title: Synaptosomal tryptophan uptake and efflux following lesion of central 5-hydroxytryptaminergic neurones.
abstract: 1. This study attempted to determine whether the activation of the tryptophan carrier in rat forebrain synaptosomes caused by depolarization or by extracellular sodium depletion occurred exclusively in 5-hydroxytryptaminergic nerve endings. 2. Ascending 5-hydroxytryptaminergic neurones were lesioned either electrolytically or by intraventricular administration of 5,7-dihydroxytryptamine. The extent of the lesion was assessed by comparing the uptake of [3H]-5-hydroxytryptamine (5-HT) in lesioned animals and in sham-operated controls. [3H]-5-HT uptake was reduced by 85.9 +/- 1.63% (mean +/- s.e. mean) in animals receiving electrolytic lesions, and by 87.4 +/- 4.51% in those receiving 5,7-dihydroxytryptamine. 3. The uptake of [3H]-tryptophan by synaptosomes from lesioned animals incubated in standard Na(+)-rich media was slightly lower (278.8 +/- 27.3 pmol mg-1 protein min-1) than that observed in sham-operated controls (360.6 +/- 30.3 pmol mg-1 protein min-1). However, uptake in the absence of extracellular Na+ was increased to a similar extent in both the sham-operated (539 +/- 54.5 pmol mg-1 protein min-1) and lesioned animals (507.2 +/- 42.4 pmol mg-1 protein min-1). 4. The efflux of [3H]-tryptophan in response to extracellular Na+ depletion was similar in sham-operated and lesioned animals. Release expressed as a percentage of tissue [3H]-tryptophan released in response to the pulse of Na(+)-free medium was 6.691 +/- 0.585 (n = 4) in sham-operated controls and 8.195 +/- 0.906 in lesioned animals. 5. The efflux of [3H]-tryptophan in response to K+ depolarization was also unchanged in lesioned animals when compared with sham-operated controls. Release, expressed as described above was, in sham-operated controls 3.76 +/- 0.41 (n = 4) and 4.09 +/- 0.30 in lesioned animals. 6. The results of this study show that the tryptophan carrier which is activated by depolarization or by extracellular Na+ depletion is not located exclusively on 5-hydroxytryptaminergic nerve endings. Moreover the contribution made by 5-hydroxytryptaminergic neurones appears to be only minor.
authors.affiliation: Department of Physiology, University of Wales College of Cardiff.
authors.forename: L S
authors.initials: LS
authors.lastname: Wilkinson
authors.forename: K J
authors.initials: KJ
authors.lastname: Collard
mesh_terms: D015116:5,7-Dihydroxytryptamine / Q000494:pharmacology; D000818:Animals; D004566:Electrodes; D008297:Male; D009474:Neurons / Q000378:metabolism*; D011903:Raphe Nuclei / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012701:Serotonin / Q000502:physiology*; D012964:Sodium / Q000172:deficiency; D013238:Stereotaxic Techniques; D013574:Synaptosomes / Q000378:metabolism*; D014364:Tryptophan / Q000378:metabolism*
chemical_list: D015116:5,7-Dihydroxytryptamine; D012701:Serotonin; D014364:Tryptophan; D012964:Sodium