Somatostatin immunoreactive neurons in the human hippocampus and cortex shown by immunogold/silver intensification on vibratome sections: Coexistence with neuropeptide Y neurons, and effects alzheimer‐type dementia

Abstract

The distribution of somatostatinlike immunoreactivity was studied in the hippocampal formation, retrohippocampal region, and temporal cortex in the human brain. Tissues from surgical biopsy and postmortem cases were used, and the immunogold/silver method on vibratome sections was introduced for routine applications in conjunction with primary antisera that recognise somatostatin-14 or somatostatin-28. Somatostatin-28 antisera readily stained numerous neurons, dendrites, and extensive axonal networks throughout the hippocampus and neighbouring cortex. Liquid phase absorption provided controls for specificity. The most prominent accumulations of Somatostatin immunoreactive neurons and axons occurred in the hilus of the area dentata, in CA1, and in the entorhinal and perirhinal cortices. Axonal plexuses occurred throughout the hippocampal subfields but were particularly dense in those regions rich in Somatostatin neurons. The distribution of Somatostatin immunoreactive neurons and fibers parallels the distribution of neuropeptide Y (NPY) neurons and fibers in the hippocampus and cerebral cortex to a remarkable extent. Double labelling experiments with antisera against neuropeptide Y and Somatostatin indicate a considerable frequency of coexistence of the two peptides in single neurons, particularly in large multipolar cortical neurons and also in the small bipolar white matter neurons. Regional variations exist in the amounts of coexistence found in the hippocampal subfields; somatostatin-NPY coexistence is particularly high in the hilus of the area dentata, the subicular complex, and the deep layers of the entorhinal and perirhinal cortices. In the hippocampi and temporal cortices in cases of Alzheimer-type dementia compared to those of age-matched control brains, there is a significant to severe loss of Somatostatin immunoreactive neurons and axons. This loss is most severe in those regions with the highest indices of neurofibrillary tangles and neuritic plaques–the hilus of the area dentata, CA1, and the entorhinal and perirhinal cortices. Surviving Somatostatin neurons are distorted with short dendrites and truncated axons. Neuritic plaques identified on double label experiments with thioflavin include Somatostatin axons but not neurons.