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Autoreceptors may be located in any part of the cell membrane: in the dendrites, the cell body, the axon, or the axon terminals.[1] Canonically, a presynaptic neuron releases a neurotransmitter across a synaptic cleft to be detected by the receptors on a postsynaptic neuron. Autoreceptors on the presynaptic neuron will also detect this neurotransmitter and often function to control internal cell processes, typically inhibiting further release or synthesis of the neurotransmitter. Thus, release of neurotransmitter is regulated by negative feedback. Autoreceptors are usually G protein-coupled receptors (rather than transmitter-gated ion channels) and act via a second messenger.[2]
자가수용체는 수상돌기, 신경세포체, 액손, axon terminal 세포 벽의 일부에 존재할 수 있다. 시냅스 전 신경세포는 postsynaptic 신경의 수용체에 의해 발견되는 synaptic cleft를 가로질러 신경전달물질을 분비한다. postsynaptic 신경세포의 자가수용체는 이러한 신경전달물질을 발견할 수 있고, 때로는 internal cell process 조절기능을 하는 .. 전형적으로는 신경전달물질의 합성이나 분비를 억제함으로서...그래서 신경전달물질의 분비는 음성되먹이기에 의해서 조절된다. 자가 수용체는 일반적으로 g protein-coupled 수용체(transmitter-gated ion channels)이고 second messenger를 통해 작용한다.
As an example, norepinephrine released from sympathetic neurons may interact with the alpha-2A and alpha-2C adrenoreceptors to inhibit further release of norepinephrine. Similarly, acetylcholine released from parasympathetic neurons may interact with M2 and M4 receptors to inhibit further release of acetylcholine. An atypical example is given by the β-adrenergic autoreceptor in the sympathetic peripheral nervous system, which acts to increase transmitter release.[1]
예를들어, 교감신경으로 부터 분비되는 노르에피네프린은 ...
The D2sh autoreceptor interacts with the trace amine-assorted receptor 1 (TAAR1), a recently discovered GPCR, to regulate monoaminergic systems in the brain.[3] Active TAAR1 opposes the autoreceptor's activity by inactivating the dopamine transporter (DAT).[4] 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 of trace amines in the cytoplasm and activation of cyclic nucleotide-gated ion channels, which further activate TAAR1 and dump dopamine into the synapse. Through a series of phosphorylation events related to PKA and PKC, active TAAR1 inactivates DAT, preventing uptake of dopamine from the synapse.[5] 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 paired-pulse facilitation (PPF).[citation needed] 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.
첫댓글 감사합니다^^
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감사헙나다^^