QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Johnson, F. Articles by Bottjer, S. W. Search for Related Content PubMed PubMed Citation Articles by Johnson, F. Articles by Bottjer, S. W.

 Previous Article  |  Next Article 

Journal of Neuroscience, Vol 13, 2452-2462, Copyright © 1993 by Society for Neuroscience

ARTICLE

Induced cell death in a thalamic nucleus during a restricted period of zebra finch vocal development

F Johnson and SW Bottjer
Department of Biological Sciences, University of Southern California, Los Angeles 90089-2520.

A discrete network of forebrain nuclei underlies vocal learning and production in male zebra finches. Three nuclei within this network form a neural pathway that is particularly important for vocal learning in juveniles: area X of the avian striatum projects to the medial dorsolateral nucleus of the anterior thalamus (DLM), which in turn projects to the lateral magnocellular nucleus of the anterior neostriatum (IMAN). Lesions of any of these nuclei in juvenile birds disrupt normal vocal development, whereas the same lesions in adult birds have no effect on already-learned song. Because numerous studies have shown that neuronal survival in the developing nervous system depends on access to efferent targets, we have investigated the possibility that the survival of DLM neurons is similarly regulated over the course of vocal learning. Thus, the efferent target of DLM (IMAN) was lesioned electrolytically in male birds at various stages of vocal development (20, 40, 60 d of age and adult) and birds were killed either 2, 4, or 6 d postlesion. Electrolytic lesions of IMAN removed the single identified efferent target of DLM projection neurons and axotomized the terminal arborizations of these neurons. Although DLM does not normally lose neurons during vocal development, IMAN lesions in 20-d-old birds yielded numerous pyknotic cells throughout DLM by 4 d postlesion and a two-thirds reduction in DLM neuron density by 6 d postlesion. In contrast, IMAN lesions in adult birds had little or no effect on neuronal survival in DLM. Analysis of 40-d-old birds revealed significant but less substantial cell loss than in 20-d-old birds, whereas 60-d-old birds were not different from adults. The age-related decline in the vulnerability of DLM cells to IMAN lesion-induced death suggests that factors that regulate DLM neuron survival may also be involved in the acquisition of learned vocal behavior in songbirds.

This article has been cited by other articles:

				R. Mooney and J. F. Prather The HVC Microcircuit: The Synaptic Basis for Interactions between Song Motor and Vocal Plasticity Pathways J. Neurosci., February 23, 2005; 25(8): 1952 - 1964. [Abstract] [Full Text] [PDF]

				A. D. Tramontin, V. N. Hartman, and E. A. Brenowitz Breeding Conditions Induce Rapid and Sequential Growth in Adult Avian Song Control Circuits: A Model of Seasonal Plasticity in the Brain J. Neurosci., January 15, 2000; 20(2): 854 - 861. [Abstract] [Full Text] [PDF]

				F. Johnson, S. E. Hohmann, P. S. DiStefano, and S. W. Bottjer Neurotrophins Suppress Apoptosis Induced by Deafferentation of an Avian Motor-Cortical Region J. Neurosci., March 15, 1997; 17(6): 2101 - 2111. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help