GABA immunoreactive neurons in rat visual cortex

Abstract

An antiserum to gamma-aminobutyric acid (GABA) was used in a light and electron microscopic immunocytochemical study to determine the morphology and distribution of GABA-containing neurons in the rat visual cortex and to ascertain whether all classes of nonpyramidal neurons in this cortex are GABAergic. The visual cortex used for light microscopy was prepared in such a way that the antibody penetrated completely through tissue sections, and in these sections large numbers of GABA immunoreactive neurons were apparent. The labeled neurons could be identified as being either multipolar, bitufted, bipolar, or horizontal neurons. In layers II through VIa, GABA immunostained cells were distributed uniformly and accounted for approximately 15% of all neurons, but in layer I all neurons appeared to be immunostained. Electron microscopy of GABA immunostained visual cortex prepared to ensure good fine structural preservation confirmed the presence in layers II through VIa of numerous immunoreactive bipolar neurons, both small and large varieties, as well as multipolar and bitufted neurons. Additionally, electron microscopy reveals that astrocytes are frequently GABA immunoreactive. From a correlated light and electron microscopic evaluation of neurons in GABA immunostained visual cortex, it was possible to confirm which kinds of neurons are GABAergic and what proportion of the neuronal population they represent. Thus, from an analysis of some 950 neurons, it was found that pyramidal neurons were never immunoreactive and that except for 20% of the bipolar cell population, all examples of other types of nonpyramidal neurons encountered in this material were GABA immunoreactive.

Lineage analysis reveals neurotransmitter (GABA or glutamate) but not calcium-binding protein homogeneity in clonally related cortical neurons

“…Moreover, the distribution of GABA-, Asp-, and Glu-immunoreactive elements was in accordance with previous reports in which preembedding immunohistochemical protocols were applied (Conti et al, 1987a;Meinecke and Peters, 1987;Dori et al, 1989). The only exception was the degree of coexistence of Glu and Asp immunoreactivity in pyramidal neurons.…”

“…In the mature cerebral cortex, the two populations of neurons can be reliably marked by the presence of the classical neurotransmitters Glu or GABA. The numerical relationship between these two neuronal cell types is very similar in different cortical areas and in various mammalian species (Rockel et al, 1980;Hendt-y et al, 1987;Meinecke and Peters, 1987) with a large preponderance of pyramidal over nonpyramidal neurons, suggesting that their production is regulated by rigidly controlled mechanisms. Any imbalance of excitatory and inhibitory stimuli can seriously alter cortical functions leading to epileptogenesis (Traub et al, 1987) and degeneration of neuronal circuits (Mattson and Kater, 1989).…”

Presynaptic GABAB Receptors Modulate Thalamic Excitation of Inhibitory and Excitatory Neurons in the Mouse Barrel Cortex

“…Post hoc morphological analysis demonstrates that this cell exhibits a nonpyramidal morphology with aspiny dendrites (Fig. 1B), confirming its electrophysiological classification as an inhibitory cortical neuron (Meinecke and Peters 1987;Ribak 1978). Furthermore, in this example the neuron forms putative synaptic contacts with an unlabeled cell body.…”

Metabotropic Glutamate Receptor Type 5-Dependent Long-Term Potentiation of Excitatory Synapses on Fast-Spiking GABAergic Neurons in Mouse Visual Cortex

“…The possibility to record excitatory synaptic responses from GABAergic neurons in the visual cortex is low, because the proportion of GABAergic neurons is only 15-25% of all neurons in the rodent neocortex and their soma sizes are generally smaller than those of excitatory neurons (Meinecke and Peters, 1987;Ren et al, 1992;Gonchar and Burkhalter, 1997;Kawaguchi and Kubota, 1997). To overcome this problem we used transgenic mice, in which expression of green fluorescence protein (GFP) is regulated by glutamate decarboxylase 67 (GAD67) gene promoter (GAD67-GFP knock-in mice) (Tamamaki et al, 2003).…”