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Erowid/BlueLight Neuropharmacology Text

Hmm, might I suggest that people only write things that they believe they have an extensive interest in.
 
^^^ I hoped that was kind of implied... either interest or knowledge...

Anyways, heres my first attempt at a chapter, have fun hacking it to bits (Figures will come much later).

Electrical properties of the Neuron

As already mentioned, one of the most distinctive and functionally important property of a neuron is that it is electrically excitable. This excitability is an emergent property of the neurons ability to alter its membrane potential (the word potential can be used interchangeably with voltage). All cells have a membrane potential, and it is generated by the uneven distribution of charged atoms (ions) across the cells membrane, which is impermeable to these ions. The most important ions for generating and altering the membrane potential are the positively charged sodium (Na+) and potassium ions (K+), and the negatively charged chloride ions (Cl-). In general, Na+ and Cl- is found at a higher concentration outside the cell, while K+ is found at high concentration inside the cell. The distribution is found because a protein, usually called the Na+-K+ pump (or ATPase), swaps three intracellular Na+ ions for two extracellular K+ ions. Not only does this action produce a chemical gradient of high extracellular Na+ and intracellular K+, but it also produces a electrical gradient because it swaps three intracellular positive charges, for two extracellular positive charges i.e. a net movement of one positive charge out of the cell. The eventually leads to a difference of charges, i.e. a voltage, of somewhere around –50 to –80mV. This is called the resting potential

Because particles have a natural urge to equally distribute themselves (2nd law of thermodynamics), it can be said that there is a chemical driving force on these unevenly spread ions. Na+ wants to flow into the cell, and K+ wants to flow out of the cell (i.e. into the areas where the particular ion is at low concentration). Because charged particles are attracted to areas of opposite charge, there is also an electrical driving force on the ions. Na+ wants to flow into the negatively charged cell, which would make the cell more positive, and if this was allowed to happen, it would make the cell increasing positive until the cell became so positive it began to repel the positively charged Na+. Eventually, the electrical force pushing Na+ out would become equal to the chemical force drawing it in. The voltage at which a cell would usually reach this Na+ equilibrium is around +55mV (called the Na+ equilibrium potential or reversal potential).

K+ wishes to leave the cell because of its high intracellular concentration and if it did so, it would make the cell increasing negative, until the electrical force drawing K+ back into the cell caused K+ flow to reach equilibrium. This K+ equilibrium potential is around –75mV. Because Cl- is a negative ion, it is repelled from entering the negative cell, even though there is a chemical force drawing it in (because of the high extracellular concentration). So Cl- has its equilibrium potential around –60mV, or very close to the membrane potential. This means that if the cell at resting potential became permeable to Cl-, not much Cl- would flow. Ca2+ is another important ion, which is distributed nearly exclusively extracellularly, and has an equilibrium potential of around +60mV. Importantly, you can see that the distribution of a particular ion, and the charge of the cell, dictates that ions equilibrium potential, which is the voltage that ion is trying to pull the cell towards.

This brings us back to the important property of the neuron: it is excitable. A neuron’s cell membrane can rapidly change its permeability to particular ions, by opening ion channels. Ion channels are pores formed by proteins that allow the flow of ions (usually a particular kind). Usually, these ion channels are can be opened (i.e. gated), by chemicals or by the cells voltage, which leads these kinds of ion channels to be called ligand, or voltage gated ion channels respectively. These channels are explained in more detail in the next chapters.

If the membrane of a cell were to suddenly become permeable to K+ ions due to potassium channels opening, potassium would flow out of the cell. This would make the cell more negative than its usual resting potential, down to a maximum of the K+ equilibrium potential of –75mV. When a cell becomes more negative than usual, it can be described as being hyperpolarised. If, on the other hand, the cell became permeable to Na+ ions, because of sodium channels opening, Na+ would flow into the cell, making the cell less negative, and up to a maximum of +55mV. When a cell becomes less negative than usual it can be described as being depolarised.

You can see that the neuron has a mechanism for changing its membrane potential. While it may not be obvious to you now why this is so important, it will be explained in the following chapters how this allows the neuron integrate as well as transmit information over long distances.
 
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Voltage gated ion channels

As already mentioned ion channels are pores in the membrane of a cell which allow ions to pass through the otherwise impermeable membrane. These channels can be gated (i.e. opened) by various things. In this chapter we will look at ion channels which can be gated by the voltage across the cells membrane itself, or voltage-gated ion channels.

There are many individual kinds of voltage-gated ion channels, but all we will be concerned about are three large families, voltage-gated sodium, potassium and calcium ion channels; channels, which when open pass sodium, potassium and calcium respectively.

The most important function of two of these voltage gated ion channels is to generate the action potential. The action potential is a often thought of as an electrical signal which passes down the axons of neurons, like current down a wire. In reality it is caused by a chain reaction of voltage gated ion channels opening. The third channel is responsible for converting the electrical nature of the action potential into chemical signals a neuron can deal with.

If a part of a neuron expressing voltage gated sodium and potassium channels (usually the axon and cell body) became depolarized (less positive) to around –50mV, voltage gated ion channels start to become active i.e. they reach threshold. At the cell body, the fastest activating voltage gated ion channel is the sodium channel. The sodium channels start to open, allowing Na+ to enter the cell, further depolarizing the cell, encouraging more sodium channels to open. The Na+ passively diffuses down the axon of the neuron, causing neighboring areas of neurons to become depolarized, where further voltage gated sodium channels open. This causes a chain reaction of Na+ entering the cell, depolarizing close-by areas of cell, opening further sodium channels, causing more Na+ to pour into the cell etc… If this were to happen unabated, the neuron would fire one action potential, Na+ would reach its equilibrium potential and the cell would become electrically dead. But two things happen to stop this, 1) sodium channels inactivate and 2) slower activating potassium channels being to open.

Inactivation of sodium channels happens normally around 1 millisecond after they begin to open. Inactivation is a transient block of a channel, which in the case of voltage gated sodium channels is caused by a length of the protein which forms the channel, physically blocking the channel like a cork. This inactivation limits both the time and voltage of the action potential. As stated, inactivation is transient, and if the neuron wasn’t returned to its resting potential, or at least below threshold, as soon as inactivation passed, the sodium channels would open again. This is when voltage gated potassium channels began to play their part. As potassium channels take about 1-2ms to open after they reach threshold, they are beginning to become fully activated when sodium channel inactivation is in full swing. K+ ions being to flood out of the cell, rapidly making the neuron more negative (repolarizing). Potassium channels do not show inactivation, but as they act to repolarize the cell the pull it below the threshold for sodium and potassium channel activation, which closes the potassium channels.

Importantly the action potential is all-or-none, that is to say, the body can’t code information in the amplitude of the action potential, the action potential either happens or it doesn’t. The body codes information in the frequency of action potentials. For instance, in neurons which transmit pain, more painful stimuli causes the neurons to fire more frequently, but with the same amplitude. Cocaine, apart from its well-known action of increasing dopamine, also blocks voltage gated sodium channels, which stops the formation and propagation of the action potential. This is why it causes numbness, by blocking the transmission in sensory neurons.

Finally, when the action potential has travelled the whole length of the axon, it depolarizes the ends of the neuron, (usually -synaptic terminals-), here voltage gated calcium channels can open, causing Ca2+ to enter the cell. This Ca2+ influx causes neurotransmitter release (as described in the synapse). Although this Ca2+ influx shares many properties with the sodium/potassium action potential, it is not all-or-none. Alcohol is believed to inhibit Ca2+ channel function directly (Hendricson et al., 2003), and many common drugs effects Ca2+ channel indirectly. For instance, D9-THC from cannabis and yohimbine from Yohimbe. By effecting Ca2+ influx, these drugs effect neurotransmitter release (discussed further in the synapse and G-Protein Coupled Receptors, and signalling cascades).

References
Hendricson AW, Thomas MP, Lippmann MJ, Morrisett RA. Suppression of L-type voltage-gated calcium channel-dependent synaptic plasticity by ethanol: analysis of miniature synaptic currents and dendritic calcium transients. J Pharmacol Exp Ther. 2003;307(2):550-8
 
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Ligand gated ion channels

Ligand gated ion channels are, as their name suggests, channels in a cells membrane that are gated by ligands, i.e. drugs/chemicals. The physiological role of nearly all ligand gated ion channels is to receive chemical signals in the way of neurotransmitters (discussed further in the synapse), and to transduce them to electrical signals. In order for these ion channels to be gated by a neurotransmitter, they have a receptor for the specific neurotransmitter as part of the proteins that make up the receptors. Therefore the ion channel complex is often refereed to by the name of the neurotransmitter/chemical/drug which is has a receptor for, and for the rest of this chapter we will largely use this style.

The two most common types ligand gated ion channels (also called ionotropic receptors) are the ion channels that are opened by the neurotransmitters glutamate and GABA, or ionotropic glutamate and GABA receptors. The ionotropic glutamate receptors may be further divided up into AMPA, kainic acid and NMDA receptors (named after drugs that specifically activate these types). While it is possible to further subdivide these receptors based on the individual proteins that make them up, it is outside the scope of this text. AMPA and kainic acid receptors are generally similar; both are opened by glutamate and both are largely selective for the flow of Na+ ions, which in all physiological situations is into the neuron. This flow of Na+ depolarizes the cell, making it more positive and bringing it closer to the threshold for firing an action potential. Because of this, it can be said that AMPA and kainic acid receptors are “excitatory”. The NMDA receptor is an anomaly amongst ligand gated ion channels, in that it is also partially voltage gated. The channel of the NMDA receptor has a site in which Mg2+ ions can sit. This Mg2+ is much larger than the normal ions that flow through the NMDA receptor (Na+ and Ca2+) and hence blocks it. When the cell partially depolarized, positive Mg2+ ions begin to be pushed out of the NMDA receptor channel (presumably because of the positive charge inside the neuron repelling it). Also, because the NMDA receptor is very permeable to Ca2+ channels, not only does it depolarize (excite) the cell, it also can cause many of the chemical changes within the cell caused by Ca2+ (see G-Protein Coupled Receptors, and signalling cascades). Largely, it is the release of glutamate, and its action of ionotropic glutamate receptors that allow one cell to excite another cell into firing (although usually it requires 100s of cells to release glutamate onto a cell to cause this).

The most famous drugs which directly effect ionotropic glutamate receptors are the so called “anaesthetic dissociates”, e.g. ketamine, PCP and DXM. These drugs all block the NMDA receptors ion channel, i.e. they are NMDA channel antagonists. Alcohol's actions is thought to be at least in part due to its ability to block NMDA receptor channels (Woodward, 2000).

The ligand gated ion channel that is gated by GABA is called the GABA-A receptor (to distinguish it from the non-ion channel GABA-B receptor). This channel is largely selective for the transit of Cl- ions. As stated before, Cl- ions have a reversal potential of around -60mV, so if a cell has a resting membrane potential of around –60mV GABA-A receptors do not cause much of an effect on membrane potential i.e. they neither hyperpolarise nor depolarise the cell. But if the cell is being depolarised by the action of ionotropic glutamate receptors, then GABA-A receptors strongly oppose this, and hence its action is often referred to as inhibitory).

A wealth of drugs directly effect GABA-A receptors, specifically benzodiazepines and barbiturates which bind to sites apart from the GABA binding site or the channel, to increase channel opening only when GABA normally opens the receptor. This is an example of allosteric modulation, and is a common feature of ligand gated ionc channels. Muscimol is a direct agonist, acting like GABA. Alcohol is also though to stimulate GABA-A receptors, though whether this is a direct action is still debated (Aguaya et al., 2002)

There are other kinds of ligand gated ion channels, though the only ones which have much relevance to recreational drugs are the ionotropic acetylcholine and serotonin receptors, also called the nicotinic and 5-HT3 receptors. Both of these receptors are ligand gated sodium channels. Nicotine activates the nicotinic receptor, and serotonin, which could be released by the action of MDMA, can activate 5-HT3 receptors (which may cause MDMA-induced vomiting). There are also the glycine, P2X and VR1 ligand gated ion channels expressed in the central nervous system.

As you can see, ligand gated ion channels are an important (probably the most important) mechanism of neuron-to-neuron communication, and drugs acting on this form of chemical to electrical transmission have a powerful way to alter neuronal activity (discussed more in Signalling properties of neurons).

References
Woodward JJ. Ethanol and NMDA receptor signaling. Crit Rev Neurobiol. 2000;14(1):69-89.


Aguayo LG, Peoples RW, Yeh HH, Yevenes GE. GABA(A) receptors as molecular sites of ethanol action. Direct or indirect actions? Curr Top Med Chem. 2002; 2(8):869-85.
 
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^^^ 2400 words in a day, not bad... The bolded words are where I think we should have links to other chapters...
 
Im sure there's plenty of people with adequate undergrad + cell biology and chemistry to make redundant anything i might have to offer, but id just like to say what a fantastic idea this is, and mad props to you all for undertaking such a piece of work.
 
What is a Receptor?

Pharmacologically speaking, a receptor is a structure where a chemical/drug binds with some kind of specificity, and produces some kind of biological effect. A chemical that binds to a receptor is called a ligand. Receptors are usually locations on proteins where ligand binding can cause a change in the shape (conformation) and cause the protein to become ‘active’ in some way. Ligands basically come in two main types: ones that bind to a receptor and activate it, or ones that bind to the receptor and do not activate it, these are called agonists and antagonists respectively. Ligand binding also happens in two main ways, reversibly and irreversibly. Simply a ligand may either approach, bind to and dissociate from a receptor, in a fully reversibly manner, or when a ligand binds to a receptor chemical bonds (covalent) form between them, effectively locking the ligand onto the receptor. Most recreational drugs are reversible ligands, though there are some exceptions (deprenyl).

The reversible binding of ligands is caused by an electrostatic attraction between the ligand and the receptor. Parts of the ligand that may be positively charged might have corresponding negatively charged areas on the receptor, and the converse for negatively charged parts of the ligand to positively charged sections of the receptor. This is why ligands that bind to the same receptors often have similar structures: they must all fit into the same location.

Generally speaking, neurotransmitters and hormones are agonists at receptors. However many drugs are antagonists at receptors. Although strictly speaking a receptor is simply a location on a protein, with the exception of enzymes, often the entire protein is labeled as the receptor for its most famous ligand e.g. the entire protein which is activated by nicotine is called the nicotinic receptor. This double use of the word receptor can become confusing when a protein has many receptor sites on it e.g. the GABA-A receptor protein not only has a receptor for the neurotransmitter GABA, but it also has independent receptors for benzodiazepines, barbiturates and thujone. These different ligands alter the activity of the same protein, but do not compete for the same receptor, hence one can describe them as non-competitive ligands, e.g. thujone is a non-competitive antagonist of the GABA-A receptor. On the other hand many drugs are competitive, for instance most antipsychotic drugs compete for the same binding site as dopamine on dopamine receptors so it can be said they antipsychotives are competitive antagonists at the dopamine receptor. One can also have situations whether neither of these terms explain the drug in quesiton. The classical example of this are the benzodiazepines, drugs which bind to, and modulate the GABA-A receptor. These drugs are neither truely agonists nor antagonists, as they have no effect on the receptor themselves, however, they massively potentiate the activity of GABA. This is often called allosteric modulation, specifically positive allosteric modulation.

The situation gets more complicated still, when ligands can be not just agonists or antagonists, but somewhere in-between, or so called partial agonists. Partial agonists bind to and activate receptors, but not to the same extent as full agonists. This ability of a ligand to activate a receptors is called it' efficacy, and is usually given as a percentage of a full agonist, so an antagonist has 0% efficacy, while a full agonist has 100%, and a partial agonist has somewhere in-between. LSD and most other tryptamine and phenethylamine hallucinogens are partial agonists at a subtype of serotonin receptors called 5-HT2A receptors.

Ligands also can bind to receptors with varying affinities. The affinity for a receptor is a ratio of the rate at which a ligand binds to a receptor to the rate at which it unbinds, but it is usually thought of as just the attraction a ligand has for the receptor. One can think of a ligands affinity and efficacy like a key in a lock. A keys ability to fit into the lock is its affinity, but its ability to open the lock is its efficacy. A drugs affinity is also sometimes called its potency.
 
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One extra bit

For the section "what is a receptor", I don't know if you wanted to include one extra bit, or whether you'd rather deal with it somewhere else; namely the area of agonists/antagonist/inverse agonists where a drug can modulate an ion channel (the benzodiazepine/flumazinil example is the one that springs to mind). Although it might seem that an inverse agonist is an antagonist, an antagonist will simply reverse the effect of an agonist, whereas the inverse agonist will have the opposite pharmacological effect.

Using the benzodiazepine example, an agonist (your common benzos) are anticonvulsants; the antagonist flumazenil reverses the actions of the agonist, but it also reverses the actions of an inverse agonist (convulsant). On its own, in the absense of an agonist or inverse agonist, an antagonist has no physiological effect
 
Well I talk about it a bit in the ligand gated ion channel section.. maybe I'll talk about it a bit more.
 
....

As far as helping to compile a glossary goes, I've vocabulary is something that I'm intersted in as a hobby of late... but I don't want to commit to taking on the whole thing.

That you arlready have key words in bold makes it easier, and if you want I could use those to begin.

If you'd rather someone with a stronger background tackle this, or if you don't think its important at this juncture, I won't take offense.

Also if i should go through my notes to see what i have for diagrams, let me know. (I should have some relevent to the text you already have).
 
Yeah, the bolded words are also words I'd like to have in a glossary/index.

When it comes to diagrams, I know they are vitaly important, unfortunatly I don't have Adobe Illustrator, and I'm not very skilled with it... so I'm really going to have to rely on others to create the images needed. Though next weekend, or perhaps sooner, I'm gonna go through and do some rough images...
 
2 | The neuron

The neuron is a type of cell that is located in your body. The brain is the part of your body where the most neurons are located. There are about 10 billion interconnected neurons. These cells function by biochemical reactions. Through these reactions they can receive, process and transmit data from one cell to another (see the synaps chapter).

So there are alot of interconnected neurons. They can all communicate with eachother. On one cell there are more neurons which communicate with that cell. A neuron first needs to get signals from other neurons before they can fire. That can happen through spatial and temporal summation. When alot of impulses are added together it's called a spatial summation. When there is a serie of weak impulses this can form a bigger one. That's called temporal summation. The input of these impulses will lead to the cell body. This cell body and his nucleus wont play any significant roll in the signaling between neurons. Their roll is to maintain the neuron so they can still signal eachother.

The part of the neuron that is important for the signal is called the axon hillock. If the threshold value is crossed, then the neuron will give an action potential (for details behind this mechanism see the chapter Electrical properties of the neuron). This signal will be passed down the axon
and wil be converted to a biochemical signal instead of a voltage signal in the synaps. The strength of this signal is always the same. If the original impulses are one hundred times greater then the threshold, the axon hillock will still send a signal of the same strength. So the output of the signal down the axon in a neuron is always the same.


(neuron picture (axon/dendrite/soma))
 
I was imagining less about the signalling properties of neurons (as that can get discussed more fully in the 'signalling properties of neurons' chapter), and more just about basic anatomy... the cell body, the dendrites, the axon...
 
The synapse

As already mentioned in the “What is a neuron”, the synapse is junction between axonal terminals and another cell (nearly always a neuron, but sometimes a muscle, or a cell specialized hormone release cell) what has been modified for the release and effect of neurotransmitters. There are also so called “electrical synapses”, where neurons are electrically coupled by channels (gap junctions) that pass through both of the cells’ membranes and allow the passage of ions and small organic molecules, but these synapses are poorly understood and are outside the scope of this text.

The action at the synapse in its simplest form is easy to understand. When an action potential invades the axonal terminal, it causes voltage sensitive calcium channels to open (see Voltage Gated Ion Channels) and Ca2+ floods into the channel. The Ca2+ influx causes the neurotransmitter containing vesicles to fuse with the membrane of the cells, and to release their contents into the synapse. Here the neurotransmitter diffuses across the synapse and can interact with its appropriate receptor and depending on the neurotransmitter and the receptor, this can have any of the myriad of effects that receptors are capable of inducing in a cell (See Ligand Gated Ion Channels and G-Protein Coupled Receptors). The neurotransmitter could also diffuse back and activate presynaptic receptors.

As stated above, the Ca2+ influx caused by the action potential invading the presynaptic terminal and opening voltage sensitive calcium channels is the signal for neurotransmitter release. Not only can drugs directly effect calcium channels, like alcohol, which inhibits them, and hence decrease Ca2+ influx and neurotransmitter release, but presynaptic receptors can effect their activity. For instance, when the CB1 receptor is activated, it causes the activation of a multi-subunit protein called a G-protein (discussed further in G-protein coupled receptors and signalling networks). The particular type of G-protein which CB1 receptors activates binds to and inhibits calcium channels, which inhibits the release of neurotransmitter. That G-protein also activates a potassium channel, which causes potassium to leave the presynaptic terminal that lowers the presynaptic depolarization and reduces the number of open Ca2+ channels, and neurotransmitter release.

You can see that the important role of the synapse is a place to release neurotransmitters in order to transmit signals from one cell to the other. However, just as important as the release of neurotransmitter is the termination of their action, because if neurotransmitters weren’t cleared they would continue to act indefinitely. Also, in order for any neuronal signals to have any degree of temporal, spatial or amplitudinal resolution they must be able to be discerned from each other, i.e. they can not ‘blur’ together. Neurotransmitters are cleared by the action of enzymes and/or by molecular carriers (generally called transporters). The enzymes metabolize the neurotransmitter to inactive compounds (i.e. they do not act at receptors) and the transporters carry the neurotransmitter from the extracellular fluid to the intracellular compartment, so that they can not act on receptors any more. Drugs that effect neurotransmitter transporters or enzymes that break down neurotransmitters increase the action of the appropriate neurotransmitter. Cocaine is the classic example of a transporter inhibitor (aka a reuptake inhibitor), it inhibits the uptake of dopamine by the dopamine transporter. The enzyme which breaks down monoamine neurotransmitters (dopamine, serotonin, noradrenaline and adrenaline) monoamine oxidase (MAO), is the target of many pharmaceutical drugs like the antidepressant, MAO inhibitors (MAOIs), and most amphetamines have some action as MAOIs.

So, the synapse is place where two neurons connect and signal to each other. By effect release, reuptake or degradation of neurotransmitters, drugs have a powerful way of modulating synaptic transmission. Indeed, it would be safe to say that the vast majority of psychoactive drugs act directly at the synapse.
 
What is an enzyme? By Anonymous

Enzymes are proteins that could be simply described as molecular catalysts; that is to say, they massively increase the rate of specific chemical reactions. Enzymes generally have a small cleft or crevice in their surface where the chemicals they act on (substrates) can bind; this is referred to as the enzyme’s “active site”. Importantly, the activity of most enzymes can be regulated, either by chemicals that reversibly bind to receptors on the enzyme, or by the action of other enzymes that can bond small chemicals to the enzyme. For instance, the dopamine precursor L-DOPA inhibits the enzyme that produces it, tyrosine hydroxylase. Also dopamine receptors alter the activity tyrosine hydroxylase by covalent bonding or removing of phosphate molecules through activating other enzymes call protein kinases or protein phosphatases respectively. In the case of tyrosine hydroxylase the addition of a phosphate (phosphorylation) increases the rate at which it forms L-DOPA, while dephosphorylation slows it down. This is not the case with all enzymes, but generally, phosphorylation/dephosphorylation alters the rate of enzymes and also effects the behavior of receptors (discussed further in G-protein coupled receptors and signaling networks). Indeed, this kinda of enzyme cascade, where one enzyme activates another enzyme, which activates another enzyme etc. is a very common theme in neurons and other cells in the body.

Enzymes are not a particularly common target for recreational drugs. Monoamine oxidase (MAO) is an enzyme that breaks down both natural (endogenous) neurotransmitters but also chemicals which are ingested. Several antidepressants block MAO that inhibits its normal function of breaking down dopamine, serotonin and norepinephrine (also called noradrenaline). Beta carbolines from Banisteriopsis caapi or syrian rue are also MAO inhibitors, and are vital components of ayahuasca, because they stop the breakdown of DMT caused by MAO in the gut.

The most important thing to appreciate about enzymes is that they cause a selected chemical process, and that their activity can be modulate in many ways.

For more information, the interested reader should consult: Campbell, N.A. & Reece, J.B. (2002). Biology. pp. 24-103. San Francisco: Benjamin Cummings.
 
there are still a bit of topics which arent in the planning of making.. (yet)
so if there are still volunteers i think bilz0r is glad to get some help on some of the topics.
 
wanna talk about kinase cascades and phosphorylases in signalling, LTP and LTD?
otherwise, that was well written
 
What is a cell?

What is a cell?

A cell is “the lowest level of structure capable of performing all the activities of life” (Campbell et al., 1996). Physically, a cell is a collection of molecules contained within a membrane of some kind, capable of reproducing itself, energy utilization and other hallmarks of life. While some forms of life exist as single cells, so-called “higher life forms” can only sustain life as a collection of cells; they are multi-cellular. In many multi-cellular life forms groups of cells have undergone some form of specialization and aggregated into tissue so that the individual cells (and hence the tissue) are well suited to a particular task. Hepatocytes are the primary cells of the liver, and contain a huge array of metabolic enzymes, allowing the liver to degrade potentially dangerous chemicals and create complex molecules. Myocytes are the primary cells of muscles, and contain specially produced protein fibers which can change their length, allowing the muscle to contract and produce movement. Neurons are the cells of the nervous system, these unique cells allow information to be quickly sent from one part of the body to another. Neurons make rapid sensation and reaction possible and allow animals to change and learn new behaviors so that they are better suited to their environment.
 
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