Serotonergic and cholinergic mechanisms during disruption of approach and avoidance behavior
Injections of d,l-5-hydroxytryptophan (d,l-5-HTP) into pigeons and rats’ working on approach schedules produce a period of behavioral depression that is temporally correlated to increased levels of total serotonin (5-HT) in the telencephalon and diencephalon. Administration of α-methyl-meta-tyrosine (α-MMT) also results in depressed responding; however, the temporal correlation is with decreased levels of total 5-HT in brain. Our hypothesis to explain these two apparent opposite biochemical states which result in similar behavioral disruptions is that in both cases more 5-HT is released within certain key serotonergic synapses mediating this behavior. Evidence from subcellular studies supports this concept. Not only are the levels of 5-HT significantly higher in preparations of nerve endings isolated from the telencephalon and diencephalon of pigeons given injections of d,l-5-HTP, but in vitro studies also show that low concentrations of l-5-HTP significantly increased the release of radioactive 5-HT from serotonergic nerve endings. On the other hand, l-5-HTP in much higher concentrations had no effect on the release of labeled dopamine or norephinephrine. A major metabolite of α-MMT, α-methyl-meta-tyramine, also caused a significant increase in the release of labeled 5-HT from similar preparations of nerve endings. Whereas serotonin appears to be involved in the disruption of approach behavior, another series of studies have indicated that acetylcholine may play a role in excitation during avoidance behavior. Behavioral excitation observed following administration of tetrabenazine 18 hr after iproniazid pretreatment to rats working on shock-avoidance schedules was temporally correlated with lowered levels of acetylcholine in the telencephalon. Pretreatment with 0.8 mg/kg of atropine blocked excitation whereas one-eighth of this dose increased the duration. Excitation in these rats was shortened by 50% following bilateral septal lesions, which lowered brain acetylcholine levels. Mechanisms to explain these neurochemical correlates of behavior are discussed.—Aprison, M. H., J. N. Hingtgen, and W. J. Mcbride. Serotonergic and cholinergic mechanisms during disruption of approach and avoidance behavior. Federation Proc. 34: 1813–1822, 1975.
KeywordsNerve Ending Avoidance Behavior Optic Lobe Approach Behavior Brain Part
- Mult FR 50 FI 10
multiple fixed-ratio 50, fixed-interval 10 minutes.
Unable to display preview. Download preview PDF.
- 7.Aprison, M. H., and J. N. Hingtgen. Life Sci. 5: 1971, 1966.Google Scholar
- 8.Aprison, M. H., and J. N. Hingtgen. Recent Adv. Biol. Psychiatry 8: 87, 1966.Google Scholar
- 11.Aprison, M. H., and J. N. Hingtgen. Federation Proc. 31: 121, 1972.Google Scholar
- 19a.Hingtgen, J. N., and M. H. Aprison. Life Sci. In press.Google Scholar
- 26.Porter, C. C., J. A. Totaro and C. M. Leibyj. Pharmacol Exp. Ther. 134: 139, 1961.Google Scholar