Modulation by arginine vasopressin of glutamate excitation in the ventral septal area of the rat brain

Arginine vasopresin is hypothesized to act as a neurotransmitter or neuromodulator in the ventral septal area of the rat brain. To examine this role of vasopressin further, it was applied by microiontophoresis or micropressure from multiple-barrelled micropipettes onto spontaneously active or glutamate-activated neurons. Applied in this manner, vasopressin reduced glutamate-evoked excitation in 32 of the 47 cells studied. Further, micropressure application of the vasopressin antagonist d(CH2)5Tyr(Me)AVP reversed the vasopressin effects. In contrast, administration of vasopressin had no effect on excitations evoked by acetylcholine iontophoresis or on the spontaneous activity of the majority of the ventral septal neurons studied. These observations suggest that vasopressin may be acting on a V1-like receptor on specific neurons in the ventral septal area as a modulator of glutamate actions. Evoked responses were also obtained in the same population of ventral septal cells following stimulation of a variety of limbic areas. Inhibitory input onto most of the vasopressin responsive neurons studied was obtained following electrical stimulation of the paraventricular nucleus and bed nucleus of the stria terminalis, two cell groupings that are potential sources of vasopressin to the ventral septal area. Thus, the similarity in action of exogenously applied vasopressin and the evoked responses following paraventricular nucleus and bed nucleus stimulation suggests that vasopressin may be a neurotransmitter in this pathway.

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The Anteroventral Bed Nucleus of the Stria Terminalis Differentially Regulates Hypothalamic-Pituitary-Adrenocortical Axis Responses to Acute and Chronic Stress

Endocrinology ◽

10.1210/en.2007-0883 ◽

2007 ◽

Vol 149 (2) ◽

pp. 818-826 ◽

Cited By ~ 70

Author(s):

Dennis C. Choi ◽

Nathan K. Evanson ◽

Amy R. Furay ◽

Yvonne M. Ulrich-Lai ◽

Michelle M. Ostrander ◽

...

Keyword(s):

Chronic Stress ◽

Hpa Axis ◽

Paraventricular Nucleus ◽

Restraint Stress ◽

Body Weight Gain ◽

Stria Terminalis ◽

Thymic Involution ◽

Bed Nucleus ◽

Acute And Chronic Stress

The anteroventral region of the bed nucleus of the stria terminalis (BST) stimulates hypothalamic-pituitary-adrenocortical (HPA) axis responses to acute stress. However, the role of the anterior BST nuclei in chronic drive of the HPA axis has yet to be established. Therefore, this study tests the role of the anteroventral BST in physiological responses to chronic drive, using a chronic variable stress (CVS) model. Male Sprague-Dawley rats received either bilateral ibotenate lesions, targeting the anteroventral BST, or vehicle injection into the same region. Half of the lesion and control rats were exposed to a 14-d CVS paradigm consisting of twice-daily exposure to unpredictable, alternating stressors. The remaining rats were nonhandled control animals that remained in home cages. On the morning after the end of CVS exposure, all rats were exposed to a novel restraint stress challenge. CVS induced attenuated body weight gain, adrenal hypertrophy, thymic involution, and enhanced CRH mRNA in hypophysiotrophic neurons of the hypothalamic paraventricular nucleus, none of which were affected by anteroventral BST lesions. In the absence of CVS, lesions attenuated the plasma corticosterone and paraventricular nucleus c-fos mRNA responses to the acute restraint stress. In contrast, lesions of the anteroventral BST elevated plasma ACTH and corticosterone responses to novel restraint in the rats previously exposed to CVS. These data suggest that the anterior BST plays very different roles in integrating acute stimulation and chronic drive of the HPA axis, perhaps mediated by chronic stress-induced recruitment of distinct BST cell groups or functional reorganization of stress-integrative circuits.

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Vasopressin and fever: evidence supporting the existence of an endogenous antipyretic system in the brain

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-211 ◽

1987 ◽

Vol 65 (6) ◽

pp. 1333-1338 ◽

Cited By ~ 30

Author(s):

A. M. Naylor ◽

K. E. Cooper ◽

W. L. Veale

Keyword(s):

Paraventricular Nucleus ◽

Septal Area ◽

Stria Terminalis ◽

Antipyretic Effect ◽

Bed Nucleus ◽

Cell Groups ◽

Bacterial Pyrogen ◽

The Brain ◽

Vasopressinergic Neurons ◽

Reducing Properties

Vasopressin administered into the ventral septum exerts a dose-related antipyresis. This site of action is similar in a number of species. The fever-reducing properties of vasopressin are both site and neuropeptide specific. Evidence supporting a role for endogenous vasopressin in fever suppression is the demonstration that the release of the peptide from the ventral septal area is altered during fever: the amount released correlates negatively with febrile changes in body temperature. In addition, changes in the concentration of vasopressin in the septum and amygdala have been demonstrated immunocytochemically during fever: an activation of vasopressinergic neurons occurs which is similar to that observed in pregnant animals at term when fever is absent. Specific antibodies directed against vasopressin or specific vasopressin antagonist analogues (e.g., d(CH2)5Tyr(Me)AVP) enhanced the febrile response to a pyrogen challenge when injected into the ventral septum. The same antagonist also can antagonize the antipyretic effect of exogenously administered vasopressin. The use of relatively specific antagonists and agonists of vasopressin, directed against the V1 and V2 subtypes of the peripheral vasopressin receptor, suggests that the central receptor responsible for the antipyretic effect of vasopressin may resemble the V1 subtype. Recent experiments using electrophysiological techniques have demonstrated the existence of thermoresponsive units in the ventral septal area whose activity may be altered by vasopressin which is possibly derived from the paraventricular nucleus and bed nucleus of the stria terminalis. Electrical stimulation of one of these cell groups in the paraventricular nucleus can reduce the fever evoked by systemic administration of bacterial pyrogen in the rabbit. Collectively, these data strongly support the hypothesis that a system of endogenous antipyresis involving vasopressin exists in the brain. There also may exist another antipyretic system in the brain involving α-melanotropin. This peptide is antipyretic when injected into the dorsal septum and concentrations of α-melanotropin are altered in this area of the brain during fever. Further, passive immunoneutralization using antiserum specific to α-melanotropin results in prolonged fever. A possible connection between the two systems has not yet been investigated. However, in future studies the mechanisms and significance of such a system will be investigated further.

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The role of the anteriolateral bed nucleus of the stria terminalis in stress-induced nociception

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00501.2011 ◽

2012 ◽

Vol 302 (11) ◽

pp. G1301-G1309 ◽

Cited By ~ 18

Author(s):

Lee Tran ◽

Brandt Wiskur ◽

Beverley Greenwood-Van Meerveld

Keyword(s):

Stria Terminalis ◽

Mrna Levels ◽

Bed Nucleus ◽

Corticotrophin Releasing Factor ◽

Visceromotor Response ◽

Dependent Mechanism ◽

Von Frey Filaments ◽

Stimulation Of

Activation of the central amygdala (CeA) by corticosterone (CORT) induces somatic and colonic hypersensitivity through corticotrophin-releasing factor (CRF)-dependent mechanisms. However, the importance of the bed nucleus of the stria terminalis (BNST), part of the extended amygdala, on nociception remains unexplored. In the present study, we test the hypothesis that stimulation of the CeA by CORT induces somatic and colonic hypersensitivity through activation of the anteriolateral BNST (BNSTAL). Animals were implanted with micropellets of CORT or cholesterol (CHOL) onto the CeA or the BNSTAL. Mechanical sensitivity was quantified using electronic von Frey filaments, and colonic nociception was measured by quantifying a visceromotor response to graded colorectal distension. In situ hybridization was used to determine mRNA levels for CRF, CRF1, and CRF2 receptors in the BNSTAL. In a second group, animals were implanted bilaterally with 1) CORT or CHOL micropellets onto the CeA; and 2) cannulas localized to the BNSTAL to administer a CRF1 receptor antagonist (CP376395). Animals implanted with CORT onto the CeA, but not the BNSTAL, exhibited increased expression of CRF mRNA and increased CRF1-to-CRF2 receptor ratio in the BNST, as well as somatic and colonic hypersensitivity compared with CHOL controls. Infusion of CP376395 into the BNSTAL inhibited somatic and colonic hypersensitivity in response to elevated amygdala CORT. Somatic and colonic hypersensitivity induced by elevated amygdala CORT is mediated via a CRF1 receptor-dependent mechanism in the BNSTAL. The CeA through a descending pathway involving the BNSTAL plays a pivotal role in somatic and colonic nociception.

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