Galanin fails to alter both acquisition of a two trial per day water maze task and neurochemical markers of cholinergic or serotonergic neurones in adult rats.

The co-existence of galanin with acetylcholine in ventral forebrain neurones combined with evidence that galanin attenuates cholinergic function and is present in senile plaques in Alzheimer's disease all implicate this neuropeptide in the regulation of cognition. This study simultaneously examines the effect of galanin on acquisition in a Morris water maze and post-training markers of cholinergic and serotonergic forebrain neurones thought to be involved in cognition. Synthetic porcine galanin (10(-9) to 10(-6) M) produced dose-related inhibition of atropine sensitive indirectly-evoked contractions of an isolated guinea-pig ileum which was unaffected by naloxone (10(-7) M). This confirmed the bioactivity of synthetic galanin, which reduces acetylcholine, but not opiate, release from the ileal myenteric plexus. Galanin pretreatment (1 or 10 micrograms i.c.v., -15 min) failed to alter acquisition of a Morris water maze task (2 trials per day) in Hooded Lister rats. Following behavioural acquisition, five days of galanin administration did not alter choline acetyltransferase activity, thyrotrophin-releasing hormone-like immunoreactivity or 5-hydroxytryptamine levels or turnover in the frontal cortex, hippocampus or septum, although dopamine levels were significantly elevated in the frontal cortex. These findings suggest that galanin does not affect acquisition in a simple visual-spatial task which taxes reference more than working memory and questions the assumption that a cholinergic mechanism is the major contributor to previously reported cognitive effects of galanin.