GABAergic neurotransmission at the nucleus tractus solitarii in the suppression of reflex bradycardia by parabrachial nucleus
GABAergic neurotransmission at the nucleus tractus solitarii in the suppression of reflex bradycardia by parabrachial nucleus
复制标题
孤束核 GABA 能神经传递在臂旁核抑制反射性心动过缓中的作用
作者:
W. Len;J. Chan
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 γ‐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 GABAA receptor antagonist, bicuculline methiodide (5 pmol), or a GABAB 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 GABAA and GABAB receptors at the NTS. Synapse 42:27–39, 2001. © 2001 Wiley‐Liss, Inc.
影响因子:
3.7
作者:
BOURDELAIS, AJ;DEUTCH, AY
通讯作者:
DEUTCH, AY
DOI:
10.1016/0165-1838(88)90023-9
发表时间:
1988
期刊:
Journal of the autonomic nervous system
影响因子:
--
作者:
Urbanski,RW;Sapru,HN
通讯作者:
Sapru,HN