Ventral hippocampal nicotinic acetylcholine receptors mediate stress-induced analgesia in mice

• Exposure to acute elevated platform stress produced analgesia in mice.
• Intra-VH microinjection of nicotine potentiated stress-induced analgesia (SIA).
• Blockade of ventral hippocampal nicotinic receptors by injection of mecamylamine inhibited SIA.
• Intra-VH injection of nicotine or mecamylamine by itself had no effect on SIA.
• Mecamylamine reversed the potentiative effect of nicotine on SIA.

Evidence suggests that various stressful procedures induce an analgesic effect in laboratory animals commonly referred to as stress-induced analgesia (SIA). The aim of the present study was to assess the role of ventral hippocampal (VH) nicotinic acetylcholine receptors (nAChRs) in SIA in adult male NMRI mice. The VHs of animals were bilaterally cannulated and nociceptive threshold was measured using infrared source in a tail-flick apparatus. Acute stress was evoked by placing the animals on an elevated platform for 10, 20 and 30 min. The results showed that exposure to 20 and 30 min acute stress produced analgesia, while exposure to 10 min stress had no effect on the pain response. Intra-VH microinjection of nicotine (0.001–0.1 μg/mouse), 5 min before an ineffective stress (10 min stress), induced analgesia, suggesting the potentiative effect of nicotine on SIA. It is important to note that bilateral intra-VH microinjections of the same doses of nicotine without stress had no effect on the tail-flick test. On the other hand, intra-VH microinjection of mecamylamine (0.5–1 μg/mouse) 5 min before 20-min stress inhibited SIA. However, bilateral intra-VH microinjections of the same doses of mecamylamine without stress had no effect on the tail-flick response. In addition, the microinjection of mecamylamine into the VH reversed the potentiative effect of nicotine on SIA. Taken together, it can be concluded that exposure to acute stress induces SIA in a time-dependent manner and the ventral hippocampal cholinergic system may be involved in SIA via nAChRs.