Involvement of midbrain tectum neurokinin-mediated mechanisms in fear and anxiety

Electrical stimulation of midbrain tectum structures, particularly the dorsal periaqueductal gray (dPAG) and inferior colliculus (IC), produces defensive responses, such as freezing and escape behavior. Freezing also ensues after termination of dPAG stimulation (post-stimulation freezing). These defensive reaction responses are critically mediated by γ-aminobutyric acid and 5-hydroxytryptamine mechanisms in the midbrain tectum. Neurokinins (NKs) also play a role in the mediation of dPAG stimulation-evoked fear, but how NK receptors are involved in the global processing and expression of fear at the level of the midbrain tectum is yet unclear. The present study investigated the role of NK-1 receptors in unconditioned defensive behavior induced by electrical stimulation of the dPAG and IC of male Wistar rats. Spantide (100 pmol/0.2 μL), a selective NK-1 antagonist, injected into these midbrain structures had anti-aversive effects on defensive responses and distress ultrasonic vocalizations induced by stimulation of the dPAG but not of the IC. Moreover, intra-dPAG injections of spantide did not influence post-stimulation freezing or alter exploratory behavior in rats subjected to the elevated plus maze. These results suggest that NK-1 receptors are mainly involved in the mediation of defensive behavior organized in the dPAG. Dorsal periaqueductal gray-evoked post-stimulation freezing was not affected by intra-dPAG injections of spantide, suggesting that NK-1-mediated mechanisms are only involved in the output mechanisms of defensive behavior and not involved in the processing of ascending aversive information from the dPAG.

Galanin stimulates hCG induced testicular steroidogenesis in adult but not in immature male rats.

The present study was undertaken to understand the role of galanin on testosterone secretion. Leydig cells from adult (60-80 days old) and immature (21-30 days old) rat testis were incubated with galanin (100 nM), galantide (100 nM) and Human Chorionic Gonadotropin (hCG, 25 I.U.) alone or in combinations and testosterone release was measured. It was observed that in adults, galanin failed to alter the basal testosterone release from the dispersed Leydig cells but potentiated the hCG induced testosterone release significantly. While galantide, prevented this galanin potentiating effect, but it did not alter the hCG alone induced testosterone release. On the other hand, the Leydig cells obtained from immature male rats were sensitive to hCG alone but not to galanin or galantide, both of which failed to alter the hCG induced testosterone release from these cells. Based on these results it can be postulated that galanin's role at the level of the male gonad is age dependent since its potentiating effects on hCG induced testosterone release were visible only in the adult and not in the immature male rats.