The role of amygdala and hypothalamus in GABAA antagonist bicuculline-induced cardiovascular responses in conscious rats

Gören, Zafer; Aslan, Neslihan; Berkman, Kemal; Oktay, Şule; Onat, Filiz

doi:10.1016/0006-8993(96)00201-6

Cited by 24 publications

(11 citation statements)

References 29 publications

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“…These findings are consistent with our previous experiments, indicating the existence of a GABAergic inhibitory mechanism through the hypothalamus in the modulation of cardiovascular functions. It has been previously shown that the blockade of GABA A receptors by bicuculline injected into the DMH or paraventricular nucleus causes dose-related, reversible elevations in both blood pressure and heart rate in conscious rats (12,13,22). The bicuculline-induced increase in these cardiovascular parameters is more prominent when bicuculline is given into the DMH, suggesting an important role of the DMH in GABAergic control of cardiovascular functions.…”

Section: Figmentioning

confidence: 98%

“…Previous studies have indicated that tonic GABAergic inhibition through GABA A receptors in several nuclei of the hypothalamus but specifically dorsomedial hypothalamic nucleus (DMH) is responsible for the control of cardiovascular responses (11,12). We have reported that the pressor effects of intracerebroventricular administration of bicuculline (BMI), a GABA A -receptor antagonist, are mediated primarily by the posterior parts of the hypothalamus (13). Furthermore, the activation of GABA A receptors by microinjection of muscimol, a GABA Areceptor agonist, into the DMH blocks air stress and cholinomimetic-induced pressor responses (10,14).…”

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confidence: 99%

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Cardiovascular Regulation through Hypothalamic GABA_A Receptors in a Genetic Absence Epilepsy Model in Rat

Aker

Onat

2002

Epilepsia

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Summary:Purpose: ␥-Aminobutyric acid (GABA) plays a vital role in both central cardiovascular homeostasis and pathogenesis of epilepsy. Epilepsy affects autonomic nervous system functions. In this study, we aimed to clarify the role of GABA A receptors in hypothalamic cardiovascular regulation in a genetically determined animal model of absence epilepsy.Methods: Nonepileptic Wistar rats and genetic absence epilepsy rats from Strasbourg (GAERS) were instrumented with a guide cannula for drug injection and extradural electrodes for EEG recording. After a recovery period, iliac arterial catheters were inserted for direct measurement of mean arterial pressure and heart rate. Bicuculline, a GABA A -receptor antagonist, was injected into the dorsomedial (DMH) or posterior (PH) hypothalamic nuclei of nonepileptic control rats or GAERS. Blood pressure, heart rate, and EEG recordings were performed in conscious unrestrained animals.Results: Bicuculline injections into the hypothalamus produced increases in blood pressure and heart rate of both control rats and GAERS. The DMH group of GAERS showed a twofold increase in the blood pressure and the heart rate compared with those of control rats. Pressor responses to bicuculline, when microinjected into the PH, were similar in the nonepileptic animals and GAERS. Conversely, the amplitude of tachycardic responses to the administration of bicuculline into the PH was significantly higher in GAERS compared with those of control rats. Conclusions:The bicuculline-induced increases in blood pressure and heart rate were more prominent when given in the DMH of GAERS. These results indicate an increased GABA A receptor-mediated cardiovascular response through the DMH in conscious rats with absence epilepsy.

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Section: Figmentioning

confidence: 98%

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confidence: 99%

Cardiovascular Regulation through Hypothalamic GABA_A Receptors in a Genetic Absence Epilepsy Model in Rat

Aker

Onat

2002

Epilepsia

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“…However, Goren et al (39) have demonstrated that GABA A receptors located in the CeA do not have and essential role in cardiovascular regulation. These investigators showed that bicuculline injection into the CeA produced a slight increase in blood pressure (3 min at least, which returned to basal levels and did not change heart rate).…”

Section: Discussionmentioning

confidence: 99%

GABA in the central amygdaloid nucleus modulates the electrolyte excretion and hormonal responses to blood volume expansion in rats

Margatho

Elias

2009

Braz J Med Biol Res

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We investigated the involvement of GABAergic mechanisms of the central amygdaloid nucleus (CeA) in unanesthetized rats subjected to acute isotonic or hypertonic blood volume expansion (BVE). Male Wistar rats bearing cannulas unilaterally implanted in the CeA were treated with vehicle, muscimol (0.2 nmol/0.2 μL) or bicuculline (1.6 nmol/0.2 μL) in the CeA, followed by isotonic or hypertonic BVE (0.15 or 0.3 M NaCl, 2 mL/100 g body weight over 1 min). The vehicle-treated group showed an increase in sodium excretion, urinary volume, plasma oxytocin (OT), and atrial natriuretic peptide (ANP) levels compared to control rats. Muscimol reduced the effects of BVE on sodium excretion (isotonic: 2.4 ± 0.3 vs vehicle: 4.8 ± 0.2 and hypertonic: 4.0 ± 0.7 vs vehicle: 8.7 ± 0.6 μEq·100 g -1 ·40 min -1 ); urinary volume after hypertonic BVE (83.8 ± 10 vs vehicle: 255.6 ± 16.5 μL·100 g -1 ·40 min -1 ); plasma OT levels (isotonic: 15.3 ± 0.6 vs vehicle: 19.3 ± 1 and hypertonic: 26.5 ± 2.6 vs vehicle: 48 ± 3 pg/ mL), and ANP levels (isotonic: 97 ± 12.8 vs vehicle: 258.3 ± 28.1 and hypertonic: 160 ± 14.6 vs vehicle: 318 ± 16.3 pg/mL). . .. . Bicuculline reduced the effects of isotonic or hypertonic BVE on urinary volume and ANP levels compared to vehicle-treated rats. However, bicuculline enhanced the effects of hypertonic BVE on plasma OT levels. These data suggest that CeA GABAergic mechanisms are involved in the control of ANP and OT secretion, as well as in sodium and water excretion in response to isotonic or hypertonic blood volume expansion.

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“…Our previous experiments demonstrated the roles of GABA A -mediated inhibitory and NMDA-mediated excitatory mechanisms in the modulation of cardiovascular functions [16,18]. Limbic structures such as amygdala and hippocampus are richly interconnected with hypothalamic regions.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that the dorsomedial nucleus plays a vital role in physiological regulatory processes [13,14]. Previous studies demonstrated that disruption of GABAergic neurotransmission in the dorsomedial nucleus evokes increases in arterial blood pressure, heart rate, peripheral sympathetic nerve activity and plasma catecholamine levels in both conscious and anesthetized rats, suggesting that the GABAergic system in the dorsomedial nucleus exerts a tonic inhibitory influence over the sympathetic nervous system [15][16][17]. Moreover, we demonstrated that the activation of N-methyl-D-aspartate (NMDA) receptors in the dorsomedial nucleus evokes significant increases in blood pressure and heart rate [18].…”

Section: Introductionmentioning

confidence: 99%

Extracellular Concentrations of Catecholamines and Amino Acids in the Dorsomedial Hypothalamus of Kindled Rats

Gören

Aker²,

Yananlı³

et al. 2003

Pharmacology

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Epilepsy affects homeostasis and autonomic nervous system functions. It has been thought that the dysfunction in the autonomic neural mechanisms could be a cause of sudden unexpected death in patients with epilepsy. The kindling model of epilepsy is considered to be an animal model for complex partial seizures with secondary generalization. The objectives of this study were to investigate the extracellular γ-aminobutyric acid (GABA), glutamate, noradrenaline and dopamine levels in the dorsomedial nucleus of the hypothalamus in non-epileptic and kindled epileptic rats and to explain some of the cardiovascular changes in the kindling model of epilepsy. Stimulation electrodes were stereotaxically implanted into the basolateral amygdala and electrical stimulation was applied 3 times a day at a constant current. The rats were then kindled to full stage 5 seizures. Microdialysis experiments were performed to demonstrate the neurotransmitter levels in the dorsomedial nucleus of the hypothalamus 3–5 days after being kindled. Decreases in noradrenaline and dopamine levels in the dorsomedial nucleus were detected in the conscious kindled animals. This finding is in agreement with prior findings that the noradrenergic system has a negative role in the process of kindling. The basal level of glutamic acid and GABA remained unchanged in the kindled group when compared to non-epileptic animals, and similarly, neither blood pressure nor heart rate responses to bicuculline or N-methyl-D-aspartate were affected by the acute kindled state. These findings suggest that the autonomic changes in kindling require further studies.

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The role of amygdala and hypothalamus in GABAA antagonist bicuculline-induced cardiovascular responses in conscious rats

Cited by 24 publications

References 29 publications

Cardiovascular Regulation through Hypothalamic GABA_A Receptors in a Genetic Absence Epilepsy Model in Rat

Cardiovascular Regulation through Hypothalamic GABA_A Receptors in a Genetic Absence Epilepsy Model in Rat

GABA in the central amygdaloid nucleus modulates the electrolyte excretion and hormonal responses to blood volume expansion in rats

Extracellular Concentrations of Catecholamines and Amino Acids in the Dorsomedial Hypothalamus of Kindled Rats

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The role of amygdala and hypothalamus in GABAA antagonist bicuculline-induced cardiovascular responses in conscious rats

Cited by 24 publications

References 29 publications

Cardiovascular Regulation through Hypothalamic GABAA Receptors in a Genetic Absence Epilepsy Model in Rat

Cardiovascular Regulation through Hypothalamic GABAA Receptors in a Genetic Absence Epilepsy Model in Rat

GABA in the central amygdaloid nucleus modulates the electrolyte excretion and hormonal responses to blood volume expansion in rats

Extracellular Concentrations of Catecholamines and Amino Acids in the Dorsomedial Hypothalamus of Kindled Rats

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Cardiovascular Regulation through Hypothalamic GABA_A Receptors in a Genetic Absence Epilepsy Model in Rat

Cardiovascular Regulation through Hypothalamic GABA_A Receptors in a Genetic Absence Epilepsy Model in Rat