Injection of L-allylglycine into the posterior hypothalamus in rats causes decreases in local gaba which correlate with increases in heart rate

1988 ◽  
Vol 27 (11) ◽  
pp. 1171-1177 ◽  
Author(s):  
V.M. Abshire ◽  
K.D. Hankins ◽  
K.E. Roehr ◽  
J.A. DiMicco
2013 ◽  
Vol 114 (1) ◽  
pp. 119-130 ◽  
Author(s):  
Georg M. Stettner ◽  
Leszek Kubin

The perifornical (PF) region of the posterior hypothalamus promotes wakefulness and facilitates motor activity. In anesthetized rats, local disinhibition of PF neurons by GABAA receptor antagonists activates orexin (OX) neurons and elicits a systemic response, including increases of hypoglossal nerve activity (XIIa), respiratory rate, heart rate, and blood pressure. The increase of XIIa is mediated to hypoglossal (XII) motoneurons by pathways that do not require noradrenergic or serotonergic projections. We hypothesized that the pathway might include OX-dependent activation locally within the PF region or direct projections of OX neurons to the XII nucleus. Adult, male Sprague-Dawley rats were urethane anesthetized, vagotomized, paralyzed, and ventilated. Gabazine (GABAA receptor antagonist, 0.18 mM, 20 nl) was injected into the PF region, and ∼2 h later, a second gabazine injection was performed preceded by injection of a dual OX1/2 receptor antagonist (almorexant; 90 mM) either into the XII nucleus (40–60 nl at 2–3 rostrocaudal levels; n = 6 rats), or into the PF region (40–60 nl; n = 6 rats). XIIa, respiratory rate, heart rate, and arterial blood pressure were analyzed for 70 min after each gabazine injection. The excitatory effects of PF gabazine on XIIa, respiratory, and heart rates were significantly reduced by up to 44–82% when gabazine injections were preceded by PF almorexant injections, but not when almorexant was injected into the XII nucleus. These data suggest that a significant portion of XII motoneuronal and cardiorespiratory activation evoked by disinhibition of PF neurons is mediated by local OX-dependent mechanisms within the posterior hypothalamus.


1986 ◽  
Vol 25 (9) ◽  
pp. 1063-1066 ◽  
Author(s):  
J.A. DiMicco ◽  
V.M. Abshire ◽  
K.D. Hankins ◽  
R.H.B. Sample ◽  
J.H. Wible

1988 ◽  
Vol 254 (4) ◽  
pp. R680-R687 ◽  
Author(s):  
J. H. Wible ◽  
F. C. Luft ◽  
J. A. DiMicco

We studied the cardiovascular effects of altering GABA-ergic tone in the posterior hypothalamus in rats. Animals were equipped with chronic guide cannulas placed in the posterior hypothalamus, arterial and venous catheters, and a bipolar electrode on the splanchnic nerve. Microinjected bilaterally into the posterior hypothalamus in conscious rats, the postsynaptic gamma-aminobutyric acid (GABA) antagonists bicuculline methiodide and picrotoxin rapidly increased heart rate, blood pressure, and sympathetic nerve activity. Microinjection of the GABA agonist muscimol into this same region decreased heart rate, blood pressure, and sympathetic nerve activity in conscious rats. In contrast, muscimol infused into the posterior hypothalamus of anesthetized rats failed to alter heart rate or blood pressure. We conclude that 1) the posterior hypothalamus contains a sympathoexcitatory system that is modulated by changes in GABA-ergic tone and 2) tonic GABA-ergic inhibition is sufficient to completely suppress the activity of this hypothalamic sympathoexcitatory system in anesthetized animals but not in conscious rats.


1997 ◽  
Vol 272 (5) ◽  
pp. R1447-R1453 ◽  
Author(s):  
H. Hashiguchi ◽  
S. H. Ye ◽  
F. Ross-Cisneros ◽  
N. Alexander

An earlier study showed that norepinephrine (NE) was released in the paraventricular nucleus (PVN) and posterior hypothalamus (PH) along with increases of mean arterial pressure (MAP) and heart rate (HR) during shaker stress (SS). Here we investigated the possibility that nitric oxide (NO) donors, infused into hypothalamus, could modulate responses to SS. In conscious rats, an injector-microdialysis probe, for direct application of donor and collection of extracellular NE, respectively, was inserted into PVN or PH; MAP and HR were recorded continuously from conscious rats. The NO donor, molsidomine (Mol), infused 5 or 30 min before SS, did not alter baseline values of NE, MAP, or HR, but did attenuate changes elicited by 5 min of SS; methylene blue blocked the effects of Mol. The NO donor, sodium nitroprusside, was much less effective than Mol as a modulator of stress-related effects. The results indicate that MAP, HR, and hypothalamic NE responses to environmental stress, but not baseline values, can be modulated by NO donors in the hypothalamus.


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