Elsevier

Neuroscience Letters

Volume 75, Issue 3, 10 April 1987, Pages 259-264
Neuroscience Letters

A morphogenic role for transiently expressed acetylcholinesterase in developing thalamocortical systems?

https://doi.org/10.1016/0304-3940(87)90531-3Get rights and content

Abstract

Experiments in infant rats have revealed patterns of intense acetylcholinesterase (AChE) activity in primary sensory thalamic nuclei and thalamocortical recipient zones of primary sensory areas of cerebral cortex. The distribution and appearance of AChE staining indicates that the transient AChE in these areas is characteristic of thalamocortical neurons. The patterns of AChE are detectable during the first postnatal week of life, reach peak intensity during the second postnatal week, and decline to normal adult levels by the end of the third postnatal week. These temporal parameters correlate well with the time of thalamocortical axon growth into the cerebral cortex. These data suggest that the transient AChE may be playing a morphogenic role in the development of thalamocortical connections.

References (23)

  • L.L. Butcher et al.

    Histochemical distribution of acetylcholinesterase in the central nervous system: clues to the localization of cholinergic neurons

    Handb. Chem. Neuroanat.

    (1984)
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