Long-term effects of postnatal aluminium exposure on acetylcholinesterase activity and biogenic amine neurotransmitters in rat brain.

The long-term effects of early postnatal exposure to aluminium on acetyl choline esterase (AChE) activity and on biogenic amines were studied in different brain regions. The subjects were eight days old male Wistar rat pups. They were grouped into normal control and aluminium exposed groups. For aluminium exposure, the pups were gastric intubated with aluminium chloride (40 mg/Kg body weight) for two weeks. Control rats were given equal volumes of distilled water. After the treatment, they were rehabilitated for forty days. On the sixtieth day, the rats from both the groups were sacrificed and AChE activity, levels of dopamine, noradrenaline and serotonin were estimated in the cerebral cortex, hippocampus, septum, brainstem and striatum. In the aluminium exposed group: the AChE activity was significantly decreased in the hippocampus, septum, striatum and brainstem; serotonin levels were reduced by 20% in the cortex, hippocampus, septum and striatum; in brain stem, the serotonin level was decreased by 40%. A 60% reduction in noradrenaline levels was observed in the striatum whereas it was reduced by 25% in other regions except in hippocampus. Though dopamine levels were not altered in the cortex, septum and brainstem, they were reduced by 40% in the striatum. The study documents the long-term consequences of exposure to aluminium during the developmental periods.

Success of autonomic operant conditioning of heart rate without involving contractions of somatic skeletal muscles.

In conscious Wistar rats neuromuscularly paralysed by gallamine, operantly conditioned reduction of heart rate was achieved under both negative and positive reinforcement schedules using the tail shock avoidance or the rewarding brain-stimulations in 20-min test sessions. The primary aim was to assess whether it would be possible to achieve operant conditioning of the heart rate, evoked not as a secondary reflex response of any voluntary skeletal muscular contractions of trunk but as a conditioned voluntary function of the central autonomic regulation of a visceral organ, since this entire subject was peculiarly left in confusion by Miller (5, 8) who wanted that others should independently study it. This study revealed interestingly that not every subject might be able to achieve the visceral learning in a given set of conditions, and suggested that this type of a special learning might be dependent on individual predisposition in the central nervous system. In the present study, 15 showed the learning, out of the 58 subjects assessed. It was also observed that there was a variation in the magnitude of the learning response among different learners, and, also, in the same subject in different sessions conducted on different days. This is considered as an indication that this type of conditioned autonomic function is probably not easily recruited into the long-term memory mechanisms. The overall average of the operant lowering of the heart rate progressively achieved by the end part of the learning session was about 10.5% from the basal average rate, and the score of reinforcement (per cent of painful tail shocks avoided, or of increase in number of brain shocks achieved) was over 80%. The extinction test confirmed the learning. Control experiments revealed that the conditioned heart rate changes were not due to any unconditioned stimulus effects. The learning observed under the brain-stimulation reinforcement was confirmed by losing the learning response after lesioning the site of the rewarding stimulation. The visceral operant learning occurring in state of somatomotor paralysis under both negative and positive types of reinforcement was blocked by haloperidol. Morphine delayed the onset of the pain avoidance operant learning, whereas it speeded up the hedonic brain-stimulation operant learning. The results, considered from all the above angles, dispell the doubt previously expressed about the occurrence of the operant conditioning of heart rate under a visceral learning paradigm.