Monoaminergic mechanisms in stress-induced analgesia

Male albino rats given brief transcutaneous electric footshock showed an elevation in tail-flick response latency--an effect called stress-induced analgesia (SIA). The influence of pretreatments altering monoaminergic neurotransmission on SIA were studied. Inhibition of monoamine storage in presynaptic vesicles reduced SIA, while additional inhibition of serotonin synthesis abolished the SIA response. In contrast, inhibition of serotonin synthesis alone failed to influence SIA. Blockade of dopaminergic receptors reduced SIA, while induction of dopaminergic receptor supersensitivity failed to affect footshock-induced analgesia. Neither inhibition of monoamine oxidase nor blockade of noradrenergic neurotransmission affected SIA significantly. The results suggest that serotonergic and dopaminergic rather than noradrenergic mechanisms contribute to SIA.