Premium
Inhibition of Hypothalamic Paraventricular Nucleus (PVN) Attenuates Responses of Preganglionic Adrenal (pre‐ASNA) but not Renal (RSNA) Sympathetic Nerve Activity Evoked by Disinhibition of Dorsomedial Hypothalamus (DMH)
Author(s) -
Scislo Tadeusz J,
O’Leary Donal S
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a361-a
Subject(s) - endocrinology , medicine , disinhibition , chemistry , stimulation , bicuculline , hypothalamus , medulla , psychology , neuroscience , gabaa receptor , receptor
Different components of the autonomic responses elicited via stimulation/disinhibition of DMH, a center mediating the hypothalamic defense response, are transmitted via different brainstem pathways without contribution of PVN. Disinhibition of DMH increases circulating epinephrine. However, the pathways mediating activation of the adrenal medulla following disinhibition of DMH have not been studied. Since PVN exert humoral control of the adrenal gland and stimulation of PVN preferentially activates pre‐ASNA, it is likely that PVN may also mediate activation of the adrenal medulla in response to disinhibition of DMH. Therefore in urethane/chloralose anesthetized male Sprague Dawley rats (n=5) we compared hemodynamic and sympathetic responses evoked by disinhibition of DMH with microinjections of bicuculline (50 pmol/50 nL) before and after inhibition of PVN with microinjections of muscimol (500 pmol/50 nL). Inhibition of PVN decreased pre‐ASNA (101.3±1.3 vs. 55.4±4.4%) and mean arterial pressure (MAP) (87.3±6.8 vs. 75.7±5.9 mmHg) without significant changes in heart rate (HR) (354.7±11.0 vs. 357.5±12.6 bpm) and RSNA (101.3±1.3 vs. 96.5±5.8%). Following the inhibition of PVN, the DMH elicited increases in pre‐ASNA were attenuated ~ 3 fold whereas the responses in RSNA, MAP and HR remained virtually unaltered. We conclude that PVN may selectively mediate the activation of the adrenal medulla in response to disinhibition of DMH and generate tonic activation of pre‐ASNA. Supported by NIH Grant HL‐67814.