Talk:Neurotransmitter

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We need: criteria for being a neurotransmitter (1. endogenous synthesis 2. quantities in the presynaptic neuron must be of sufficient quantity to exert an effect on the post-synaptic neuron 3. externally administered, it must mimic the endogenously released substance 4. a biochemical mechanism for inactivation must be present).

More information about inactivation mechanisms. Diffusion and reuptake by astrocytes in the CNS is not mentioned.

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The current definition does not seem right: "Neurotransmitters are chemicals that are used to relay, amplify and modulate electrical signals between a neuron and another cell." My objection is that the Neurotransmitter is the signal between the cells - there is usually no electrical signal between cells/neurons - electrical signals primarily exsists within a neuron.

• I agree that the current sentence (quoted above) mixes together two concepts. Maybe it could be split into two sentences: "Neurotransmitters are chemicals that can function as signals released from neurons. Neurotransmitters influence the behavior of nearby cells, often by modifying electrical signals that propagate along cell surface membranes."

Electrical is not essential as it is and is a bit misleading without the additional sentence. DCDuring 17:47, 8 September 2007 (UTC)

Contents 1 production? 2 Neurotransmitter effects 2.1 Notes 3 Improvements

[edit] production?

Where are transmitters produced??—Preceding unsigned comment added by 141.30.206.172 (talk • contribs)

I'm not sure for all of them, but glutamate is formed in neurons. Since it would activate glutamate receptors on neurons, it is uptaken by glia, transformed into glutamine, which is released into the extracellular space. Neurons take up the glutamine and transform it back into glutamate. You may not want to quote me on that, since I'm recalling from memory. See synaptic vesicle and neurotransmitter transporter for more info. delldot talk 19:44, 28 February 2007 (UTC)

[edit] Neurotransmitter effects

Recently, I have been recovering from an MAOI discontinuation syndrome due to hospital mismanagement which has put me in a unique position to identify the effects of fluctuating dopamine, norepinephrine, and serotonin levels (due to departures from homeostasis incurred by physical dependence) in relative isolation from each other. On November 9, 2007, unlike on prior days, my serotonin level underwent considerable variation, allowing me to experience its effects in addition to those of the other two neurotransmitters, which I had experienced previously. As a result, I believe I have experienced "pure" forms of several mental disorders, which are generally caused by messy combinations of multiple neurotransmitters. Serendipitously, this occurred at the office of my psychiatrist in Sacramento, allowing me to discuss my experiences with him as they occurred throughout the day.

Neurotransmitter production appears to require glucose, as eventually all three reached low levels simultaneously, accompanied by symptoms of hypoglycemia. Food led to gradual recovery.

Please note that norepinephrine appears to be solely responsible for causing effects to be displeasurable; that is, dysphoria and even extreme effects such as pseudoparkinsonism are not in themselves unpleasant regardless of whether they may be disturbing at a cognitive level. This suggests the most urgently needed new drug is a norepinephrine stabilizer. By far, the most pleasurable effect is the catatonic fixation induced by extremely low serotonin, which may have profound implications for meditative behavior.

In these tables, decreasing levels are indicated by left arrows, while increasing levels are indicated by right arrows. Regrettably, the following is based only on subjective observations, without objective measurements. All of the listed effects are temporary, although it seems I may now have limited direct control over each neurotransmitter.

bruxism dyskinesia dysphagia dysphasia pseudoparkinsonian gait disturbance1	←	Dopamine	→	euphoria	→	attention pressured speech	→	...	→	psychosis (presumed)
	→		←	dysphoria	←		←	...	←

cholinergic syndrome discomfort sadness2 (with decreased serotonin)	←	dysthymia (with decreased serotonin)	←	Norepinephrine	→	anticholinergic syndrome anxiety
	→		→		←

catatonia diplopia hallucination3 (with increasing dopamine) visual fixation4	←	Serotonin	→	amicability communicativeness eye contact improved senses psychological bonding	→	serotonin syndrome (!)
	→		←		←

¹ Following a demonstration of this for my psychiatrist, I was informed it differs from the effects of parkinsonism.

² Note that sadness appears linked to cholinergic syndrome, which produces tears.

³ These hallucinations resemble certain effects of LSD, as have been described to me. Floor tiles appeared to slide past each other; lines between them disappeared at random, suggesting blind spots; closed magazines on a table appeared to curl upward at their edges; carpeting with a simple, repetitive pattern appeared to develop tectonics.

⁴ This effectively produces tunnel vision. Faces produce stronger fixation than all other images and may have a positive effect on dopamine.

— 66.218.55.142 14:45, 10 November 2007 (UTC)

[edit] Notes

• It seems like "hyperthymia" belongs in the space below "dysthymia", but so far it's been difficult to characterize the positive transition from low to baseline norepinephrine. An attempt to do so would require entering a sad or dysthymic state, and exiting states with such strong emotional content may be indistinguishable from a truly unique positive state.
• I've found that diplopia can occur selectively, presumably during the low serotonin state. Bars can form double images more easily than other objects, even without inducing double images of nearby objects.
• Increasing serotonin seems to cause yawning.
• Serotonin appears to have a dangerously low therapeutic index; a relatively small increase in serotonin separates its social effects from serotonin syndrome. This became apparent this morning following an unexpected interaction with clonazepam.
• Review of LSD, Cluster headache, and Serotonergic psychedelic suggests to me that control of neurotransmitter reuptake is not equivalent to control of presynaptic release or postsynaptic uptake. Additionally, receptor agonism does not appear to imply increased stimulation.
• The noted fluctuations follow a consistent pattern. Initially the effects of neurotransmitter deficiency occur (suggesting acclimation to exogenous supplementation which was no longer present), and over time these are replaced by effects of neurotransmitter excess (presumably due to increased endogenous production, but perhaps involving receptor sensitization as well).
• Serotonin may be necessary for proper integration of sense experience, especially stereopsis. Loss of integration would naturally result in psychedelic effects.
  • NMDA antagonism produces effects similar to serotonin deficiency. NMDA may be partially responsible for regulating serotonin activity.

— 66.218.55.142 18:15, 10 November 2007 (UTC)

[edit] Improvements

mattycoze and I have been discussing ways to expand and improve the article. He suggested a bunch of additions on my talk page, including explanations of how they're synthesized and broken down. I think a section on the 'lifecycle' (what would be a better word for this?) might be a good idea, i.e. a depiction of what typically happens from synthesis to release to reuptake and breakdown. What do others think? delldot on a public computer talk 07:05, 5 May 2008 (UTC)

Oh heh, sorry guys I'm kinda new to the Wikipedia editing thing... maybe next time i should check out the discussion pages before i start adding my own crap to the articles! Anyway will know better next time Mattycoze (talk) 11:14, 5 May 2008 (UTC)

Nonsense! You're doing awesome. Anyway, even if you were to do something wrong, it would be easily fixable. Keep it up! delldot on a public computer talk 11:16, 5 May 2008 (UTC)