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Somatostatin‐immunoreactive interneurons contribute to lateral inhibitory circuits in the dentate gyrus of control and epileptic rats
Author(s) -
Boyett Jesse M.,
Buckmaster Paul S.
Publication year - 2001
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.1056
Subject(s) - dentate gyrus , neuroscience , inhibitory postsynaptic potential , somatostatin , axon , glutamate decarboxylase , chemistry , biology , hippocampus , biochemistry , enzyme
Lateral inhibition, a feature of neuronal circuitry that enhances signaling specificity, has been demonstrated in the rat dentate gyrus. However, neither the underlying neuronal circuits, nor the ways in which these circuits are altered in temporal lobe epilepsy, are completely understood. This study examines the potential contribution of one class of inhibitory interneurons to lateral inhibitory circuits in the dentate gyrus of both control and epileptic rats. The retrograde tracer wheat germ agglutinin‐apo‐horse radish peroxidase‐gold (WGA‐apo‐HRP‐gold) was injected into the septal dentate gyrus. Neurons double‐labeled for glutamic acid decarboxylase (GAD) and the retrograde tracer are concentrated in the hilus and may contribute to lateral inhibition. Neurons double‐labeled for somatostatin and the retrograde tracer account for at least 28% of GAD‐positive neurons with axon projections appropriate for generating lateral inhibition in control rats. Despite an overall loss of somatostatin‐expressing cells in epileptic animals, the number of somatostatin‐positive interneurons with axon projections appropriate for generating lateral inhibition is similar to that seen in controls. These findings suggest that somatostatinergic interneurons participate in lateral inhibitory circuits in the dentate gyrus of both control and epileptic rats, and that surviving somatostatinergic interneurons might sprout new axon collaterals in epileptic animals. Hippocampus 2001;11:418–422. © 2001 Wiley‐Liss, Inc.

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