Distribution of glutamate‐decarboxylase‐immunoreactive neurons and synapses in the rat and monkey hippocampus: Light and electron microscopy

Abstract

We have studied the distribution of gamma-aminobutyric acid (GABA) neurons, axons, and synapses in the rat and monkey hippocampal formation by using glutamate decarboxylase (GAD) immunocytochemistry together with Nissl stains, electron microscopy, and double-labeled retrograde transport of horseradish peroxidase. The numbers of GAD-containing (putative GABA) neurons and their percentages compared to all Nissl-stained neurons were calculated throughout all the various fields and strata of the mammalian hippocampus. Although their numbers are greatest in the polymorph region of the fascia dentata (FD) and in the principal cell layers stratum pyramidale (SP) and stratum granulosum (SG), GAD immunoreactive (GAD-IR) cells are numerous in other strata that contain mostly dendrites and scattered cells. These GAD-IR (putative GABA) neurons in dendritic regions may be involved in feedforward dendritic inhibition or may directly inhibit nearby neurons. We used a postmortem delay technique, which resulted in apparent diffusion of GAD into dendrites and axons and allowed better visualization of the extensive dendritic domain of GAD-IR neurons. Computerized image analysis of GAD-IR puncta indicated that putative GABA terminals were numerous on apical and basilar dendrites of all pyramidal cells but unexpectedly highest in the monkey presubiculum. In the rat, GAD-IR neurons projected axons ipsilaterally from every region to the fascia dentata and CA1; however, commissural GAD-IR axons to the fascia dentata arose from GAD-IR neurons in only the contralateral fascia dentata and subiculum. Electron microscopy of GAD-stained hippocampus identified GAD-IR neurons with non-GAD-IR (possibly excitatory) synapses and GAD-IR terminals on somata and dendrites, 80% being the symmetric type and 20% the asymmetric type. In contrast, non-GAD-IR terminals were asymmetric 80% of the time.

GABAergic neurons in the rat hippocampal formation: ultrastructure and synaptic relationships with catecholaminergic terminals

“…This distribution is consistent with previous studies in the same or different species which similarly used antibodies to GABA (Gamrani et al, 1986;Peterson and Ribak, 1987;Sloviter and Nilaver, 1987;Babb et al, 1988) or to glutamic acid decarboxylase (GAD), the GABA-synthesizing enzyme, in colchicine pretreated animals (Ribak et al, 1978;Amaral and Kurz, 1985;Babb et al, 1988). The majority of GABAergic neurons and processes overlapped TH-labeled processes in the infragranular hiius of the DG and CA3 region of the hippocampus, suggesting that GABA and catecholamines could prominently interact in these regions.…”

Prolonged Cyclooxygenase-2 Induction in Neurons and Glia Following Traumatic Brain Injury in the Rat

“…However, exclusively excitatory (possibly mossy cell) fibers have been found to cross from the prosubiculum to the contralateral medial entorhinal cortex (van Haeften et al, 1998). Reports of crossing inhibitory (γ-amino butyric acid, GABA) fibers have long been available (Leranth and Frotscher, 1987;Babb et al, 1988). Lowenstein et al (1992) reported that the loss of hilar neurons caused a hyperexcitability in dentate granule cells within 4 h after TBI in the rat.…”

Electrophysiological diversity of pyramidal‐shaped neurons at the granule cell layer/hilus border of the rat dentate gyrus recorded in vitro

“…These cells have several anatomical characteristics of interneurons, such as few spines, an axon that usually arborizes locally, and ultrastructural characteristics such as infolded nuclei and intranuclear rods and sheets (Ramón y Cajal, 1911;Lorenté de Nó, 1934;Ribak and Anderson, 1980;Léranth and Frotscher, 1986). They are thought to be inhibitory because they are immunoreactive for the inhibitory neurotransmitter γ-aminobutyric acid (GABA; Somogyi et al, 1984;Gamrani et al, 1986;Sloviter and Nilaver, 1987;Babb et al, 1988;Woodson et al, 1989;Goodman and Sloviter, 1992) as well as the synthetic enzyme for GABA, glutamic acid decarboxylase (GAD; Ribak et al 1978;Somogyi et al, 1984;Kosaka et al, 1985;Babb et al, 1988). In addition, they make symmetric synapses on their postsynaptic targets (Ribak and Anderson, 1980).…”