GABAergic neurotransmission at the nucleus tractus solitarii in the suppression of reflex bradycardia by parabrachial nucleus.

We investigated the role of GABAergic neurotransmission at the nucleus tractus solitarii (NTS) in the suppression of cardiac baroreceptor reflex (BRR) response induced by parabrachial nucleus (PBN) complex in adult Sprague-Dawley rats maintained under pentobarbital anesthesia. Based on in vivo microdialysis coupled with high-performance liquid chromatography-fluorescence detection for gamma-aminobutyric acid (GABA), we found that electrical stimulation of the ventrolateral regions and Koelliker-Fuse (KF) subnucleus of PBN complex resulted in a site-specific increase in GABA concentration in the dialysate collected from the NTS. The temporal increase in extracellular GABA concentration in the NTS coincided with the time course of PBN-induced cardiac BRR inhibition. In addition, the PBN-induced cardiac BRR suppression was reversed by microinjection bilaterally into the NTS of a GABA(A) receptor antagonist, bicuculline methiodide (5 pmol), or a GABA(B) receptor antagonist, 2-OH saclofen (500 pmol). Blockade of neuronal activity in the ventrolateral regions and KF subnucleus of PBN complex with lidocaine (5%) elicited an enhancement of the same reflex response. The time course of this facilitatory effect of lidocaine correlated positively with the temporal decrease in extracellular GABA concentration in the NTS. Anatomically, Fast Blue-labeled neurons were identified in the same subnuclei of the PBN complex after microinjection of the retrograde transport tracer into the NTS. Some of these Fast Blue-labeled neurons were also immunoreactive to glutamic acid decarboxylase. These results suggest that a direct GABAergic descending projection from the KF subnucleus and surrounding areas of the PBN complex to the NTS may inhibit cardiac BRR response by activating GABA(A) and GABA(B) receptors at the NTS. Copyright 2001 Wiley-Liss, Inc.