engleski

Alternations of the passive avoidance acquisition in rats with damaged neocortical cholinergic innervation

Dementia of the Alzheimer type is characterized by an acquired global impairment of higher cortical functions. It has been found that a reduction in cholinergic function in the telencephalon is a result of dysfunction in the basal forebrain cholinergic system, particularly in the nucleus basalis (NB). Performance of learning and memory tasks is enhanced by cholinomimetic drugs. On the opposite, learning and memory deficits can often he induced by anticholinergic treatment (atropine, NB lesions). It was of interest to study the effects of various cholinomymetics on the avoidance behaviour in the rat with bilateral electrolytic lesions of NB equivalent. Male, Wistar albino rats weighing 350-450 g were used. The coordinates for NB lesions were: 1.8 mm anterior, 2.5 mm lateral to the bregma, 7 mm below the dura. In sham lesioned rats the electrode was only lowered into the NB without turning on the current. After 10 day postoperative recovery period the passive avoidance acquisition according to the procedure of Ashford and Jones (1976) under the influence of various drugs (i.p.) was measured. Drugs used were: lecithin (3.2 x 10-4 mol/kg), arecoline (6.4 x 10-6 mol/kg), lecithin (3.2 x 10-4 mol/kg) + arecoline (6.4 x 10-6 mol/kg), THA (5.0 x 10-6 mol/kg), galantamine (3.4 x 10-6 mol/kg), physostigmine (3.0 x 10-7 mol/kg). It has been found out that the avoidance acquisition deficit in NB lesioned rats was improved by arecoline and lecithin alone or, in combination, while mentioned AChE reversible inhibitors didn't influence it significantly.

nucleus basalis lesion; passive avoidance; lecithin; arecoline; THA; galantamine; physostigmine; rat

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