Activity-dependent plasticity

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Activity-dependent_plasticity

Activity-dependent plasticity is a form of functional and structural neuroplasticity that arises from the use of cognitive functions and personal experience; hence, it is the biological basis for learning and the formation of new memories. Activity-dependent plasticity is a form of neuroplasticity that arises from intrinsic or endogenous activity, as opposed to forms of neuroplasticity that arise from extrinsic or exogenous factors, such as electrical brain stimulation- or drug-induced neuroplasticity. The brain's ability to remodel itself forms the basis of the brain's capacity to retain memories, improve motor function, and enhance comprehension and speech amongst other things. It is this trait to retain and form memories that is associated with neural plasticity and therefore many of the functions individuals perform on a daily basis. This plasticity occurs as a result of changes in gene expression which are triggered by signaling cascades that are activated by various signaling molecules (e.g., calcium, dopamine, and glutamate, among many others) during increased neuronal activity.

The brain's ability to adapt toward active functions allows humans to specialize in specific processes based on relative use and activity. For example, a right-handed person may perform any movement poorly with his/her left hand but continuous practice with the less dominant hand can cause one to become ambidextrous. Another example is if someone was born with a neurological disorder such as major depressive disorder or had a stroke that resulted in a disorder, then they are capable of retrieving much of their lost function through practice, which in turn "rewires" the brain to mitigate neurological dysfunction.

History

The idea of neural plasticity was first proposed during 1890 by William James in Principles of Psychology. During the first half of the 1900s, the word 'plasticity' was directly and indirectly rejected throughout science. Many scientists found it hard to receive funding because nearly everyone unanimously supported the fact that the brain was fully developed at adulthood and specific regions were unable to change functions after the critical period. It was believed that each region of the brain had a set and specific function. Despite this, several pioneers pushed the idea of plasticity through means of various experiments and research. There are others that helped to the current progress of activity-dependent plasticity but the following contributed very effective results and ideas early on. 

Pioneers of activity-dependent plasticity

The history of activity-dependent plasticity begins with Paul Bach y Rita. With conventional ideology being that the brain development is finalized upon adulthood, Bach y Rita designed several experiments in the late 1960s and 1970s that proved that the brain is capable of changing. These included a pivotal visual substitution method for blind people provided by tactile image projection in 1969. The basis behind this experiment was to take one sense and use it to detect another: in this case use the sense of touch on the tongue to visualize the surrounding. This experiment was years ahead of its time and lead to many questions and applications. A similar experiment was reported again by Bach y Rita in 1986 where vibrotactile stimulation was delivered to the index fingertips of naive blindfolded subjects. Even though the experiment did not yield great results, it supported the study and proposed further investigations. In 1998, his design was even further developed and tested again with a 49-point electrotactile stimulus array on the tongue. He found that five sighted adult subjects recognized shapes across all sizes 79.8% of the time, a remarkable finding that has led to the incorporation of the tongue electrotactile stimulus into cosmetically acceptable and practical designs for blind people. In later years, he has published a number of other articles including "Seeing with the brain" in 2003 where Bach y Rita addresses the plasticity of the brain relative to visual learning. Here, images are enhanced and perceived by other plastic mechanisms within the realm of information passing to the brain. 

Another pioneer within the field of activity-dependent plasticity is Michael Merzenich, currently a professor in neuroscience at the University of California, San Francisco. One of his contributions includes mapping out and documenting the reorganization of cortical regions after alterations due to plasticity. While assessing the recorded changes in the primary somatosensory cortex of adult monkeys, he looked at several features of the data including how altered schedules of activity from the skin remap to cortical modeling and other factors that affect the representational remodeling of the brain. His findings within these studies have since been applied to youth development and children with language-based learning impairments. Through many studies involving adaptive training exercises on computer, he has successfully designed methods to improve their temporal processing skills. These adaptive measures include word-processing games and comprehension tests that involve multiple regions of the brain in order to answer. The results later translated into his development of the Fast ForWord program in 1996, which aims to enhance cognitive skills of children between kindergarten and twelfth grade by focusing on developing "phonological awareness". It has proven very successful at helping children with a variety of cognitive complications. In addition, it has led to in depth studies of specific complications such as autism and intellectual disability and the causes of them. Alongside a team of scientists, Merzenich helped to provide evidence that autism probes monochannel perception where a stronger stimulus-driven representation dominates behavior and weaker stimuli are practically ignored in comparison. 

Structure of neurons

Diagram displaying components of a myelinated vertebrate motorneuron.

Neurons are the basic functional unit of the brain and process and transmit information through signals. Many different types of neurons can be identified based on their function, such as sensory neurons or motor neurons. Each responds to specific stimuli and sends respective and appropriate chemical signals to other neurons. The basic structure of a neuron is shown here on the right and consists of a nucleus that contains genetic information; the cell body, or the soma, which is equipped with dendritic branches that mostly receive the incoming inputs from other neurons; a long, thin axon that bears axon terminals which carry the output information to other neurons. The dendrites and axons are interfaced through a small connection called a synapse. This component of the neuron contains a variety of chemical messengers and proteins that allow for the transmission of information. It is the variety of proteins and effect of the signal that fundamentally lead to the plasticity feature. 

Structures and molecular pathways involved

Activity-dependent plasticity of one form or another has been observed in most areas of the brain. In particular, it is thought that the reorganization of sensory and motor maps involves a variety of pathways and cellular structures related to relative activity.

Many molecules have been implicated in synaptic plasticity. Notably, AMPA and NMDA receptors are key molecules in mechanisms of long and short-term potentiation between neurons. NMDA receptors can detect local activity due to activation and therefore modify signaling in the post-synaptic cell. The increased activity and coordination between pre- and post-synaptic receptors leads to more permanent changes and therefore result in plasticity. Hebb's postulate addresses this fact by stating that synaptic terminals are strengthened by correlated activity and will therefore sprout new branches. However, terminals that experience weakened and minimal activity will eventually lose their synaptic connection and deteriorate.

A major target of all molecular signaling is the inhibitory connections made by GABAergic neurons. These receptors exist at postsynaptic sites and along with the regulation of local inhibitory synapses have been found to be very sensitive to critical period alterations. Any alteration to the receptors leads to changed concentrations of calcium in the affected cells and can ultimately influence dendritic and axonal branching. This concentration change is the result of many kinases being activated, the byproduct of which may enhance specific gene expression.

Illustration of the elements incorporated in synaptic transmission. An action potential is generated and travels down the axon to the axon terminal, where it is released and provokes a neurotransmitter release that acts on the post-synaptic end.

 

In addition, it has been identified that the wg postsynaptic pathway, which is responsible for the coding and production of many molecules for development events, can be bidirectionally stimulated and is responsible for the downstream alteration of the postsynaptic neuron. When the wg presynaptic pathway is activated, however, it alters cytoskeletal structure through transcription and translation.

Cell adhesion molecules (CAMs) are also important in plasticity as they help coordinate the signaling across the synapse. More specifically, integrins, which are receptors for extracellular matrix proteins and involved with CAMs, are explicitly incorporated in synapse maturation and memory formation. They play a crucial role in the feedback regulation of excitatory synaptic strength, or long-term potentiation (LTP), and help to control synaptic strength by regulating AMPA receptors, which result in quick, short synaptic currents. But, it is the metabotropic glutamate receptor 1 (mGlu1) that has been discovered to be required for activity-dependent synaptic plasticity in associative learning.

Activity-dependent plasticity is seen in the primary visual cortex, a region of the brain that processes visual stimuli and is capable of modifying the experienced stimuli based on active sensing and arousal states. It is known that synaptic communication trends between excited and depressed states relative to the light/dark cycle. By experimentation on rats, it was found that visual experience during vigilant states leads to increased responsiveness and plastic changes in the visual cortex. More so, depressed states were found to negatively alter the stimulus so the reaction was not as energetic. This experiment proves that even the visual cortex is capable of achieving activity-dependent plasticity as it is reliant on both visual exploration and the arousal state of the animal.

Role in learning

Activity-dependent plasticity plays a very important role in learning and in the ability of understanding new things. It is responsible for helping to adapt an individual's brain according to the relative amount of usage and functioning. In essence, it is the brain's ability to retain and develop memories based on activity-driven changes of synaptic strength that allow stronger learning of information. It is thought to be the growing and adapting quality of dendritic spines that provide the basis for synaptic plasticity connected to learning and memory. Dendritic spines accomplish this by transforming synaptic input into neuronal output and also by helping to define the relationship between synapses. 

In recent studies, a specific gene has also been identified as having a strong role in synapse growth and activity-dependent plasticity: the microRNA 132 gene (miR132). This gene is regulated by the cAMP response element-binding (CREB) protein pathway and is capable of enhancing dendritic growth when activated. The miR132 gene is another component that is responsible for the brain's plasticity and helps to establish stronger connections between neurons. 

Another plasticity-related gene involved in learning and memory is Arc/Arg3.1. The Arc gene is activity-regulated and the transcribed mRNA is localized to activated synaptic sites where the translated protein plays a role in AMPA receptor trafficking. Arc is a member of a class of proteins called immediate early genes (IEG) that are rapidly transcribed in response to synaptic input. Of the estimated 30-40 genes that comprise the total neuronal IEG response, all are prototypical activity-dependent genes and a number have been implicated in learning and memory. For example, zif268, Arc, beta-activin, tPA, Homer, and COX-2 have all been implicated in long-term potentiation (LTP), a cellular correlate of learning and memory. 

Mechanisms involved

There are a variety of mechanisms involved in activity-dependent plasticity. These include LTP, long-term depression (LTD), synaptic elimination, neurogenesis, and synaptogenesis. The mechanisms of activity-dependent plasticity result in membrane depolarization and calcium influx, which in turn trigger cellular changes that affect synaptic connections and gene transcription. In essence, neuronal activity regulates gene expression related to dendritic branching and synapse development. Mutations in activity-dependent transcription-related genes can lead to neurological disorders. Each of the studies' findings aims to help proper development of the brain while improving a wide variety of tasks such as speech, movement, comprehension, and memory. More so, the findings better explain the development induced by plasticity. 

It is known that during postnatal life a critical step to nervous system development is synapse elimination. The changes in synaptic connections and strength are results from LTP and LTD and are strongly regulated by the release of brain-derived neurotrophic factor (BDNF), an activity-dependent synapse-development protein. In addition to BDNF, Nogo-66 receptors, and more specifically NgR1, are also involved in the development and regulation of neuronal structure. Damage to this receptor leads to pointless LTP and attenuation of LTD. Both situations imply that NgR1 is a regulator of synaptic plasticity. From experiments, it has been found that stimulation inducing LTD leads to a reduction in synaptic strength and loss of connections but, when coupled simultaneously with low-frequency stimulation, helps the restructuring of synaptic contacts. The implications of this finding include helping people with receptor damage and providing insight into the mechanism behind LTP.

Another research model of activity-dependent plasticity includes the excitatory corticostriatal pathway that is involved in information processing related to adaptive motor behaviors and displays long-lasting synaptic changes. The change in synaptic strength is responsible for motor learning and is dependent on the simultaneous activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. These are the same pathways affected in Parkinson's disease, and the degeneration of synapses within this disorder may be responsible for the loss of some cognitive abilities.

Relationship to behavior

Intellectual disability

Since plasticity is such a fundamental property of brain function due to its involvement in brain development, brain repair, and cognitive processes, its proper regulation is necessary for normal physiology. Mutations within any of the genes associated with activity-dependent plasticity have been found to positively correlate with various degrees of intellectual disability. The two types of intellectual disability related to plasticity depend on dysfunctional neuronal development or alterations in molecular mechanisms involved in synaptic organization. Complications within either of these types can greatly reduce brain capability and comprehension.

Stroke rehabilitation

On the other hand, people with such conditions have the capacity to recover some degree of their lost abilities through continued challenges and use. An example of this can be seen in Norman Doidge's The Brain That Changes Itself. Bach y Rita's father suffered from a disabling stroke that left the 65-year-old man half-paralyzed and unable to speak. After one year of crawling and unusual therapy tactics including playing basic children's games and washing pots, his father's rehabilitation was nearly complete and he went back to his role as a professor at City College in New York. This remarkable recovery from a stroke proves that even someone with abnormal behavior and severe medical complications can recover nearly all of the normal functions by much practice and perseverance. 

Recent studies have reported that a specific gene, FMR1, is highly involved in activity-dependent plasticity and fragile X syndrome (FraX) is the result of this gene's loss of function. FMR1 produces FMRP, which mediates activity-dependent control of synaptic structure. The loss or absence of this gene almost certainly leads to both autism and intellectual disability. Dr. Gatto has found that early introduction of the product FMRP results in nearly complete restructuring of the synapses. This method is not as effective, though, when introduced into a mature subject and only partially accommodates for the losses of FMR1. The discovery of this gene provides a possible location for intervention for young children with these abnormalities as this gene and its product act early to construct synaptic architecture.

Stress

A common issue amongst most people in the United States is high levels of stress and also disorders associated with continuous stress. Many regions of the brain are very sensitive to stress and can be damaged with extended exposure. More importantly, many of the mechanisms involved with increased memory retention, comprehension, and adaptation are thought to involve LTP and LTD, two activity-dependent plasticity mechanisms that stress can directly suppress. Several experiments have been conducted in order to discover the specific mechanisms for this suppression and also possible intervention methods. Dr. Li and several others have actually identified the TRPV1 channel as a target to facilitate LTP and suppress LTD, therefore helping to protect the feature of synaptic plasticity and retention of memory from the effects of stress.

Future studies

The future studies and questions for activity-dependent plasticity are nearly endless because the implications of the findings will enable many treatments. Despite many gains within the field, there are a wide variety of disorders that further understanding of activity-dependent mechanisms of plasticity would help treat and perhaps cure. These include autism, different severities of intellectual disability, schizophrenia, Parkinson's disease, stress, and stroke. In addition to a better understanding of the various disorders, neurologists should and will look at the plasticity incurred by the immune system, as it will provide great insight into diseases and also give the basis of new immune-centered therapeutics. A better perspective of the cellular mechanisms that regulate neuronal morphology is the next step to discovering new treatments for learning and memory pathological conditions.

Neuroplastic effects of pollution

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Neuroplastic_effects_of_pollution

Research indicates that living in areas of high pollution has serious long term health effects. Living in these areas during childhood and adolescence can lead to diminished mental capacity and an increased risk of brain damage. People of all ages who live in high pollution areas for extended periods place themselves at increased risk of various neurological disorders. Both air pollution and heavy metal pollution have been implicated as having negative effects on central nervous system (CNS) functionality. The ability of pollutants to affect the neurophysiology of individuals after the structure of the CNS has become mostly stabilized is an example of negative neuroplasticity.

Air pollution

Air pollution is known to affect small and large blood vessels throughout the body. High levels of air pollution are associated with increased risk of strokes and heart attacks. By permanently affecting vascular structures in the brain, air pollution can have serious effects on neural functioning and neural matter. In dogs air pollution shows to cause damage to the CNS by altering the blood–brain barrier, causing neurons in the cerebral cortex to degenerate, destroying glial cells found in white matter, and by causing neurofibrillary tangles. These changes can permanently alter brain structure and chemistry, resulting in various impairments and disorders. Sometimes, the effects of neural remodeling do not manifest themselves for a prolonged period of time.

Effects in adolescents and canines

A study from 2008 compared children and dogs raised in Mexico City (a location known for high pollution levels) with children and dogs raised in Polotitlán, Mexico (a city whose pollution levels meet the current US National Ambient Air Quality Standards). According to this study, children raised in areas of higher pollution scored lower in intelligence (i.e. on IQ tests), and showed signs of lesions in MRI scanning of the brain. In contrast, children from the low pollution area scored as expected on IQ tests, and did not show any significant sign of the risk of brain lesions. This correlation was found to be statistically significant, and shows that pollution levels may be related to, and contribute to, brain lesion formation and IQ scores, which, in turn, manifests as impaired intellectual capacity and/or performance. Living in high pollution areas thus places adolescents at risk of premature brain degeneration and improper neural development—these findings could have significant implications for future generations.

Effects in adults

There are indications that the effects of physical activity and air pollution on neuroplasticity counteract. Physical activity is known for its health-enhancing benefits, particularly on the cardiovascular system, and has also demonstrated benefits for brain plasticity processes, cognition and mental health. The neurotrophine, brain-derived neurotrophic factor (BDNF) is thought to play a key role in exercise-induced cognitive improvements. Brief bouts of physical activity have been shown to increase serum levels of BDNF, but this increase may be offset by increased exposure to traffic-related air pollution. Over longer periods of physical exercise, cognitive improvements that were demonstrated in rural joggers were found to be absent in urban joggers taking the same 12-week start-2-run training programme.

Epilepsy

Researchers in Chile found statistically-significant correlations between multiple air pollutants and the risk of epilepsy using a 95% confidence interval. The air pollutants that the researchers attempted to correlate with increased incidence of epilepsy included carbon monoxide, ozone, sulfur dioxide, nitrogen dioxide, large particulate matter, and fine particulate matter. The researchers tested these pollutants across seven cities and, in all but one case, a correlation was found between pollutant levels and the occurrence of epilepsy. All of the correlations found were shown to be statistically significant. The researchers hypothesized that air pollutants increase epilepsy risk by increasing inflammatory mediators, and by providing a source of oxidative stress. They believe that these changes eventually alter the functioning of the blood–brain barrier, causing brain inflammation. Brain inflammation is known to be a risk factor for epilepsy; thus, the sequence of events provides a plausible mechanism by which pollution may increase epilepsy risk in individuals who are genetically vulnerable to the disease. 

Dioxin poisoning

Organohalogen compounds, such as dioxins, are commonly found in pesticides or created as by-products of pesticide manufacture or degradation. These compounds can have a significant impact on the neurobiology of exposed organisms. Some observed effects of exposure to dioxins are altered astroglial intracellular calcium ion (Ca²⁺), decreased glutathione levels, modified neurotransmitter function in the CNS, and loss of pH maintenance. A study of 350 chemical plant employees exposed to a dioxin precursor for herbicide synthesis between 1965 and 1968 showed that 80 of the employees displayed signs of dioxin poisoning. Of these 350 employees, 15 were contacted again in 2004 to submit to neurological tests to assess whether the dioxin poisoning had any long-term effects on neurological capabilities. The amount of time that had passed made it difficult to assemble a larger cohort, but the results of the tests indicated that eight of the 15 subjects exhibited some central nervous system impairment, nine showed signs of polyneuropathy, and electroencephalography (EEG) showed various degrees of structural abnormalities. This study suggested that the effects of dioxins were not limited to initial toxicity. Dioxins, through neuroplastic effects, can cause long-term damage that may not manifest itself for years or even decades. 

Metal exposure

Heavy metal exposure can result in an increased risk of various neurological diseases. Research indicates that the two most neurotoxic heavy metals are mercury and lead. The impact that these two metals will have is highly dependent upon the individual due to genetic variations. Mercury and lead are particularly neurotoxic for many reasons: they easily cross cell membranes, have oxidative effects on cells, react with sulfur in the body (leading to disturbances in the many functions that rely upon sulfhydryl groups), and reduce glutathione levels inside cells. Methylmercury, in particular, has an extremely high affinity for sulfhydryl groups. Organomercury is a particularly damaging form of mercury because of its high absorbability Lead also mimics calcium, a very important mineral in the CNS, and this mimicry leads to many adverse effects. Mercury's neuroplastic mechanisms work by affecting protein production. Elevated mercury levels increase glutathione levels by affecting gene expression, and this in turn affects two proteins (MT1 and MT2) that are contained in astrocytes and neurons. Lead's ability to imitate calcium allows it to cross the blood–brain barrier. Lead also upregulates glutathione.

Autism

Heavy metal exposure, when combined with certain genetic predispositions, can place individuals at increased risk for developing autism. Many examples of CNS pathophysiology, such as oxidative stress, neuroinflammation, and mitochondrial dysfunction, could be by-products of environmental stressors such as pollution. There have been reports of autism outbreaks occurring in specific locations. Since these cases of autism are related to geographic location, the implication is that something in the environment is complementing an at-risk genotype to cause autism in these vulnerable individuals. Mercury and lead both contribute to inflammation, leading scientists to speculate that these heavy metals could play a role in autism. These findings are controversial, however, with many researchers believing that increasing rates of autism are a consequence of more accurate screening and diagnostic methods, and are not due to any sort of environmental factor.

Accelerated neural aging

Neuroinflammation is associated with increased rates of neurodegeneration. Inflammation tends to increase naturally with age. By facilitating inflammation, pollutants such as air particulates and heavy metals cause the CNS to age more quickly. Many late-onset diseases are caused by neurodegeneration. Multiple sclerosis, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and Alzheimer's disease are all believed to be exacerbated by inflammatory processes, resulting in individuals displaying signs of these diseases at an earlier age than is typically expected.

Multiple sclerosis occurs when chronic inflammation leads to the compromise of oligodendrocytes, which in turn leads to the destruction of the myelin sheath. Then axons begin exhibiting signs of damage, which in turn leads to neuron death. Multiple sclerosis has been correlated to living in areas with high particulate matter levels in the air.

In Parkinson's disease, inflammation leading to depletion of antioxidant stores will ultimately lead to dopaminergic neuron degeneration, causing a shortage of dopamine and contributing to the formation of Parkinson's disease. Chronic glial activation as a result of inflammation causes motor neuron death and compromises astrocytes, these factors leading to the symptoms of amyotrophic lateral sclerosis (ALS, aka Lou Gehrig's disease).

In the case of Alzheimer's disease, inflammatory processes lead to neuron death by inhibiting growth at axons and activating astrocytes that produce proteoglycans. This product can only be deposited in the hippocampus and cortex, indicating that this may be the reason these two areas show the highest levels of degeneration in Alzheimer's disease. Airborne metal particulates have been shown to directly access and affect the brain through olfactory pathways, which allows a large amount of particulate matter to reach the blood–brain barrier.

These facts, coupled with air pollution's link to neurofibrillary tangles and the observed subcortical vascular changes observed in dogs, imply that the negative neuroplastic effects of pollution could result in increased risk for Alzheimer's disease, and could also implicate pollution as a cause of early-onset Alzheimer's disease through multiple mechanisms. The general effect of pollution is increased levels of inflammation. As a result, pollution can significantly contribute to various neurological disorders that are caused by inflammatory processes.

Recrystallization (chemistry)

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Recrystallization_(chemistry)

 

Crystallization
Concepts
Crystallization · Crystal growth Recrystallization · Seed crystal Protocrystalline · Single crystal
Methods and technology
Boules Bridgman–Stockbarger technique Crystal bar process Czochralski process Epitaxy Flux method Fractional crystallization Fractional freezing Hydrothermal synthesis Kyropoulos process Laser-heated pedestal growth Micro-pulling-down Shaping processes in crystal growth Skull crucible Verneuil process Zone melting
Fundamentals
Nucleation · Crystal Crystal structure · Solid

In chemistry, recrystallization is a technique used to purify chemicals. By dissolving both impurities and a compound in an appropriate solvent, either the desired compound or impurities can be removed from the solution, leaving the other behind. It is named for the crystals often formed when the compound precipitates out. Alternatively, recrystallization can refer to the natural growth of larger ice crystals at the expense of smaller ones.

Chemistry

In chemistry, recrystallization is a procedure for purifying compounds. The most typical situation is that a desired "compound A" is contaminated by a small amount of "impurity B". There are various methods of purification that may be attempted, recrystallization being one of them. There are also different recrystallization techniques that can be used such as: 

Single-solvent recrystallization

Typically, the mixture of "compound A" and "impurity B" is dissolved in the smallest amount of hot solvent to fully dissolve the mixture, thus making a saturated solution. The solution is then allowed to cool. As the solution cools the solubility of compounds in solution drops. This results in the desired compound dropping (recrystallizing) from solution. The slower the rate of cooling, the bigger the crystals form. 

→ Solvent added (clear) to compound (orange) → Solvent heated to give saturated compound solution (orange) → Saturated compound solution (orange) allowed to cool over time to give crystals (orange) and a saturated solution (pale-orange).

 

Crystallization of Ibuprofen in HCl(aq)

In an ideal situation the solubility product of the impurity, B, is not exceeded at any temperature. In that case the solid crystals will consist of pure A and all the impurity will remain in solution. The solid crystals are collected by filtration and the filtrate is discarded. If the solubility product of the impurity is exceeded, some of the impurity will co-precipitate. However, because of the relatively low concentration of the impurity, its concentration in the precipitated crystals will be less than its concentration in the original solid. Repeated recrystallization will result in an even purer crystalline precipitate. The purity is checked after each recrystallization by measuring the melting point, since impurities lower the melting point. NMR spectroscopy can also be used to check the level of impurity. Repeated recrystallization results in some loss of material because of the non-zero solubility of compound A.

The crystallization process requires an initiation step, such as the addition of a "seed" crystal. In the laboratory a minuscule fragment of glass, produced by scratching the side of the glass recrystallization vessel, may provide the nucleus on which crystals may grow. Successful recrystallization depends on finding the right solvent. This is usually a combination of prediction/experience and trial/error. The compounds must be more soluble at the higher temperature than at the lower temperatures. Any insoluble impurity is removed by the technique of hot filtration. 

Multi-solvent recrystallization

This method is the same as the above but where two (or more) solvents are used. This relies on both "compound A" and "impurity B" being soluble in a first solvent. A second solvent is slowly added. Either "compound A" or "impurity B" will be insoluble in this solvent and precipitate, whilst the other of "compound A"/"impurity B" will remain in solution. Thus the proportion of first and second solvents is critical. Typically the second solvent is added slowly until one of the compounds begins to crystallize from solution and then the solution is cooled. Heating is not required for this technique but can be used. 

→ Solvent added (clear) to compound (orange) → Solvent heated to give saturated compound solution (orange) → Second solvent (blue) added to compound solution (orange) to give mixed solvent system (green) → Mixed solvent system (green) allowed to cool over time to give crystals (orange) and a saturated mixed solvent system (green-blue).

 

The reverse of this method can be used where a mixture of solvent dissolves both A and B. One of the solvents is then removed by distillation or by an applied vacuum. This results in a change in the proportions of solvent causing either "compound A" or "impurity B" to precipitate.

→ First solvent added (clear) to compound (orange) → Solvent heated to give saturated compound solution (orange) → Second solvent (blue) added to compound solution (orange) to give first mixed solvent system (green) → Volatile first solvent (clear) is removed (e.g. evaporation) from first mixed solvent system (green) to give a second mixed solvent system (dark-green) → Second mixed solvent system (dark-green) allowed to cool over time to give crystals (orange) and a saturated second mixed solvent system (green-blue).

 

Hot filtration-recrystallization

Hot filtration can be used to separate "compound A" from both "impurity B" and some "insoluble matter C". This technique normally uses a single-solvent system as described above. When both "compound A" and "impurity B" are dissolved in the minimum amount of hot solvent, the solution is filtered to remove "insoluble matter C". This matter may be anything from a third impurity compound to fragments of broken glass. For a successful procedure, one must ensure that the filtration apparatus is hot in order to stop the dissolved compounds crystallizing from solution during filtration, thus forming crystals on the filter paper or funnel.

One way to achieve this is to heat a conical flask containing a small amount of clean solvent on a hot plate. A filter funnel is rested on the mouth, and hot solvent vapors keep the stem warm. Jacketed filter funnels may also be used. The filter paper is preferably fluted, rather than folded into a quarter; this allows quicker filtration, thus less opportunity for the desired compound to cool and crystallize from the solution.

Often it is simpler to do the filtration and recrystallization as two independent and separate steps. That is dissolve "compound A" and "impurity B" in a suitable solvent at room temperature, filter (to remove insoluble compound/glass), remove the solvent and then recrystallize using any of the methods listed above. 

→ Solvent added (clear) to a mixture of compound (orange) + insoluble substance (purple) → Solvent heated to give saturated compound solution (orange) + insoluble substance (purple) → Saturated compound solution (orange) filtered to remove insoluble substance (purple) → Saturated compound solution (orange) allowed to cool over time to give crystals (orange) and a saturated solution (pale-orange).

 

Seeding

Crystallization requires an initiation step. This can be spontaneous or can be done by adding a small amount of the pure compound (a seed crystal) to the saturated solution, or can be done by simply scratching the glass surface to create a seeding surface for crystal growth. It is thought that even dust particles can act as simple seeds.

Single perfect crystals (for X-ray analysis)

Growing crystals for X-ray crystallography can be quite difficult. For X-ray analysis, single perfect crystals are required. Typically a small amount (5–100 mg) of pure compound is used, and crystals are allowed to grow very slowly. Several techniques can be used to grow these perfect crystals:

• Slow evaporation of a single solvent - typically the compound is dissolved in a suitable solvent and the solvent is allowed to slowly evaporate. Once the solution is saturated crystals can form.

→ Solvent added (clear) to compound (orange) to give compound solution (orange) → Vessel sealed but a small hole allows solvent vapour (clear) to slowly evaporate from compound solution (orange) over time to give crystals (orange) and a saturated solution (pale-orange).

• Slow evaporation of a multi-solvent system - the same as above, however as the solvent composition changes due to evaporation of the more volatile solvent. The compound is more soluble in the volatile solvent, and so the compound becomes increasingly insoluble in solution and crystallizes.

→ Solvent added (clear) to compound (orange) to give compound solution (orange) → Second solvent added (blue) to compound solution (orange) to give mixed solvent system (green) → Vessel sealed but a small hole allows solvent vapour (clear) to slowly evaporate over time to give crystals (orange) and a saturated mixed solvent solution (blue-green).

• Slow diffusion - similar to the above. However, a second solvent is allowed to evaporate from one container into a container holding the compound solution (gas-diffusion). As the solvent composition changes due to an increase in solvent that has gas-diffused into solution, the compound become increasingly insoluble in solution and crystallizes.

→ Solvent added (clear) to compound (orange) in first vessel to give compound solution (orange) → First vessel is placed in a second vessel contain second solvent (blue). The second vessel is sealed, the first vessel is also sealed, although a small hole in the first vessel is present. This hole allows volatile solvent vapour (blue) to slowly evaporate from second vessel and condensate (that is infuse) into the first vessel, to give a mixed solvent system (green) → Over time this gives crystals (orange) and a saturated mixed solvent system (green-blue).

• Interface/slow mixing (often performed in an NMR tube). Similar to the above, but instead of one solvent gas-diffusing into another, the two solvents mix (diffuse) by liquid-liquid diffusion. Typically a second solvent is "layered" carefully on top of the solution containing the compound. Over time the two solution mix. As the solvent composition changes due to diffusion, the compound becomes increasingly insoluble in solution and crystallizes, usually at the interface. Additionally, it is better to use a denser solvent as the lower layer, and/or a hotter solvent as the upper layer because this results in the slower mixing of the solvents.

→ Solvent added (clear) to compound (orange) to give compound solution (orange) → Second solvent added (blue) carefully so that the two solvents do not mix. → The two solvents mix (diffuse) slowly over time to give crystals (orange) at solvent interface (green)

• Specialized equipment can be used in the shape of a "H" to perform the above, where one of the vertical line of the "H" is a tube containing a solution of the compound, and the other vertical line of the "H" is a tube containing a solvent which the compound is not soluble in, and the horizontal line of the "H" is a tube which joins the two vertical tubes, which also has a fine glass sinter that restricts the mixing of the two solvents.

→ Solvent added (clear) to compound (orange) to give a compound solution (orange) → Second solvent added (blue) to the second tube chamber → The two solvents mix slowly over time, the mixing is slowed by a fine sinter separating the two solvent chambers, to give crystals (orange) at solvent interface (green) over time

• Once single perfect crystals have been obtained, it is recommended that the crystals are kept in a sealed vessel with some of the liquid of crystallisation to prevent the crystal from 'drying out'. Single perfect crystals may contain solvent of crystallisation in the crystal lattice. Loss of this internal solvent from the crystals can result in the crystal lattice breaking down, and the crystals turning to powder.

Ice

For ice, recrystallization refers to the growth of larger crystals at the expense of smaller ones. Some biological antifreeze proteins have been shown to inhibit this process, and the effect may be relevant in freezing-tolerant organisms.

Igneous differentiation

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In geology, igneous differentiation, or magmatic differentiation, is an umbrella term for the various processes by which magmas undergo bulk chemical change during the partial melting process, cooling, emplacement, or eruption.

Definitions

Primary melts

When a rock melts to form a liquid, the liquid is known as a primary melt. Primary melts have not undergone any differentiation and represent the starting composition of a magma. In nature, primary melts are rarely seen. Some leucosomes of migmatites are examples of primary melts. Primary melts derived from the mantle are especially important and are known as primitive melts or primitive magmas. By finding the primitive magma composition of a magma series, it is possible to model the composition of the rock from which a melt was formed, which is important because we have little direct evidence of the Earth's mantle.

Parental melts

Where it is impossible to find the primitive or primary magma composition, it is often useful to attempt to identify a parental melt. A parental melt is a magma composition from which the observed range of magma chemistries has been derived by the processes of igneous differentiation. It need not be a primitive melt.

For instance, a series of basalt lava flows is assumed to be related to one another. A composition from which they could reasonably be produced by fractional crystallization is termed a parental melt. To prove this, fractional crystallization models would be produced to test the hypothesis that they share a common parental melt. 

Cumulate rocks

Fractional crystallization and accumulation of crystals formed during the differentiation process of a magmatic event are known as cumulate rocks, and those parts are the first which crystallize out of the magma. Identifying whether a rock is a cumulate or not is crucial for understanding if it can be modelled back to a primary melt or a primitive melt, and identifying whether the magma has dropped out cumulate minerals is equally important even for rocks which carry no phenocrysts.

Underlying causes of differentiation

The primary cause of change in the composition of a magma is cooling, which is an inevitable consequence of the magma being created and migrating from the site of partial melting into an area of lower stress - generally a cooler volume of the crust.

Cooling causes the magma to begin to crystallize minerals from the melt or liquid portion of the magma. Most magmas are a mixture of liquid rock (melt) and crystalline minerals (phenocrysts). 

Contamination is another cause of magma differentiation. Contamination can be caused by assimilation of wall rocks, mixing of two or more magmas or even by replenishment of the magma chamber with fresh, hot magma.

The whole gamut of mechanisms for differentiation has been referred to as the FARM process, which stands for Fractional crystallization, Assimilation, Replenishment and Magma mixing.

Fractional crystallization of igneous rocks

Fractional crystallization is the removal and segregation from a melt of mineral precipitates, which changes the composition of the melt. This is one of the most important geochemical and physical processes operating within the Earth's crust and mantle.

Fractional crystallization in silicate melts (magmas) is a very complex process compared to chemical systems in the laboratory because it is affected by a wide variety of phenomena. Prime amongst these are the composition, temperature, and pressure of a magma during its cooling.

The composition of a magma is the primary control on which mineral is crystallized as the melt cools down past the liquidus. For instance in mafic and ultramafic melts, the MgO and SiO₂ contents determine whether forsterite olivine is precipitated or whether enstatite pyroxene is precipitated.

Two magmas of similar composition and temperature at different pressure may crystallize different minerals. An example is high-pressure and high-temperature fractional crystallization of granites to produce single-feldspar granite, and low-pressure low-temperature conditions which produce two-feldspar granites.

The partial pressure of volatile phases in silicate melts is also of prime importance, especially in near-solidus crystallization of granites. 

Assimilation

Assimilation is a popular mechanism for explaining the felsification of ultramafic and mafic magmas as they rise through the crust. Assimilation assumes that a hot primitive melt intruding into a cooler, felsic crust will melt the crust and mix with the resulting melt. This then alters the composition of the primitive magma. Also pre-existing mafic host rocks can be assimilated, with little effect on the bulk magma chemistry.

 

Effects of this kind are to be expected, and have been clearly proven in many places. There is, however, a general reluctance to admit that they are of great importance. The nature and succession of the rock types do not as a rule show any relation to the sedimentary or other materials which may be supposed to have been dissolved; and where solution is known to have gone on the products are usually of abnormal character and easily distinguishable from the common rock types.

Replenishment

When a melt undergoes cooling along the liquid line of descent, the results are limited to the production of a homogeneous solid body of intrusive rock, with uniform mineralogy and composition, or a partially differentiated cumulate mass with layers, compositional zones and so on. This behaviour is fairly predictable and easy enough to prove with geochemical investigations. In such cases, a magma chamber will form a close approximation of the ideal Bowen's reaction series. However, most magmatic systems are polyphase events, with several pulses of magmatism. In such a case, the liquid line of descent is interrupted by the injection of a fresh batch of hot, undifferentiated magma. This can cause extreme fractional crystallisation because of three main effects:

• Additional heat provides additional energy to allow more vigorous convection, allows resorption of existing mineral phases back into the melt, and can cause a higher-temperature form of a mineral or other higher-temperature minerals to begin precipitating
• Fresh magma changes the composition of the melt, changing the chemistry of the phases which are being precipitated. For instance, plagioclase conforms to the liquid line of descent by forming initial anorthite which, if removed, changes the equilibrium mineral composition to oligoclase or albite. Replenishment of the magma can see this trend reversed, so that more anorthite is precipitated atop cumulate layers of albite.
• Fresh magma destabilises minerals which are precipitating as solid solution series or on a eutectic; a change in composition and temperature can cause extremely rapid crystallisation of certain mineral phases which are undergoing a eutectic crystallisation phase.

Magma mixing

Magma mixing is the process by which two magmas meet, comingle, and form a magma of a composition somewhere between the two end-member magmas. 

Magma mixing is a common process in volcanic magma chambers, which are open-system chambers where magmas enter the chamber, undergo some form of assimilation, fractional crystallisation and partial melt extraction (via eruption of lava), and are replenished.

Magma mixing also tends to occur at deeper levels in the crust and is considered one of the primary mechanisms for forming intermediate rocks such as monzonite and andesite. Here, due to heat transfer and increased volatile flux from subduction, the silicic crust melts to form a felsic magma (essentially granitic in composition). These granitic melts are known as an underplate. Basaltic primary melts formed in the mantle beneath the crust rise and mingle with the underplate magmas, the result being part-way between basalt and rhyolite; literally an 'intermediate' composition. 

Other mechanisms of differentiation

Interface entrapment Convection in a large magma chamber is subject to the interplay of forces generated by thermal convection and the resistance offered by friction, viscosity and drag on the magma offered by the walls of the magma chamber. Often near the margins of a magma chamber which is convecting, cooler and more viscous layers form concentrically from the outside in, defined by breaks in viscosity and temperature. This forms laminar flow, which separates several domains of the magma chamber which can begin to differentiate separately.

Flow banding is the result of a process of fractional crystallization which occurs by convection, if the crystals which are caught in the flow-banded margins are removed from the melt. The friction and viscosity of the magma causes phenocrysts and xenoliths within the magma or lava to slow down near the interface and become trapped in a viscous layer. This can change the composition of the melt in large intrusions, leading to differentiation.

Partial melt extraction
With reference to the definitions, above, a magma chamber will tend to cool down and crystallize minerals according to the liquid line of descent. When this occurs, especially in conjunction with zonation and crystal accumulation, and the melt portion is removed, this can change the composition of a magma chamber. In fact, this is basically fractional crystallization, except in this case we are observing a magma chamber which is the remnant left behind from which a daughter melt has been extracted.

If such a magma chamber continues to cool, the minerals it forms and its overall composition will not match a sample liquid line of descent or a parental magma composition. 

Typical behaviours of magma chambers

It is worth reiterating that magma chambers are not usually static single entities. The typical magma chamber is formed from a series of injections of melt and magma, and most are also subject to some form of partial melt extraction.

Granite magmas are generally much more viscous than mafic magmas and are usually more homogeneous in composition. This is generally considered to be caused by the viscosity of the magma, which is orders of magnitude higher than mafic magmas. The higher viscosity means that, when melted, a granitic magma will tend to move in a larger concerted mass and be emplaced as a larger mass because it is less fluid and able to move. This is why granites tend to occur as large plutons, and mafic rocks as dikes and sills.

Granites are cooler and are therefore less able to melt and assimilate country rocks. Wholesale contamination is therefore minor and unusual, although mixing of granitic and basaltic melts is not unknown where basalt is injected into granitic magma chambers.

Mafic magmas are more liable to flow, and are therefore more likely to undergo periodic replenishment of a magma chamber. Because they are more fluid, crystal precipitation occurs much more rapidly, resulting in greater changes by fractional crystallisation. Higher temperatures also allow mafic magmas to assimilate wall rocks more readily and therefore contamination is more common and better developed. 

Dissolved gases

All igneous magmas contain dissolved gases (water, carbonic acid, hydrogen sulfide, chlorine, fluorine, boric acid, etc.). Of these water is the principal, and was formerly believed to have percolated downwards from the Earth's surface to the heated rocks below, but is now generally admitted to be an integral part of the magma. Many peculiarities of the structure of the plutonic rocks as contrasted with the lavas may reasonably be accounted for by the operation of these gases, which were unable to escape as the deep-seated masses slowly cooled, while they were promptly given up by the superficial effusions. The acid plutonic or intrusive rocks have never been reproduced by laboratory experiments, and the only successful attempts to obtain their minerals artificially have been those in which special provision was made for the retention of the "mineralizing" gases in the crucibles or sealed tubes employed. These gases often do not enter into the composition of the rock-forming minerals, for most of these are free from water, carbonic acid, etc. Hence as crystallization goes on the residual melt must contain an ever-increasing proportion of volatile constituents. It is conceivable that in the final stages the still uncrystallized part of the magma has more resemblance to a solution of mineral matter in superheated steam than to a dry igneous fusion. Quartz, for example, is the last mineral to form in a granite. It bears much of the stamp of the quartz which we know has been deposited from aqueous solution in veins, etc. It is at the same time the most infusible of all the common minerals of rocks. Its late formation shows that in this case it arose at comparatively low temperatures and points clearly to the special importance of the gases of the magma as determining the sequence of crystallization.

When solidification is nearly complete the gases can no longer be retained in the rock and make their escape through fissures towards the surface. They are powerful agents in attacking the minerals of the rocks which they traverse, and instances of their operation are found in the kaolinization of granites, tourmalinization and formation of greisen, deposition of quartz veins, and the group of changes known as propylitization. These "pneumatolytic" processes are of the first importance in the genesis of many ore deposits. They are a real part of the history of the magma itself and constitute the terminal phases of the volcanic sequence.

Quantifying igneous differentiation

There are several methods of directly measuring and quantifying igneous differentiation processes;

• Whole rock geochemistry of representative samples, to track changes and evolution of the magma systems
  • Using the above, calculating normative mineralogy and investigating trends
• Trace element geochemistry
• Isotope geochemistry
  • Investigating the contamination of magma systems by wall rock assimilation using radiogenic isotopes

In all cases, the primary and most valuable method for identifying magma differentiation processes is mapping the exposed rocks, tracking mineralogical changes within the igneous rocks and describing field relationships and textural evidence for magma differentiation.