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The calretinin interneurons of the striatum: comparisons between rodents and primates under normal and pathological conditions

  • Neurology and Preclinical Neurological Studies - Review Article
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Abstract

This paper reviews the major organizational features of calretinin interneurons in the dorsal striatum of rodents and primates, with some insights on the state of these neurons in Parkinson’s disease and Huntington’s chorea. The rat striatum harbors medium-sized calretinin-immunoreactive (CR+) interneurons, whereas the mouse striatum is pervaded by medium-sized CR+ interneurons together with numerous small and highly immunoreactive CR+ cells. The CR interneuronal network is even more elaborated in monkey and human striatum where, in addition to the small- and medium-sized CR+ interneurons, a set of large CR+ interneurons occurs. The majority of these giant CR+ interneurons, which are unique to the primate striatum, also display immunoreactivity for choline acetyltransferase (ChAT), a faithful marker of cholinergic neurons. The expression of CR and/or ChAT by the large striatal interneurons appears to be seriously compromised in Parkinson’s disease and Huntington’s chorea. The species differences noted above have to be considered to better understand the role of CR interneurons in striatal organization in both normal and pathological conditions.

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Fig. 1

Adapted from Wu and Parent (2000)

Fig. 2

Adapted from Petryszyn et al. (2014)

Fig. 3

Adapted from Petryszyn et al. (2016)

Fig. 4

ac Adapted from Petryszyn et al. (2014), dg adapted from Prensa et al. (1998)

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Acknowledgements

The study was supported by research grants from the Canadian Institutes of Health Research (CIHR MOP-115008 to M.P.) and the Natural Sciences and Engineering Research Council of Canada (NSERC 386396 to M.P.). The authors have no conflict of interest to declare.

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Correspondence to Martin Parent.

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Petryszyn, S., Parent, A. & Parent, M. The calretinin interneurons of the striatum: comparisons between rodents and primates under normal and pathological conditions. J Neural Transm 125, 279–290 (2018). https://doi.org/10.1007/s00702-017-1687-x

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  • DOI: https://doi.org/10.1007/s00702-017-1687-x

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