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GABAergic modulation of ventilatory response to acute and sustained hypoxia in obese Zucker rats.
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OBJECTIVE
To determine whether altered central and/or peripheral gamma-aminobutyric acid (GABA)ergic mechanisms acting in GABA(A) receptors contribute to the abnormal ventilatory response to acute and sustained hypoxia in obese Zucker rats.
METHODS
In all, 10 lean and 10 obese Zucker rats were
GABAergic modulation of ventilation and peak oxygen consumption in obese Zucker rats.
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Obesity is often associated with a reduced ventilatory response and a decreased maximal exercise capacity. GABA is a major inhibitory neurotransmitter in the mammalian central nervous system. Altered GABAergic mechanisms have been detected in obese Zucker rats and implicated in their hyperphagic
GABA(A) and GABA(B) receptors differentially modulate volume and frequency in ventilatory compensation in obese Zucker rats.
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The aim of this study was to investigate whether GABA(A) and/or GABA(B) receptor-mediated mechanisms contribute to the impaired ventilatory response and reduced maximal aerobic exercise capacity in obese Zucker rats. Ten lean and 10 obese Zucker rats were studied at 12 wk of age. Minute ventilation
Activation of the melanocortin-4 receptor causes enhanced excitation in presympathetic paraventricular neurons in obese Zucker rats.
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Sympathetic nerve activity is increased in obesity-related hypertension. However, the central mechanisms involved in the increased sympathetic outflow remain unclear. The hypothalamic melanocortin system is important for regulating energy balance and sympathetic outflow. To understand the mechanisms
High fat diet induced-obesity facilitates anxiety-like behaviors due to GABAergic impairment within the dorsomedial hypothalamus in rats.
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Overweight and obesity are conditions associated with an overall range of clinical health consequences, and they could be involved with the development of neuropsychiatric diseases, such as generalized anxiety disorder (GAD) and panic disorder (PD). A crucial brain nuclei involved on the
Dietary salt loading exacerbates the increase in sympathetic nerve activity caused by intravenous insulin infusion in rats.
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Obesity and type 2 diabetes mellitus frequently produce chronic elevations in blood insulin levels. Importantly, hyperinsulinemia stimulates increases in sympathetic nerve activity that may predispose to hypertension, atherosclerosis, and end-organ damage. Because depletion of dietary salt (NaCl)
Blunted GABA-mediated inhibition within the dorsomedial hypothalamus potentiates the cardiovascular response to emotional stress in rats fed a high-fat diet.
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Rats fed a high-fat diet (HFD) present an exaggerated endocrine response to stress conditions, which, like obesity, show a high correlation with cardiovascular diseases. Meanwhile the GABAergic neurotransmission within the dorsomedial hypothalamus (DMH) is involved in the regulation of the
High-fat feeding alters the cardiovascular role of the hypothalamic paraventricular nucleus.
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Increased sympathetic nerve activity is associated with obesity-related hypertension, but the underlying central neural mechanisms are not clear. We examined the role of the hypothalamic paraventricular nucleus (PVN) in the regulation of sympathetic nerve activity in rats fed a normal chow diet
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