Restraining Action of GABA on Estradiol-Induced LH Surge in the Rat: GABA Activity in Brain Nuclei and Effects of GABA Mimetics in the Medial Preoptic Nucleus

1992 ◽  
Vol 55 (1) ◽  
pp. 28-34 ◽  
Author(s):  
Alicia M. Seltzer ◽  
Alfredo O. Donoso
2002 ◽  
Vol 24 (1) ◽  
pp. 27-39 ◽  
Author(s):  
Philippe Absil ◽  
Monica Papello ◽  
Carla Viglietti-Panzica ◽  
Jacques Balthazart ◽  
GianCarlo Panzica

1988 ◽  
Vol 255 (3) ◽  
pp. H646-H650 ◽  
Author(s):  
J. S. Gutkind ◽  
M. Kurihara ◽  
J. M. Saavedra

We analyzed angiotensin II (ANG II) receptors by in vitro autoradiography in selective brain nuclei of control, salt-treated (1% NaCl in drinking water), deoxycorticosterone acetate (DOCA)-treated (DOCA pivalate, 25 mg/kg sc weekly), and DOCA-salt-treated (DOCA + salt treatments) uninephrectomized male Wistar-Kyoto rats. After 4 wk of treatment, only the DOCA-salt group developed hypertension. ANG II binding increased in median preoptic nucleus and subfornical organ of salt- and DOCA-treated rats. DOCA-treated rats also showed increased ANG II binding in paraventricular nucleus. DOCA-salt-treated rats showed higher ANG II binding in nucleus of the solitary tract and area postrema, as well as in the areas mentioned before. Although salt and/or DOCA treatments alone increased ANG II receptors in some brain nuclei, after combined DOCA-salt treatment there was significantly higher ANG II binding in all areas, except the median preoptic nucleus. These results suggest that increased ANG II receptors in selected brain areas may play a role in the pathophysiology of mineralocorticoid-salt experimental hypertension.


2010 ◽  
Vol 104 (1) ◽  
pp. 200-209 ◽  
Author(s):  
Evgenya Malinina ◽  
Michael Druzin ◽  
Staffan Johansson

To clarify the role of presynaptic L-type Ca2+ channels in GABA-mediated transmission in the medial preoptic nucleus (MPN), spontaneous, miniature, and impulse-evoked inhibitory postsynaptic currents (sIPSCs, mIPSCs, and eIPSCs, respectively) were recorded from MPN neurons in a slice preparation from rat brain. The effects of different stimulus protocols and pharmacological tools to detect contributions of L-type Ca2+ channels and of Ca2+-activated K+ (KCa) channels were analyzed. Block of L-type channels did not affect the sIPSC and mIPSC properties (frequency, amplitude, decay time course) in the absence of external stimulation but unexpectedly potentiated the eIPSCs evoked at low stimulus frequency (0.1–2.0 Hz). This effect was similar to and overlapping with the effect of KCa-channel blockers. High-frequency stimulation (50 Hz for 10 s) induced a substantial posttetanic potentiation (PTP) of the eIPSC amplitude and of the sIPSC frequency. Block of L-type channels still potentiated the eIPSC during PTP, but in contrast, reduced the sIPSC frequency during PTP. It was concluded that L-type channels provide a means for differential control of spontaneous and impulse-evoked GABA release and that this differential control is prominent during short-term synaptic plasticity. Functional coupling of the presynaptic L-type channels to KCa channels explains the observed effects on eIPSCs.


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