Autoreceptor

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An autoreceptor is a type of receptor located in the membranes of nerve cells. It serves as part of a negative feedback loop in signal transduction. It is only sensitive to the neurotransmitters or hormones released by the neuron on which the autoreceptor sits. Similarly, a heteroreceptor is sensitive to neurotransmitters and hormones that are not released by the cell on which it sits. A given receptor can act as either an autoreceptor or a heteroreceptor, depending upon the type of transmitter released by the cell on which it is embedded.

Autoreceptors may be located in any part of the cell membrane: in the

cell body, the axon, or the axon terminals.[1]

Canonically, a presynaptic neuron releases a neurotransmitter across a

second messenger.[2]

Examples

Autoreceptor inhibition leads to increase respective neurotransmitter release. Major autoreceptor which clinically important are alpha 2(

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]

The

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 Postsynaptic 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.

Autoreceptor diagram
This diagram shows pre-synaptic neuron (left) releasing a neurotransmitter, noradrenaline (norepinephrine), into the synaptic cleft. The transmitter acts on the receptors of the post-synaptic neuron (right), but also on autoreceptors of the pre-synaptic neuron. Activation of these autoreceptors typically inhibits further release of the neurotransmitter.
A pharmacodynamic model of amphetamine and TAAR1
Amphetamine, trace amines, and dopamine can activate TAAR1 in dopamine neurons, but only dopamine activates D2sh. These receptors have opposite effects on protein kinase signaling. This results in opposite effects on DAT phosporylation, and consequently, on reuptake as well.

References

  1. ^ a b Siegel GJ, Agranoff BW, Albers RW, et al., eds. (1999). "Catecholamine Receptors". Basic Neurochemistry: Molecular, Cellular and Medical Aspects (6th ed.). Lippincott-Raven.
  2. ^ Bear; Connors; Paradiso (2006). Neuroscience: Exploring the Brain (3rd ed.). p. 119.
  3. PMID 17234900
    .
  4. PMID 18310473
    .
  5. PMID 19482011
    .
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