An experimental analysis of the origins of somatostatin-like immunoreactivity in the dentate gyrus of the rat

Abstract

In previous studies, fibers demonstrating somatostatin-like immunoreactivity were observed in the outer half of the molecular layer of the dentate gyrus in the rat and monkey. They occupy the same region as those of the perforant pathway that originates in the entorhinal cortex. Numerous somatostatin immunoreactive neuronal cell bodies were also observed in the hilar region, though stained axonal profiles could not be followed from these cells into the molecular layer. In the present study, several experimental procedures were employed to determine the origin of the somatostatin-positive fibers in the molecular layer. Transection of the perforant path fibers resulted in such characteristic changes as shrinkage of the molecular layer and sprouting of AChE-positive fibers. There was no apparent decrease, however, in the density of somatostatin-positive fibers. In fact, since the stained fibers occupied a narrower band in the shrunken molecular layer, their density appeared greater. Injections of kainic acid into the hilar region produced a lesion of hilar neurons, including those positive for somatostatin. In the region of cell loss, there was a marked reduction of somatostatin-immunoreactive fibers in the ipsilateral molecular layer, with no detectable changes in the homotopic contralateral molecular layer. The distribution of AChE fibers, which presumably have an extrinsic origin, was not altered by the treatment. In a final series of experiments, the retrograde tracer wheat germ agglutinin-horseradish peroxidase (WGA-HRP) was injected into the hilar region and sections were prepared for the simultaneous demonstration of the tracer and of somatostatin-like immunoreactivity. Somatostatin-positive neurons demonstrating WGA-HRP reaction product were observed primarily in the ipsilateral hilar region, but a few double-labeled cells were also seen in the same area of the contralateral side. These studies indicate that a population of intrinsic neurons located in the polymorphic layer of the dentate gyrus projects to the outer half of the ipsilateral molecular layer. A similar, but very much smaller, projection also extends to the contralateral dentate gyrus. Taken together, these projections appear to account for much of the somatostatin-like immunoreactivity in the molecular layer of the dentate gyrus.

EPSPs of dentate gyrus granule cells during epileptiform bursts of dentate hilar "mossy" cells and area CA3 pyramidal cells in disinhibited rat hippocampal slices

“…The excitatory effects of hilar stimulation in these studies were probably due to mossy cells, since mossy cells are the only hilar cells that are known to be immunoreactive for glutamate and project to the contralateral inner molecular layer (Swanson et al, 1978, 198 1;Laurberg and Sorensen, 1981;Bakst et al, 1986;Soriano and Frotscher, in press). Stimulation in control conditions produced inhibitory effects in vivo (Douglas et al, 1983;Bilkey and Goddard, 1987) but weakly excitatory effects after systemic bicuculline (Douglas et al, 1983).…”

The dentate gyrus: fundamental neuroanatomical organization (dentate gyrus for dummies)

“…Antibodies directed against the peptide somatostatin have revealed that neurons such as the HIPP cells scattered throughout the polymorphic layer are immunoreactive for this peptide, and account for approximately 16% of the GABAergic cells in the dentate gyrus (Morrison et al, 1982;Bakst et al, 1986;Freund and Buzsaki, 1996;Sik et al, 1997;Boyett and Buckmaster, 2001). The somatostatin-positive cells all colocalize with GABA, and are the source of the somatostatin immunoreactive fibers and terminals in the outer two-thirds of the molecular layer.…”

Translamellar Disinhibition in the Rat Hippocampal Dentate Gyrus after Seizure-Induced Degeneration of Vulnerable Hilar Neurons

“…8C), which contains both excitatory mossy cells (Amaral, 1978;Ribak et al, 1985;Soriano and Frotscher, 1994) and a variety of intermingled inhibitory interneurons (Amaral, 1978;Freund and Buzsáki, 1996). To determine whether FG-labeled hilar neurons included a significant number of inhibitory interneurons capable of directly mediating translamellar inhibition, we colocalized FG with GluR2, which primarily labels mossy cells (Leranth et al, 1996), with SS, which labels the largest population of hilar inhibitory interneurons (Bakst et al, 1986;Sloviter and Nilaver, 1987), and with PV, which labels several inhibitory interneuron populations in all dentate subregions (Freund and Buzsáki, 1996;Sloviter et al, 2003).…”