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1 Neurological Sciences Institute, Oregon Health & Science University, Beaverton, OR, USA
* To whom correspondence should be addressed. E-mail: maddench{at}ohsu.edu.
We determined whether the dorsomedial hypothalamus (DMH) plays a role in the thermogenic, metabolic and cardiovascular effects evoked by centrally-administered prostaglandin E2 (PGE2). Microinjection of PGE2 (170pmol/60nl) into the medial preoptic area of the hypothalamus in urethane-chloralose anesthetized, artificially ventilated rats increased brown adipose tissue (BAT) sympathetic nerve activity (SNA; +207 ± 18% of control), BAT temperature (+1.5 ± 0.2 oC), expired CO2 (+0.9 ± 0.1%), heart rate (HR; +106 ± 12 beats/min, bpm) and mean arterial pressure (+22 ± 4 mmHg). Within five minutes of subsequent bilateral microinjections of the GABAA receptor agonist, muscimol (120pmol/60nl/side), or the ionotropic excitatory amino acid antagonist, kynurenate (6nmol/60nl/side) into the DMH, the PGE2-evoked increases were respectively attenuated by 91 ± 3% and 108 ± 7% for BAT SNA, by 73 ± 12% and 102 ± 28% for BAT temperature, by 100 ± 4% and 125 ± 21% for expired CO2, by 72 ± 11% and 70 ± 16 % for HR and by 84 ± 19% and 113 ± 16% for mean arterial pressure. Microinjections outside the DMH within the dorsal hypothalamic area adjacent to the mamillothalamic tracts or within the ventromedial hypothalamus were less effective for attenuating the PGE2-evoked thermogenic, metabolic and cardiovascular responses. These results demonstrate that activation of excitatory amino acid receptors within the DMH is necessary for the thermogenic, metabolic and cardiovascular responses evoked by microinjection of PGE2 into the medial preoptic area.
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