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 Freeman, J. H. Articles by Stanton, M. E. Search for Related Content PubMed PubMed Citation Articles by Freeman, J. H., Jr Articles by Stanton, M. E.

 Previous Article  |  Next Article 

Journal of Neuroscience, Vol 15, 7301-7314, Copyright © 1995 by Society for Neuroscience

ARTICLE

Disruption of cerebellar maturation by an antimitotic agent impairs the ontogeny of eyeblink conditioning in rats

JH Freeman Jr, S Barone Jr and ME Stanton
Department of Psychology, University of North Carolina at Chapel Hill 27599, USA.

This study represents an attempt to establish a relationship between maturation of the cerebellum and the ontogeny of eyeblink conditioning in the rat. Experiments 1 and 2 examined the effects of disrupting cerebellar maturation by neonatal exposure to the antimitotic agent methylazoxymethanol (MAM) on the ontogeny of eyeblink conditioning in infant rats. Experiment 1 demonstrated that neonatal exposure to MAM on Postnatal Day 4 (PND4) and 7 severely disrupted cerebellar maturation. This effect appeared to be specific in that there was no overt dysmorphology in other brain regions. MAM treatment also severely disrupted associative eyeblink conditioning in rats given training on PND24 and 25. However, exposure to MAM had no effect on the unconditioned response, T-maze delayed alternation, or conditioned suppression of ongoing behavior. In Experiment 2, MAM was given on PND4 and 7 and pups were tested behaviorally on PND17-18, 20-21, or 31-32. Cerebellar hypoplasia was most dramatic shortly after exposure. The cerebellar cortex continued to mature after exposure to MAM, but development of morphological endpoints examined here were static from PND19 to 33. Eyeblink conditioning was impaired at all ages, indicating that there was no functional recovery following neonatal exposure to MAM over the age range tested. These experiments suggest that normal cerebellar maturation may be important for the ontogeny of eyeblink conditioning.

This article has been cited by other articles:

				J. H. Freeman Jr. and D. A. Nicholson Developmental Changes in the Neural Mechanisms of Eyeblink Conditioning Behav Cogn Neurosci Rev, March 1, 2004; 3(1): 3 - 13. [Abstract] [PDF]

				D. A. Nicholson and J. H. Freeman Jr Developmental Changes in Eye-Blink Conditioning and Neuronal Activity in the Inferior Olive J. Neurosci., November 1, 2000; 20(21): 8218 - 8226. [Abstract] [Full Text] [PDF]

				J. H. Freeman Jr and D. A. Nicholson Developmental Changes in Eye-Blink Conditioning and Neuronal Activity in the Cerebellar Interpositus Nucleus J. Neurosci., January 15, 2000; 20(2): 813 - 819. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help