Autoreceptor: Difference between revisions

As an example, [[norepinephrine]] released from [[Sympathetic nervous system|sympathetic]] neurons may interact with the [[alpha-2 adrenergic receptor|alpha-2A]] and alpha-2C adrenoreceptors to inhibit further release of norepinephrine. Similarly, [[acetylcholine]] released from [[parasympathetic]] neurons may interact with [[muscarinic acetylcholine receptor|M₂]] and M₄ receptors to inhibit further release of acetylcholine. An atypical example is given by the [[Adrenergic_receptorAdrenergic receptor#.CE.B2_receptorsB2 receptors|β-adrenergic autoreceptor]] in the [[Sympathetic nervous system|sympathetic peripheral nervous system]], which acts to ''increase'' transmitter release.<ref name=siegel/>

The [[D2sh]] autoreceptor interacts with the [[TAAR1|trace amine-assorted receptor 1]] (TAAR1), a recently discovered [[G protein-coupled receptor|GPCR]], to regulate monoaminergic systems in the brain.<ref>{{cite pmid|17234900}}</ref> Active TAAR1 opposes the autoreceptor's activity by inactivating the [[dopamine transporter]] (DAT).<ref>{{cite pmid|18310473}}</ref> In their review of TAAR1 in [[monoaminergic]] systems, Xie and Miller proposed this schematic: synaptic dopamine binds to the dopamine autoreceptor, which activates the DAT. Dopamine enters the presynaptic cells and binds to TAAR1, which increases [[adenylyl cyclase]] activity. This eventually allows for the [[Translation (biology)|translation]] of [[trace amines]] in the cytoplasm and activation of [[cyclic nucleotide-gated ion channel]]s, which further activate TAAR1 and dump dopamine into the synapse. Through a series of [[phosphorylation]] events related to [[protein kinase A|PKA]] and [[protein kinase C|PKC]], active TAAR1 inactivates DAT, preventing uptake of dopamine from the synapse.<ref>{{cite pmid|19482011}}</ref> The presence of two presynaptic receptors with opposite abilities to regulate monoamine transporter function allows for regulation of the monoaminergic system.

Autoreceptor activity may also decrease [[neural facilitation|paired-pulse facilitation]] (PPF).{{CNCitation needed|date=January 2014}} A feedback cell is activated by the (partially) depolarized post-synaptic neuron. The feedback cell releases a neurotransmitter to which the autoreceptor of the presynaptic neuron is receptive. The autoreceptor causes the inhibition of calcium channels (slowing calcium ion influx) and the opening of potassium channels (increasing potassium ion efflux) in the presynaptic membrane. These changes in ion concentration effectively diminish the amount of the original neurotransmitter released by the presynaptic terminal into the synaptic cleft. This causes a final depression on the activity of the postsynaptic neuron. Thus the feedback cycle is complete.