Possible Indications of Noradrenergic Involvement in Behavioral Plasticity
The modifiability of neuronal substrates by early postnatal experience, as in the case of early visual experience (Hubel and Weisel, 1965), stimulated much interest in behavioral plasticity. The early hypothesis concerning central catecholamine (Carlsson et al., 1962) involvement in plasticity was demonstrated in experiments depleting catecholamines by use of the catecholamine neurotoxin 6-hydroxydopamine (Kasamatsu and Pettigrew, 1976). Subsequent investigations indicated that administration of the putative neurotransmitter norepinephrine (NE) restored plasticity abolished by catecholamine depletion after 6OHDA (Pettigrew and Kasamatsu, 1978). In the present account, two possible indications of behavioral plasticity implicating noradrenergic modulation are described: (1) the improvement of rats’ ability to perform in the Hebb—Williams maze task following post-weaning housing in a complex environment is abolished by postnatal NE depletion, and (2) central and spinal depletion of NE antagonizes the analgesia induced by the 5hydroxytryptamine (5-HT) agonist 5-methoxy-N,N-dimethyltryptamine, and the intrathecal administration of NE restores the analgesic effects of the 5-HT agonist.
KeywordsBehavioral Plasticity Ocular Dominance Spontaneous Motor Activity Monocular Deprivation Noradrenergic Modulation
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