Postnatal development of parvalbumin‐ and GABA transporter‐immunoreactive axon terminals in monkey prefrontal cortex
- 8 May 2002
- journal article
- research article
- Published by Wiley in Journal of Comparative Neurology
- Vol. 448 (2) , 186-202
- https://doi.org/10.1002/cne.10249
Abstract
In the primate prefrontal cortex, the axon terminals of the chandelier class of inhibitory local circuit neurons have a distinctive time course of postnatal development. In this study, we sought to determine whether the axon terminals of other classes of local circuit neurons are also refined during postnatal development. We examined postnatal changes in the density of punctate structures immunoreactive for the calcium binding protein parvalbumin, which identifies a subset of gamma‐aminobutyric acid (GABA) ‐containing terminals, in the prefrontal cortex of 35 rhesus monkeys ranging in age from newborn to adult. In area 46, the density of parvalbumin‐ immunoreactive puncta in the superficial and middle layers was extremely low in the newborn animals, then increased more than 10‐fold to adult levels, which were achieved by 3 to 4 years of age. In layer V, a band of labeled puncta present in the newborn animals also increased in density until 3 to 4 years of age. Developmental changes of parvalbumin‐immunoreactive puncta in area 9 were similar to those in area 46. In contrast, the density of punctate structures labeled with an antibody against a GABA membrane transporter (GAT‐1) did not change across development, suggesting that the number of GABAergic terminals is stable over time, but that the level of parvalbumin protein within the terminals varies. The time course of the observed changes in these parvalbumin‐labeled terminals is markedly different from that of parvalbumin‐immunoreactive chandelier cell terminal clusters. These findings suggest that morphologically specialized classes of inhibitory interneurons assume prominence within the prefrontal cortical network at different stages of postnatal development. J. Comp. Neurol. 448:186–202, 2002.Keywords
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