Chronic administration of the L-type calcium channel blocker nimodipine can facilitate the acquisition of sequence learning in a radial-arm maze.

Nimodipine, a dihydropyridine L-type voltage-gated calcium-channel blocker, was examined for its potential effect on the acquisition of a complex-arm sequence task in an automated radial maze. Young (60-day-old) male Wistar rats were injected with saline or nimodipine (5 mg/kg) 15 min prior to radial maze training, or immediately following the radial maze testing. The results of the learning task (over 7 days of testing) showed that rats injected with nimodipine each training session acquired the task more quickly and more efficiently compared to saline-treated animals. There were no significant differences for rats that were pre-/post-treated with nimodipine during the maze-learning task. The number of incorrect arm entries and number of additional lever presses in the same arm were found to be significantly lower in rats treated with nimodipine compared to saline-injected controls. The beneficial effect of nimodipine treatment occurred only in rats that were acquiring the task, and not in rats that had already learned the arm sequence paradigm. There were no potential non-specific influences on locomotor activity or appetite caused by chronic nimodipine treatments. These results strongly suggest that nimodipine can facilitate the acquisition of a complex learning task.

Fos-like immunoreactivity in vagal and hypoglossal nuclei in different feeding states: a quantitative study.

This study characterized the distribution of Fos-like immunoreactivity (FLI) in three hindbrain nuclei: dorsal motor nucleus of the vagus (DMN), nucleus of the solitary tract (NST) and hypoglossal nucleus (HG) in response to eating or activation of specific components of feeding behavior. The degree of FLI was quantified by automated image analysis software that provided an efficient and sensitive method for counting the number of cells labelled with Fos antibody. Ingestion, and anticipation, of a meal both increased FLI in the DMN and HG, but not in the NST. Sham feeding 1 M sucrose was a more potent stimulus for FLI activation in DMN and NST than combined oral plus gastric/postingestive stimulation provided by real feeding the same food. The results indicate that the physiological stimulus of eating is sufficient to elicit FLI in the hindbrain and that specific components of the feeding act, especially oral stimulation provided by sham feeding, can activate FLI. The results suggest further that, under specific experimental conditions, gastric and/or postgastric stimulation may decrease FLI in the NST and DMN.