Chronic systemic melatonin treatment attenuates abnormalities produced by occlusion of middle cerebral artery (MCA) in adult rats. Because the pineal gland secretes high levels of melatonin, we examined in the present study whether transplantation of pineal gland exerted similar protective effects in MCA-occluded adult rats. Animals underwent same-day MCA occlusion and either intrastriatal transplantation of pineal gland (harvested from 2-month-old rats) or vehicle infusion. Behavioral tests (from day of surgery to 3 days posttransplantation) revealed that transplanted stroke rats displayed significantly less motor asymmetrical behaviors than vehicle-infused stroke rats. Histological analysis at 3 days posttransplantation revealed that transplanted stroke rats had significantly smaller cerebral infarction than vehicle-infused rats. Additional experiments showed that pinealectomy affected transplantation outcome, in that transplantation of pineal gland only protected against stroke-induced deficits in stroke animals with intact pineal gland, but not in pinealectomized stroke rats. Interestingly, nonpinealectomized vehicle-infused stroke rats, as well as pinealectomized transplanted stroke rats, had significantly lower melatonin levels in the cerebrospinal fluid than nonpinealectomized transplanted stroke rats. We conclude that intracerebral transplantation of pineal gland, in the presence of host intact pineal gland, protected against stroke, possibly through secretion of melatonin.

Systemic or central administration of kainic acid (KA) in rats results in the expression of wet dog shakes (WDS) followed by motoric seizures and convulsions, which are associated with limbic neurotoxicity. Although a number of neurotransmitter systems are thought to be involved with this KA-induced syndrome, little is known about the possible influence of cholinergic nicotinic receptor modulation. In the study presented here, we pretreated rats with saline or 0.5 mg/kg nicotine base followed 15 minutes later by 12.0 mg/kg KA and then observed the incidence of WDS between 45 and 120 minutes post-KA injection. Rats pretreated with nicotine exhibited significantly less WDS than those pretreated with saline (p < .001). Whereas the mechanism for this nicotine effect is currently not known, future experiments will look at dose-response relationships, the role of nicotine receptors, and possible neuroprotective potential of nicotine in this KA-induced syndrome.