A heteroreceptor is a
receptor regulating the synthesis and/or the release of mediators other than its own
ligand.[1]
Heteroreceptors respond to
neurotransmitters,
neuromodulators, or
neurohormones released from adjacent neurons or cells; they are opposite to
autoreceptors, which are sensitive only to neurotransmitters or hormones released by the cell in whose wall they are embedded.[2]
Acetylcholine can influence the release of norepinephrine from sympathetic neurons by acting on
muscarinic-2 and muscarinic-4 heteroreceptors.
CB1 negatively modulates the release of
GABA[4][5] and
glutamate,[6] playing a crucial role in maintaining a homeostasis between excitatory and inhibitory transmission.
Glutamate released from an excitatory neuron escapes from the
synaptic cleft and preferentially affects
mGluR III receptors on the presynaptic terminals of interneurons. Glutamate spillover leads to inhibition of
GABA release, modulating GABAergic transmission.[7][8]
^Millan, M. J.; Lejeune, F.; Gobert, A. (2000). "Reciprocal autoreceptor and heteroreceptor control of serotonergic, dopaminergic and noradrenergic transmission in the frontal cortex: Relevance to the actions of antidepressant agents". Journal of Psychopharmacology. 14 (2): 114–138.
doi:
10.1177/026988110001400202.
PMID10890307.
S2CID18333385.
^Schlicker, E.; Malinowska, B.; Kathmann, M.; Göthert, M. (1994). "Modulation of neurotransmitter release via histamine H3 heteroreceptors". Fundamental & Clinical Pharmacology. 8 (2): 128–137.
doi:
10.1111/j.1472-8206.1994.tb00789.x.
PMID8020871.
S2CID21816655.
A heteroreceptor is a
receptor regulating the synthesis and/or the release of mediators other than its own
ligand.[1]
Heteroreceptors respond to
neurotransmitters,
neuromodulators, or
neurohormones released from adjacent neurons or cells; they are opposite to
autoreceptors, which are sensitive only to neurotransmitters or hormones released by the cell in whose wall they are embedded.[2]
Acetylcholine can influence the release of norepinephrine from sympathetic neurons by acting on
muscarinic-2 and muscarinic-4 heteroreceptors.
CB1 negatively modulates the release of
GABA[4][5] and
glutamate,[6] playing a crucial role in maintaining a homeostasis between excitatory and inhibitory transmission.
Glutamate released from an excitatory neuron escapes from the
synaptic cleft and preferentially affects
mGluR III receptors on the presynaptic terminals of interneurons. Glutamate spillover leads to inhibition of
GABA release, modulating GABAergic transmission.[7][8]
^Millan, M. J.; Lejeune, F.; Gobert, A. (2000). "Reciprocal autoreceptor and heteroreceptor control of serotonergic, dopaminergic and noradrenergic transmission in the frontal cortex: Relevance to the actions of antidepressant agents". Journal of Psychopharmacology. 14 (2): 114–138.
doi:
10.1177/026988110001400202.
PMID10890307.
S2CID18333385.
^Schlicker, E.; Malinowska, B.; Kathmann, M.; Göthert, M. (1994). "Modulation of neurotransmitter release via histamine H3 heteroreceptors". Fundamental & Clinical Pharmacology. 8 (2): 128–137.
doi:
10.1111/j.1472-8206.1994.tb00789.x.
PMID8020871.
S2CID21816655.