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Serotonergic Regulation of in Vivo Neuritogenesis in the Adult Snail

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image of Netherlands Journal of Zoology
For more content, see Archives Néerlandaises de Zoologie (Vol 1-17) and Animal Biology (Vol 53 and onwards).

Injury induces well defined changes in the cerebrobuccal neurons of the pulmonate Achatina fulica. A lesion to the cerebral-buccal connective (CBC) causes axotomized neurons to grow new processes which re-innervate their original targets via either the repaired pathway or the contralateral CBC. The lesion also induces uninjured neurons to sprout new processes which invade denervated regions. One cerebrobuccal neuron which has been particularly well studied is the metacerebral giant (MCG) cell, which provides the sole source of serotonin (5-HT) to the buccal ganglia. Since this cell possesses mostly unilateral projections in Achatina, a lesion to one CBC causes nearly complete, unilateral depletion of serotonin 5-HT from the buccal ganglia. Two lines of evidence suggest that this depletion plays a major role in the expression of sprouting responses seen after a lesion to the CBC. First, pharmacological depletion of 5-HT, using 5,7-dihydroxytryptamine, p-chlorophenylalanine or reserpine causes much the same pattern of sprouting as seen after a lesion. Second, lesion-induced sprouting can be inhibited by systemic administration of 5-HT. Such actions of 5-HT appear to be receptor mediated. Cyproheptadine, which blocks a slow, depolarizing action of 5-HT on some Achatina neurons, also blocks 5-HT inhibition of sprouting. Other 5-HT antagonists, which were less effective at blocking the depolarizing response, were also less effective in blocking the 5-HT inhibition of sprouting. Our results, thus, indicate that changing levels of 5-HT are both necessary and sufficient to explain a large amount of the sprouting response observed after a lesion to the CBC.

Affiliations: 1: Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4H7

10.1163/156854293X00412
/content/journals/10.1163/156854293x00412
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/content/journals/10.1163/156854293x00412
1993-01-01
2016-12-07

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