Stress-induced activation of median raphe serotonergic neurons in rats is potentiated by the neurotensin antagonist, SR 48692.

The activation of rostrally projecting serotonergic (5-HT) neurons by acute sound stress is blocked by exogenous administration of the tridecapeptide neurotensin (NT). 5-HT neurons respond to acute sound stress within the median raphe nucleus (MRN), but not within the dorsal raphe nucleus or hindbrain regions. By use of the NT antagonist, SR 48692, the present study examines the involvement of endogenous NT in modulating the preferential activation of MRN 5-HT neurons by sound stress, and extends the findings with sound stress to two other stressors (swim and tail shock).

Further studies on the activation of rat median raphe serotonergic neurons by inescapable sound stress.

Previous studies, using a biochemical measure of serotonergic neuronal function, show that inescapable, randomly presented sound pulses activate serotonergic neurons in the rat median raphe but not dorsal raphe nucleus. The present study reveals that this activation also occurs in serotonin projection areas, in hippocampus, nucleus accumbens and cortex but not in caudate nucleus. The selectivity of this response is examined by comparing the response to sound stress with that produced by morphine, a treatment known to selectively activate dorsal raphe but not median raphe serotonergic neurons.

Neurotensin inhibits the activation of midbrain serotonergic neurons produced by random inescapable sound.

Previous studies indicate that exposure of rats to randomly presented, inescapable loud sound, referred to as sound stress, increases central serotonin turnover as well as the ex vivo activity of tryptophan hydroxylase (EC 1.14.16.

Differential activation of the 5-hydroxytryptamine-containing neurons of the midbrain raphe of the rat in response to randomly presented inescapable sound.

Estimates of 5-hydroxytryptamine (5-HT) turnover in response to 30 min of inescapable, randomly presented, loud sound (sound stress) were obtained for regions of rat brain containing 5-HT perikarya by means of 5-hydroxytryptophan (5-HTP) accumulation after administration of an inhibitor of aromatic amino acid decarboxylase (100 mg/kg i.p., m-hydroxybenzylhydrazine, NSD 1015).

Sound stress activation of tryptophan hydroxylase blocked by hypophysectomy and intracranial RU 38486.

The rapidly reversible increase in cortical or midbrain tryptophan hydroxylase activity observed ex vivo after exposure of rats to 1-h sound stress was blocked by hypophysectomy, but not sham hypophysectomy, and restored by dexamethasone administration to the hypophysectomized animals (500 micrograms/day i.p. for 3 days).