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Tonic Glycinergic Inhibition of brown adipose tissue (BAT) Sympathetic Premotor Neurons in Rostral Raphe Pallidus (rRPa)
Author(s) -
Conceicao Ellen Santos
Publication year - 2017
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.31.1_supplement.1040.6
Subject(s) - brown adipose tissue , biology , medicine , endocrinology , adipose tissue
The rRPa contains BAT sympathetic premotor neurons controlling BAT sympathetic nerve activity (SNA) and BAT thermogenesis. We report here the contribution of a tonic activation of glycine A receptors in the rRPa at the inhibitory regulation of BAT SNA and BAT thermogenesis, as well as cardiovascular parameters, in urethane/chloralose anesthetized, artificially‐ventilated rats. Under warm conditions, nanoinjection of strychnine (STR) into the rRPa increased BAT SNA (peak: +495% of control), BAT temperature (TBAT, + 1.1 °C), expired CO 2 , (+ 0.4 %), core body temperature (TCORE, + 0.2 °C), mean arterial pressure (MAP, + 4 mmHg) and heart rate (HR, + 57 bpm). Glycine (GLY) injection into the rRPa evoked a potent, 74 % inhibition of cooling‐evoked BAT SNA, and reductions in TBAT (−0.2 °C), TCORE (−0.2 °C), expired CO 2 (−0.2 %), MAP (−8 mmHg), and HR (−22 bpm), but did not reduce any of these parameters after STR nanoinjection into rRPa. Nanoinjection of STR into the rRPa had no effect on the ability of nanoinjection of GABA into the rRPa to inhibit BAT SNA (−86 % of the cold‐evoked BAT SNA), and expired CO 2 (−0.4 %). Blockade of glutamate receptors with AP5/CNQX into rRPa markedly inhibited the STR‐evoked increases in BAT SNA (−56 %), TBAT (−0.4 °C), expired CO 2 (−0.8 %), MAP (−8 mmHg) and HR (−34 bpm). Regarding the synaptic integration occurring at the BAT sympathetic premotor neurons in the rRPa, we conclude that a tonically‐active, glycinergic inhibitory input contributes to reductions in their discharge probabilities that compete with their excitatory inputs from the DMH and brainstem sites to determine the level of BAT thermogenesis and energy expenditure. Support or Funding Information This work was supported by NIH R01‐NS091066 (S.F.M.).