GABAergic systems in the nucleus tractus solitarius regulate noradrenaline release in the subfornical organ area in the rat

5-HT Receptor Regulation of Neurotransmitter Release

“…5-HT Receptor WAY 161503, 8,9-dichloro-2,3,4,4-tetrahydro-1H-pyrazino͓1,2-a͔quinoxalin-5(6H)-one hydrochloride (5-HT 2C agonist); SR 57227, 1-(6-chloro-2-pyridinyl)-4-piperidinamine hydrochloride (5-HT 3 agonist); Y-25130, N-1-azabicyclo͓2.2.2͔-oct-3-yl-6-chloro-3,4-dihydro-4-methyl-3-oxo-2H-1,4-benzoxazine-8-carboxamide hydrochloride (azasetron; 5-HT 3 antagonist); ML10302, 2-(1-piperidinyl)ethyl-4-amino-5-chloro-2-methoxybenzoate (5-HT 4 agonist); RS 39604, 1-͓4-amino-5-chloro-2- (3,5-dimethoxyphenyl) 1998; Vazquez and Baghdoyan, 2003), dopaminergic (Ronken et al, 1993;Steiniger and Kretschmer, 2003), and noradrenergic neurons (Fung and Fillenz, 1983;Suzdak and Gianutsos, 1985;Tanaka et al, 2002;Sakamaki et al, 2004;Ushigome et al, 2004) Presynaptic 5-HT heteroreceptors play mainly a physiological role in the local fine regulation of the release of the transmitter from the axon terminal on which the receptors are located. They inhibit or facilitate transmitter release in response to action potentials invading the varicosities.…”

Opioid and α2 adrenergic mechanisms are activated by GABA agonists in the lateral parabrachial nucleus to induce sodium intake

“…The present results suggest that the activation of gabaergic mechanisms depends also on α 2 adrenoceptor activation to release sodium intake. Different types of interaction between adrenergic and gabaergic mechanisms have been proposed (Zarrindast et al, 2001;Han et al, 2002;Tanaka et al, 2002;Sakamaki et al, 2003). Although the activation of α 2 adrenoceptors located in the gabaergic neurons may reduce the spontaneous inhibitory synaptic current (Han et al, 2002), the modulation of noradrenaline release by gabaergic activation was described in the median preoptic nucleus and subfornicial organ (SFO) (Tanaka et al, 2002;Sakamaki et al, 2003).…”

“…Different types of interaction between adrenergic and gabaergic mechanisms have been proposed (Zarrindast et al, 2001;Han et al, 2002;Tanaka et al, 2002;Sakamaki et al, 2003). Although the activation of α 2 adrenoceptors located in the gabaergic neurons may reduce the spontaneous inhibitory synaptic current (Han et al, 2002), the modulation of noradrenaline release by gabaergic activation was described in the median preoptic nucleus and subfornicial organ (SFO) (Tanaka et al, 2002;Sakamaki et al, 2003). In addition, GABA B receptors are located in post-synaptic neurons that receives noradrenergic input (Suzdak and Gianutsos, 1985) and baclofen effects on memory retention was reduced by α 2 adrenoceptor blockade (Zarrindast et al, 2001).…”