Release of glutamate and GABA in the amygdala of conscious rats by acute stress and baroreceptor activation: differences between SHR and WKY rats

Citation
N. Singewald et al., Release of glutamate and GABA in the amygdala of conscious rats by acute stress and baroreceptor activation: differences between SHR and WKY rats, BRAIN RES, 864(1), 2000, pp. 138-141
Citations number
26
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH
ISSN journal
00068993 → ACNP
Volume
864
Issue
1
Year of publication
2000
Pages
138 - 141
Database
ISI
SICI code
0006-8993(20000502)864:1<138:ROGAGI>2.0.ZU;2-R
Abstract
To reveal the functional importance of amino acid neurotransmission in the amygdala (AMY) of conscious spontaneously hypertensive rats (SHR) and Wista r-Kyoto (WKY) rats, the in vivo release of glutamate (GLU) and GABA in this brain structure was studied using the push-pull superfusion technique. Bas al GLU and GABA release rates in the AMY were comparable in SI-IR and WKY r ats, although arterial blood pressure (BP) in SHR (152+/-6 mmHg) was higher than in WKY rats (102+/-4 mmWg). Neuronal depolarization by superfusion wi th veratridine enhanced the release of GLU and GABA to a similar extent in both rat strains. On the other hand, exposure to noise stress (95 dB) for 3 min led to a tetrodotoxin-sensitive increase in GLU release in the AMY of SHR, but not WKY rats. The concurrent presser response to noise was enhance d in SHR as compared to WKY rats. A rise in BP induced by intravenous infus ion of phenylephrine for 9 min had no effect on amino acid release in the A MY of both strains. The data suggest an exaggerated stress response of glut amatergic neurons in the AMY of SHR as compared with WKY rats, which might be of significance for the strain differences in the cardiovascular and beh avioural responses to stress. The results also show that, in both rat strai ns, glutamatergic and GABAergic neurons in the AMY are not modulated by bar oreceptor activation. Moreover, hypertension in adult SHR does not seem to be linked to a disturbed synaptic regulation of glutamatergic or GABAergic transmission in the AMY. (C) 2000 Elsevier Science B.V. All rights reserved .