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Synaptic transmission in nucleus tractus solitarius is depressed by Group II and III but not Group I presynaptic metabotropic glutamate receptors in rats
Author(s) -
Chen ChaoYin,
Ling Erhhsin,
Horowitz John M.,
Bonham Ann C.
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2001.012948
Subject(s) - metabotropic glutamate receptor , neurotransmission , glutamatergic , excitatory postsynaptic potential , postsynaptic potential , neuroscience , ampa receptor , glutamate receptor , metabotropic receptor , agonist , chemistry , inhibitory postsynaptic potential , biology , receptor , biochemistry
Presynaptic metabotropic glutamate receptors (mGluRs) serve as autoreceptors throughout the CNS to inhibit glutamate release and depress glutamatergic transmission. Both presynaptic and postsynaptic mGluRs have been implicated in shaping autonomic signal transmission in the nucleus tractus solitarius (NTS). We sought to test the hypothesis that activation of presynaptic mGluRs depresses neurotransmission between primary autonomic afferent fibres and second‐order NTS neurones. In second‐order NTS neurones, excitatory postsynaptic currents (EPSCs) synaptically evoked by stimulation of primary sensory afferent fibres in the tractus solitarius (ts) and currents postsynaptically evoked by α‐amino‐3‐hydroxy‐4‐isoxazoleproprionic acid (AMPA) were studied in the presence and absence of mGluR agonists and antagonists. Real‐time quantitative RT‐PCR (reverse transcription‐polymerase chain reaction) was used to determine whether the genes for the mGluR subtypes were expressed in the cell bodies of the primary autonomic afferent fibres. Agonist activation of Group II and III but not Group I mGluRs reduced the peak amplitude of synaptically (ts) evoked EPSCs in a concentration‐dependent manner while having no effect on postsynaptically (AMPA) evoked currents recorded in the same neurones. At the highest concentrations, the Group II agonist, (2 S ,3 S ,4 S )‐CCG/(2 S ,1′ S ,2′ S )‐2‐carboxycyclopropyl ( l ‐CCG‐I), decreased the amplitude of the ts‐evoked EPSCs by 39 % with an EC 50 of 21 μ m , and the Group III agonist, l (+)‐2‐amino‐4‐phosphonobutyric acid ( l ‐AP4), decreased the evoked EPSCs by 71 % with an EC 50 of 1 m m . mRNA for all eight mGluR subtypes was detected in the autonomic afferent fibre cell bodies in the nodose and jugular ganglia. Group II and III antagonists ((2 S ,3 S ,4 S )‐2‐methyl‐2‐(carboxycyclopropyl)glycine (MCCG) and ( RS )‐α‐methylserine‐ O ‐phosphate (MSOP)), at concentrations that blocked the respective agonist‐induced synaptic depression, attenuated the frequency‐dependent synaptic depression associated with increasing frequencies of ts stimulation by 13–34 % and 13–19 %, respectively ( P < 0.05, for each). We conclude that Group II and III mGluRs (synthesized in the cell bodies of the primary autonomic afferent fibres and transported to the central terminals in the NTS) contribute to the depression of autonomic signal transmission by attenuating presynaptic release of glutamate.