Glutamate receptor subtypes mediate excitatory synaptic responses of rat lateral parabrachial neurons.

Abstract

We examined the role of specific excitatory amino acid (EAA) receptors in synaptic transmission within the lateral parabrachial nucleus (LPBN) using whole cell patch-recording techniques in a slice preparation. Two types of excitatory postsynaptic responses were observed. The first involved the contribution of non-N-methyl-D-aspartate (NMDA) receptors, which mediated a fast component, and NMDA receptors, which governed the late component of the excitatory postsynaptic current (EPSC). The second EPSC response was mediated solely by non-NMDA receptors. Both EPSC responses reversed near 0 mV. The fast component of the EPSC was attenuated by the non-NMDA antagonists [6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 6,7-dinitroquinoxaline-2,3-dione (DNQX), and 6-nitro-7-sulfamobenzoquinoxaline-2-3,-dione (NBQX)]. The late component was reduced by D,L-2-amino-5-phosphonovaleric acid (APV) and augmented in Mg(2+)-free external medium. EPSCs mediated solely by non-NMDA receptors were completely blocked by CNQX and NBQX but not affected by APV or Mg(2+)-free external medium. EPSCs were also markedly attenuated by the metabotropic-receptor agonist, trans-(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (trans-ACPD). We concluded that intra-LPBN stimulation causes the synaptic release of glutamate, which depolarizes LBPN neurons via non-NMDA and NMDA receptors. We also provide evidence that glutamate can negatively influence its own release via action on presynaptic metabotropic receptors.