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Disinhibition of neurons in paraventricular hypothalamic nucleus (PVH) inhibits cold‐evoked shivering
Author(s) -
Morrison Shaun F.
Publication year - 2010
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.24.1_supplement.992.6
Subject(s) - thermogenesis , shivering , bicuculline , endocrinology , medicine , brown adipose tissue , chemistry , inhibitory postsynaptic potential , thermoregulation , antagonist , anesthesia , adipose tissue , receptor
The thermogenesis from skeletal muscle shivering contributes to the maintenance of a homeostatic body temperature during exposure to a cold environment. Activation of neurons in the PVH elicits a potent inhibition of the sympathetic outflow and thermogenesis in brown adipose tissue (Am. J. Physiol., 296:831–843, 2009) and the present study determined whether this effect of PVH neurons to inhibit sympathetically‐mediated thermogenesis extends also to thermogenesis mediated by activation of somatic motoneurons. Cooling‐evoked shivering responses were monitored as the increases in neck and gastrocnemius muscle EMG activities elicited by cooling the trunk skin to ~32¢ a C for 1–2 min with a water jacket in isoflurane‐anesthetized rats whose core temperature was lowered to ~36¢ a C. Nanoinjection of the GABAA receptor antagonist, bicuculline (60 pmol), into the PVH terminated ongoing skin cooling‐evoked EMG increases and prevented EMG increases to subsequent skin cooling episodes for ~20 minutes. These results indicate that neurons in the PVH can exert a potent inhibitory influence on cooling‐evoked shivering thermogenesis. The physiological stimulus for, and the synaptic integration sites supporting this PVH‐mediated inhibition of thermoregulatory energy consumption remain to be determined. Supported by NIH grant NS40987.