autoreceptor


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au·to·re·cep·tor

(au'tō-rē-sep'tŏr, tōr),
A site on a neuron that binds the neurotransmitter released by that neuron, which then regulates the neuron's activity.
[auto- + receptor]

autoreceptor

A neurotransmitter receptor located in the presynaptic terminal of the same neuron that produces the neurotransmitter. Autoreceptors have a higher affinity for the neurotransmitter than does the postsynaptic receptor, and thus have an autoregulatory function.

au·to·re·cep·tor

(aw'tō-rĕ-sep'tŏr)
A site on a neuron that binds the neurotransmitter released by that neuron, which then regulates the neuron's activity.

au·to·re·cep·tor

(aw'tō-rĕ-sep'tŏr)
A site on a neuron that binds the neurotransmitter released by that neuron, which then regulates the neuron's activity.
[auto- + receptor]
References in periodicals archive ?
SB-649915-B, a novel 5-[HT.sub.[1A/B]] autoreceptor antagonist and serotonin reuptake inhibitor, is anxiolytic and displays fast onset activity in the rat high light social interaction test.
Pittaluga, "Pre-synaptic glycine GlyT1 transporter--NMDA receptor interaction: relevance to NMDA autoreceptor activation in the presence of [Mg.sup.2+] ions," Journal of Neurochemistry, vol.
Vilazodone was developed based on the theory that inhibition of 5-HT1A autoreceptor inhibition was responsible for SSRIs' delayed (approximately 2 weeks) onset of antidepressant efficacy.
Results of microdialysis studies indicate relative importance of 5-[HT.sub.1A] autoreceptor to the mechanism of action of selective 5-HT reuptake inhibitors or monoamino-oxidase inhibitors (Gardier et al., 1996).
Summarizing what is nown about the biologic and clinical effects of MAO inhibition, sustained treatment with a non-selective inhibitor leads to gradual recovery of the firing activity of serotonin neurons, due to a desensitization of the 5-HTIA autoreceptor. Subsequently, an enhancement of serotonin transmission occurs.
The authors proposed that the onset of dopamine autoreceptor function in the mesolimbic dopamine system during adolescence might underlie these characteristics of adolescence in rats.
These receptors show different postsynaptic and presynaptic localizations and distributions in the brain and have different autoreceptor and heteroreceptor characteristics as mentioned above.
Use of a running wheel for 6 weeks increased the expression of the mRNA for 5-HT1A, an autoreceptor that inhibits the synthesis and release of 5-HT, in the raphe (90); six weeks of wheel running also increased the mRNA for tyrosine hydroxylase in the SNpc and for D2 receptors in the caudate-putamen (66).
Another instance of genetic susceptibility to treatment nonresponse pertains to the 5-HT1A rs6295 polymorphism; the G allele has been associated with increased presynaptic autoreceptor expression (decreasing serotonin release due to inhibitory feedback) and decreased postsynaptic receptor expression (potentially leading to heightened glutamatergic drive and contributing to anxiety and depressive symptoms) [320].
Some of these strategies include the use of muscarinic M2 autoreceptor inhibitors [81] and nicotinic agonists [82]; ACh releasers or donors [83]; ACh precursors [84]; and acetylcholinesterase (AChE) inhibitors which act by inhibiting the hydrolysis of ACh in the synaptic cleft thereby restoring the levels of the neurotransmitter [85, 86].
Presynaptically localized D2Rs regulate synthesis and release of DA as the main autoreceptor of the dopaminergic system [29, 30].
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