title: Non-NMDA and NMDA receptors in the synaptic pathway between area postrema and nucleus tractus solitarius.
abstract: Area postrema (AP) modulates cardiovascular function through excitatory projections to neurons in nucleus tractus solitarius (NTS), which also process primary sensory (including cardiovascular-related) input via the solitary tract (TS). The neurotransmitter(s) and their receptors in the AP-NTS pathway have not been fully characterized. We used whole cell recordings in voltage- and current-clamp modes in the rat brain stem slice to examine the role of ionotropic glutamatergic receptors and alpha2-adrenergic receptors in the pathway from AP to NTS neurons receiving visceral afferent information via the TS. In neurons voltage clamped at potentials from -100 to +80 mV, AP stimulation (0. 2 Hz) evoked excitatory postsynaptic currents having a fast component blocked by the non-N-methyl-D-aspartate (NMDA) receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2, 3-dioxobenzoquinoxaline-7-sulfonamide (NBQX; 3 microM, n = 7) and a slow component blocked by the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV; 50 microM, n = 8). Although NBQX (3 microM, n = 14) abolished AP-evoked action potentials, APV (50 microM, n = 9 or 500 microM, n = 6) or yohimbine, (200 nM, n = 5 or 2 microM, n = 10) did not. Thus, although AP stimulation activates both non-NMDA and NMDA receptors on NTS neurons receiving TS input, only non-NMDA receptors are required for synaptic transmission.
authors.affiliation: Division of Cardiovascular Medicine, Department of Pharmacology, University of California, Davis, California 95616, USA.
authors.forename: M L
authors.initials: ML
authors.lastname: Aylwin
authors.forename: J M
authors.initials: JM
authors.lastname: Horowitz
authors.forename: A C
authors.initials: AC
authors.lastname: Bonham
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology*; D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001933:Brain Stem / Q000502:physiology*; D002319:Cardiovascular System / Q000294:innervation*; D002552:Cerebral Ventricles / Q000502:physiology*; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D011810:Quinoxalines / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology*; D017470:Receptors, Glutamate / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D017552:Solitary Nucleus / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D018691:Excitatory Amino Acid Antagonists; D011810:Quinoxalines; D018341:Receptors, Adrenergic, alpha-2; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D015016:Yohimbine; D015763:2-Amino-5-phosphonovalerate