Modulation of noradrenaline release in the median preoptic area by GABAergic inputs from the organum vasculosum of the lamina terminalis in the rat

Ushigome, Akihiko; Nomura, Masahiko; Tanaka, Junichi

doi:10.1016/s0197-0186(03)00134-7

Cited by 22 publications

(20 citation statements)

References 26 publications

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“…5-HT Receptor WAY 161503, 8,9-dichloro-2,3,4,4-tetrahydro-1H-pyrazino͓1,2-a͔quinoxalin-5(6H)-one hydrochloride (5-HT 2C agonist); SR 57227, 1-(6-chloro-2-pyridinyl)-4-piperidinamine hydrochloride (5-HT 3 agonist); Y-25130, N-1-azabicyclo͓2.2.2͔-oct-3-yl-6-chloro-3,4-dihydro-4-methyl-3-oxo-2H-1,4-benzoxazine-8-carboxamide hydrochloride (azasetron; 5-HT 3 antagonist); ML10302, 2-(1-piperidinyl)ethyl-4-amino-5-chloro-2-methoxybenzoate (5-HT 4 agonist); RS 39604, 1-͓4-amino-5-chloro-2- (3,5-dimethoxyphenyl) 1998; Vazquez and Baghdoyan, 2003), dopaminergic (Ronken et al, 1993;Steiniger and Kretschmer, 2003), and noradrenergic neurons (Fung and Fillenz, 1983;Suzdak and Gianutsos, 1985;Tanaka et al, 2002;Sakamaki et al, 2004;Ushigome et al, 2004) Presynaptic 5-HT heteroreceptors play mainly a physiological role in the local fine regulation of the release of the transmitter from the axon terminal on which the receptors are located. They inhibit or facilitate transmitter release in response to action potentials invading the varicosities.…”

Section: -Ht Receptors Discussed In This Review Their Cellular Signmentioning

confidence: 99%

5-HT Receptor Regulation of Neurotransmitter Release

Fink¹,

Göthert²

2007

Pharmacol Rev

323

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Section: -Ht Receptors Discussed In This Review Their Cellular Signmentioning

confidence: 99%

5-HT Receptor Regulation of Neurotransmitter Release

Fink¹,

Göthert²

2007

Pharmacol Rev

323

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“…Consistent with this notion, blockade of glutamatergic receptors in the AV3V elicits inhibition of hemorrhagic AVP release [15,16], as well as hyperosmotic hormone secretion [16,19]. Regarding GABAergic innervation in the AV3V, it has been reported that GABAergic fibers, like glutamatergic fibers, extend from the SFO or organum vasculosum of the lamina terminalis (OVLT), an AV3V osmoreceptor site, to MnPO neurons to regulate their excitability via ionotropic GABA A and metabotropic GABA B receptors [20,21]. Moreover, acute fluid depletion reduces GABA synthesis in the AV3V or SFO [22].…”

Section: Animals and Surgerymentioning

confidence: 76%

“…The AV3V possesses GABA A and GABA B receptors [20,21,29], as well as the NMDA and non-NMDA receptors for l-glutamate (Glu), the major excitatory neurotransmitter in the brain [16,19,37]. The GABA A receptor is a ligand-gated Cl -ion channel that mediates rapid synaptic transmission, while the GABA B receptor is bound to G proteins and modulates synaptic transmission through intracellular effector systems, leading to the activation of K + channels and inactivation of adenylate cyclase or Ca 2+ channels [30].…”

Section: Discussionmentioning

confidence: 99%

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Changes in vasopressin release and autonomic function induced by manipulating forebrain GABAergic signaling under euvolemia and hypovolemia in conscious rats

Yamaguchi

Hama

2011

Endocr J

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Hypovolemia, as well as hyperosmolality, is a potent stimulus for accelerating arginine vasopressin (AVP) secretion [1]. In contrast to the situation that the cerebral neurons engaged in the hyperosmotic excitation of AVP cells in the hypothalamic supraoptic nucleus (SON) and paraventricular nucleus (PVN) (AV3V) is a pivotal area for osmotic responses and integration of autonomic functions. The purpose of this study was to investigate whether the gamma-aminobutyric acid (GABA)-ergic activity in the AV3V may be involved in the regulation of arginine vasopressin (AVP) secretion and related phenomena under the conditions with or without hypovolemia. Experiments were performed in conscious rats. We found that AV3V infusion with the GABA A receptor antagonist bicuculline in euvolemic rats caused prompt increases in plasma AVP, osmolality, glucose, arterial pressure and heart rate. The effects of the bicuculline infusion were abolished by prior infusion of a GABA A receptor agonist, muscimol. When repeated twice with a 10-min interval, removal of systemic blood (10 mL/ kg body weight) lowered arterial pressure and enhanced plasma AVP, osmolality, glucose and angiotensin II. Muscimol infusion in the AV3V, but not in the cerebral ventricle, inhibited the responses of plasma AVP and glucose, despite having no effect in a sham hemorrhagic state. The inhibition of the AVP response by the muscimol infusion was also verified in rats given a combined stimulus of bleeding plus an osmotic load. In contrast, AV3V infusion with the GABA B receptor agonist baclofen tended to intensify the hemorrhagic responses of plasma AVP and glucose, despite its potency to prevent the hemorrhagic fall in arterial pressure. These results, taken together with our previous data, suggest that hypovolemic stimuli, like hyperosmotic stimuli, may promote AVP secretion by causing the inhibition of AV3V GABA A -ergic activity responsible for potentiation of glutamatergic activity.Key words: Anteroventral third ventricular region (AV3V), Gamma aminobutyric acid, Antidiuretic hormone, Bleeding, Hypotension information is conveyed from the peripheral organs to the nucleus of the solitary tract (NTS) and the ventrolateral medulla (VLM) via the carotid sinus or aortic depressor nerve, and then transferred to the SON and PVN through pathways that directly connect these brainstem loci with the hypothalamic nuclei [2-5]. However, there are various observations suggesting that the neurons of the anteroventral third ventricular region (AV3V) responsible for osmotic AVP release may participate in hypovolemic and hypotensive activation of AVP cells. For example, the median preoptic nucleus (MnPO), a major AV3V structure that includes synapses of osmotic circuits [4,6,7], and the subfornical organ (SFO), a neighboring area with osmosensitivity [8], receive afferents from the NTS and VLM (A1 region) [9][10][11][12], and electrical stimulation of the A1 region activates MnPO neurons projecting to the

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“…The SFO is characterized by the absence of a blood-brain barrier [14]. The SFO has connections with the brain regions involved in the central regulation of drinking, salt appetite, blood pressure and cardiovascular function, such a region is the anteroventral region of the third ventricle which is involved in the control of drinking behaviour [15,16].…”

Section: Introductionmentioning

confidence: 99%

Hypertension effects on p73 expression in the rat circumventricular organs and cerebrospinal fluid

Carmona-Calero¹,

González-Marrero²,

Castaneyra-Martin³

et al. 2012

WJNS

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ABSTRACTand SHR were used. The paraffin sections containing the CVO were immunohistochemically processed with anti-TAp73 and by western blot, p73 bands in the CSF and circumventricular organ extract were also identified. The western blot study showed bands marked with p73 in the CSF and CVO, the p73 band expression was bigger in the SHR than in the WKY rats. We also found stronger markings in the SFO, SCO and AP of the hypertensive rats than in the WKY rats. It could be concluded that hypertension in the SHR produces alterations in the relationship between the p73 protein, circumventricular structures and CSF.

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Modulation of noradrenaline release in the median preoptic area by GABAergic inputs from the organum vasculosum of the lamina terminalis in the rat

Cited by 22 publications

References 26 publications

5-HT Receptor Regulation of Neurotransmitter Release

5-HT Receptor Regulation of Neurotransmitter Release

Changes in vasopressin release and autonomic function induced by manipulating forebrain GABAergic signaling under euvolemia and hypovolemia in conscious rats

Hypertension effects on p73 expression in the rat circumventricular organs and cerebrospinal fluid

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