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 trac tus solitarii (NTS) in the suppression of cardiac baroreceptor reflex (BRR) response induced by parabrachial nucleus (PBN) complex in adult Sprague-Da wley rats maintained under pentobarbital anesthesia. Based on in vivo micro dialysis coupled with high-performance liquid chromatography-fluorescence d etection for gamma -aminobutyric acid (GABA), we found that electrical stim ulation of the ventrolateral regions and Koelliker-Fuse (KF) subnucleus of PBN complex resulted in a site-specific increase in GABA concentration in t he dialysate collected from the NTS. The temporal increase in extracellular GABA concentration in the NTS coincided with the time course of PBN-induce d cardiac BRR inhibition. In addition, the PBN-induced cardiac BRR suppress ion was reversed by microinjection bilaterally into the NTS of a GABA(A) re ceptor antagonist, bicuculline methiodide (5 pmol), or a GABA(B) receptor a ntagonist, 2-OH saclofen (500 pmol). Blockade of neuronal activity in the v entrolateral regions and KF subnucleus of PBN complex with lidocaine (5%) e licited an enhancement of the same reflex response. The time course of this facilitatory effect of lidocaine correlated positively with the temporal d ecrease in extracellular GABA concentration in the NTS. Anatomically, Fast Blue-labeled neurons were identified in the same subnuclei of the PBN compl ex after microinjection of the retrograde transport tracer into the NTS. So me of these Fast Blue-labeled neurons were also immunoreactive to glutamic acid decarboxylase. These results suggest that a direct GABAergic descendin g projection from the KF subnucleus and surrounding areas of the PBN comple x to the NTS may inhibit cardiac BRR response by activating GABA(A) and GAB A(B) receptors at the NTS. Synapse 42:27-39, 2001. (C) 2001 Wiley-Liss, Inc .