Postnatal development of parvalbumin‐ and GABA transporter‐immunoreactive axon terminals in monkey prefrontal cortex

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.

A Specific Role for NR2A-Containing NMDA Receptors in the Maintenance of Parvalbumin and GAD67 Immunoreactivity in Cultured Interneurons

“…2 A). The expression of PV in cortical neuronal cultures followed a similar developmentally regulated pattern as that described in vivo for rodents and primates (de Lecea et al, 1995;Philpot et al, 1997;Erickson and Lewis, 2002), appearing after 8 -9 d in vitro (DIV8 -9) when the PV-positive subpopulation represented 8% of the GABAergic population (as determined by double immu-nocytochemistry using anti-PV and anti-GAD67 antibodies), and increasing thereafter reaching a plateau at approximately DIV20, when they reached ϳ50% of the GABAergic population (Fig. 2).…”

Differential expression of arc mRNA and other plasticity-related genes induced by nicotine in adolescent rat forebrain

“…The prefrontal cortex, an area of adolescent brain where we found differential induction of arc following acute nicotine, undergoes dramatic changes during adolescence including extensive synaptic pruning, alterations in dopaminergic input and changes in intrinsic circuitry (Rosenberg and Lewis, 1995;Cunningham et al, 2002;Erickson and Lewis, 2002;Cruz et al, 2003). Anatomical tracing studies indicate that projections from the amygdala to mPFC continue to increase in density throughout adolescence (Cunningham et al, 2002), suggesting that connectivity between emotional and cognitive areas undergoes refinement during this period.…”

Altered Cortical Expression of GABA-Related Genes in Schizophrenia: Illness Progression vs Developmental Disturbance

“…Animals were housed according to age as previously described. 37 All housing and experimental procedures were conducted in accordance with the guidelines of the US Department of Agriculture and the NIH Guide for the Care of Animals, and with approval from the University of Pittsburgh's Institutional Animal Care and Use Committee.…”