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The antagonisms of atropine to the EEG effects of adrenergic drugs.
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1959
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NeurotransmitterAnesthetic MechanismPsychopharmacologyPharmacotherapyAtropine AdministrationSocial SciencesMolecular PharmacologyEeg EffectsAdrenergic DrugsNeurologyNeurochemistryAnesthetic PharmacologyNeuropharmacologyEeg PatternNervous SystemDopaminePharmacologyEeg ArousalNeurotransmitter SystemsNeurobiological MechanismNeurophysiologyNeuroanatomyPhysiologyNeuroscienceCentral Nervous SystemMedicine
Atropine administration antagonized the electroencephalographic activation produced by epinephrine, methamphetamine and d -amphetamine in rabbits transected at the ponto-mesencephalic junction. Likewise, a persistent alert EEG pattern induced by d -amphetamine or methamphetamine in intact animals was abolished by atropine. Midbrain transections, however, prevented the electrocortical arousal produced by these agents, whereas sections at the ponto-mesencephalic junction did not. Thus centers in the posterior part of the midbrain are necessary for the adrenergic effects observed. Physostigmine produced an electrocortical activation in animals transected at the pontomesencephalic junction but did not in those transected in the midbrain. Therefore, the same region of the brainstem is apparently involved in the EEG arousal induced by cholinergic and adrenergic drugs. Atropine antagonized the EEG effect of physostigmine. Transection at the posterior border of the pons resulted in an animal which manifested a persistent alert EEG. This EEG pattern was changed to a synchronous one by the administration of atropine. Therefore, atropine inhibited an alert electrocortical pattern resulting from (1) brain lesions, (2) cholinergic drugs or (3) adrenergic drugs.