Effect of Intracerebroventricular [IVT] administration of endogenous opoids morphine on brain acetyl-choline release in rats

In the present study, female Wistar albino rats were employed as experimental animals. Acetylcholine [Ach] release was collected with the help of collecting cups placed on the cortex every five minuties. Collection was started 30 minutes prior to i. v. t. administration of test drug and continued for 120 minutes. Ach was bioassayed on leech muscle preparation. It was observed that morphine, beta-endorphin, etorphine and met - enkephalin ub decreased the Ach release. Morphine and beta-endorphin showed most potent effect while met - enkephalin had a minimum effect on Ach release. Etorphine induced inhibition was of a transient nature. Leu - enkephalin did not show any inhibitory effect on Ach release. Naloxone administration, 30 minutes after beta-endorphin, reversed the inhibitory effect on Ach release to pre - drug level

Clonidine effect on brain acetylcholine content and release

Clonidine, a potent centrally acting antihypertensive drug was screened for the effect on "free" and "bound" content and acetylcholine [Ach] release in brain of morphine dependent and withdrawal rats. "Free" and "total" Ach content in normal [non- dependent animals as well as animals dependent to morphone was not changed by clonidine. Naloxone produced abstinence syndrome in dependent rats with highly significant increase in "free" and release of Arh. Clonidine pretreatment decreased the rise of "free" content and release of Ach produced by Naloxone

production of morphine physical dependence by the oral route and the assessment of the withdrawal syndrome

A method for the chronical administration of morphine by the oral route is discussed. The method recommends the administration of morphine HCl dissolved in a 45% sucrose syrup and given orally for 4 weeks. The initial concentration of morphine in the syrup was 1 mg/ml and was increased weekly upto 4 mg/ml at the end of the experiment. This procedure rendered the animals physically dependent on morphine as observed by drugs withdrawal, when abstinence symptoms were easily identified. It became clear that morphine dependence phenomena [tolerance and the drug induced abstinence syndrome] in both rats and mice developed in association with, and were probably attributable to, change in the activity of cholinergic neurons