METABOLIC AND NEUROCHEMICAL PLASTICITY OF GAMMA-AMINOBUTYRIC ACID-IMMUNOREACTIVE NEURONS IN THE ADULT MACAQUE STRIATE CORTEX FOLLOWING MONOCULAR IMPULSE BLOCKADE - QUANTITATIVE ELECTRON-MICROSCOPIC ANALYSIS

The purpose of the present study was to examine the effects of retinal impulse blockade on gamma-aminobutyric acid (GABA)-immunoreactive (GA BA-IR) neurons in cytochrome oxidase (CO)-rich puffs of the adult monk ey striate cortex. Specifically, we wished to know if changes occurred in their CO activity, GABA immunoreactivity, and synaptic organizatio n. A double-labeling technique, which combined CO histochemistry and p ostembedding GABA immunocytochemistry on the same ultrathin sections, was used to reveal simultaneously the distribution of the two markers. We quantitatively compared changes in GABA-IR neurons of deprived puf fs (DPs) with respect to non-deprived puffs (NPs) 2 weeks after monocu lar tetrodotoxin treatment. We found that the proportion of darkly CO reactive mitochondria in GABA-IR neurons of DPs drastically decreased to about half of those in NPs. There was a greater reduction of CO lev els in GABA-IR axon terminals than in their cell bodies and dendrites. In contrast, most non-GABA-IR neurons displayed no significant change in their CO levels. Morphologically, GABA-IR neurons and axon termina ls in DPs showed a significant shrinkage in their mean size. GABA immu noreactivity, as indicated by the density of immunogold particles in G ABA-IR neurons, declined in DPs, and a greater decrease was also found in axon terminals than in cell bodies or dendrites. Moreover, the num erical density of GABA-IR axon terminals and synapses in DPs was signi ficantly reduced without changes in that of asymmetric and symmetric s ynapses. Thus, the present results support the following conclusions: 1) Oxidative metabolism and neurotransmitter expression in GABA-IR neu rons are tightly regulated by neuronal activity in adult monkey striat e cortex; 2) GABA-IR neurons are much more vulnerable to functional de privation than non-GABA-IR ones, suggesting that these inhibitory neur ons have stringent requirement for sustained excitatory input to maint ain their heightened oxidative capacity; and 3) intracortical inhibiti on mediated by GABA transmission following afferent deprivation may be decreased in deprived puffs, because the oxidative capacity and trans mitter level in GABAergic neurons, especially in their axon terminals, are dramatically reduced. (C) 1996 Wiley-Liss, Inc.