Mechanisms involved in the interaction of various central stimulants and reserpine

1. 1. It has been confirmed that low doses of reserpine phosphate produce spontaneous seizures and facilitate evoked seizures in the rhinecephalon without affecting thalamocortical recruiting responses and electrocortographic “arousal”. 2. 2. The occurrence of cortical low voltage fast activity after administration of large doses of reserpine phosphate can be blocked by atropine. Atropine does not interfere with evoked rhinecephalic seizure discharges. 3. 3. Activation of the reticular system of the brainstem by electrical stimulation of administration of central stimulants such as amphetamine, ibogaine, pipradol and methylphenidate exerts various graded effects according to stimulus intensity or dosage used: ◦ ( a) “Low dose — low intensity” stimulation causes a cortical arousal reaction with little or sometimes no diminution of the thalamo-cortical recruiting response. Such stimuli do not influence the electrically evoked limbic paroxyms in either control or reserpine-treated animals. ◦ ( b) “Higher dose — higher intensity” stimulation provokes not only cortical fast activity but also causes a considerable diminution of the thalamo-cortical recruiting response. It reduces the length of rhinencephalic seizures in control and reserpine-treated animals. 4. 4. The possible mechanisms involved in the interaction of reserpine and central stimulants are discussed in the light of the clinical potentiality of drug combinations of this type.