The present study was undertaken to investigate the role of acetylcholine in central vasomotor regulation in dogs. Both acetylcholine and carbachol produced a pressor response on intracerebroventricular (i.c.v.) administration. This response was completely blocked by pretreatment with i.c.v. atropine. Administration of hemicholinium into the lateral cerebral ventricle as well as its topical application to the floor of the fourth ventricle depressed the responsiveness of the medullary vasomotor center. Furthermore, choline, a precursor of acetylcholine, reversed the effects of hemicholinium. It is concluded that acetylcholine has an excitatory role in the medullary vasomotor center.

Dichlorvos (O,O-dimethyl-2:2-dichlorovinyl phosphate) was administered IP (3 mg/kg) daily for 10 days to a group of albino rats. Open field behavior was significantly depressed below the mean of the control group. On day 7, ambulation was reduced to 24% of the mean but recovered to 60% on day 10. Similarly, rearing response was decreased on day 7 and showed a fast recovery on day 10 but the preening response further declined on day 10. Defecation, on the contrary, was suppressed to 0% on day 7 and showed complete recovery on day 10. Motor activity showed a significant depression and fine movements were reduced more than gross movements in the second phase. Dopamine was significantly decreased on days 5 and 7 but showed a 13% recovery in the brain stem on day 10. Norepinephrine was significantly reduced in the cerebral hemisphere while serotonin was decreased both in cerebral hemisphere and brain stem. Neither of thse two amines showed significant recovery on day 10. Interesting concordance of the open field behavioral changes with the levels of dopamine, norepinephrine, and serotonin in the various regions of the rat brain was noticeable and has been discussed.

Lipid peroxidation in vitro homogenates of brain was examined as sequela of lead toxicity. The levels of malondialdehyde (MDA) in homogenates of rat brain (1 ml, 5% w/v) treated with lead (50 micrograms) alone or in combination with ascorbic acid (100 micrograms), alphatocopherol (100 micrograms) or hydroquinone (100 micrograms) were evaluated. The levels of MDA were consistently evoked by lead in a dose-related manner. The toxicity of lead was further advanced by the action of the pro-oxidant drug ascorbic acid on the brain. However, the anti-oxidant drugs alphatocopherol and hydroquinone decreased the toxic effect of lead on the brain. These results clearly show that the enhanced lipid peroxidation may provide a basis of lead-induced neurotoxicity.

No abstract