Corrigendum to “Stress induces CRF release in the paraventricular nucleus, and both CRF and GABA release in the amygdala” [Physiol Behav 82 (4) (30 September 2004) 751–762]

2014 ◽  
Vol 135 ◽  
pp. 230-231
Author(s):  
Christian J. Cook
Keyword(s):  
Paraventricular Nucleus ◽  
Gaba Release

scholarly journals Signalling pathway of nitric oxide in synaptic GABA release in the rat paraventricular nucleus

2003 ◽  
Vol 554 (1) ◽  
pp. 100-110 ◽  
Author(s):  
De-Pei Li ◽  
Shao-Rui Chen ◽  
Thomas F. Finnegan ◽  
Hui-Lin Pan
Keyword(s):  
Nitric Oxide ◽  
Paraventricular Nucleus ◽  
Gaba Release ◽  
Signalling Pathway

scholarly journals Enhanced astroglial GABA uptake attenuates tonic GABAA inhibition of the presympathetic hypothalamic paraventricular nucleus neurons in heart failure

2015 ◽  
Vol 114 (2) ◽  
pp. 914-926 ◽  
Author(s):  
Sudip Pandit ◽  
Ji Yoon Jo ◽  
Sang Ung Lee ◽  
Young Jae Lee ◽  
So Yeong Lee ◽  
...  
Keyword(s):  
Heart Failure ◽  
Paraventricular Nucleus ◽  
Gaba Release ◽  
Hypothalamic Paraventricular Nucleus ◽  
Ventrolateral Medulla ◽  
Gaba Uptake ◽  
Spontaneous Firing ◽  
Nipecotic Acid ◽  
The Difference ◽  
Selective Blocker

γ-Aminobutyric acid (GABA) generates persistent tonic inhibitory currents ( Itonic) and conventional inhibitory postsynaptic currents in the hypothalamic paraventricular nucleus (PVN) via activation of GABAA receptors (GABAARs). We investigated the pathophysiological significance of astroglial GABA uptake in the regulation of Itonic in the PVN neurons projecting to the rostral ventrolateral medulla (PVN-RVLM). The Itonic of PVN-RVLM neurons were significantly reduced in heart failure (HF) compared with sham-operated (SHAM) rats. Reduced Itonic sensitivity to THIP argued for the decreased function of GABAAR δ subunits in HF, whereas similar Itonic sensitivity to benzodiazepines argued against the difference of γ2 subunit-containing GABAARs in SHAM and HF rats. HF Itonic attenuation was reversed by a nonselective GABA transporter (GAT) blocker (nipecotic acid, NPA) and a GAT-3 selective blocker, but not by a GAT-1 blocker, suggesting that astroglial GABA clearance increased in HF. Similar and minimal Itonic responses to bestrophin-1 blockade in SHAM and HF neurons further argued against a role for astroglial GABA release in HF Itonic attenuation. Finally, the NPA-induced inhibition of spontaneous firing was greater in HF than in SHAM PVN-RVLM neurons, whereas diazepam induced less inhibition of spontaneous firing in HF than in SHAM neurons. Overall, our results showed that combined with reduced GABAARs function, the enhanced astroglial GABA uptake-induced attenuation of Itonic in HF PVN-RVLM neurons explains the deficit in tonic GABAergic inhibition and increased sympathetic outflow from the PVN during heart failure.

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