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Journal of Neuroscience, Vol 15, 3990-4004, Copyright © 1995 by Society for Neuroscience
Reactive synaptogenesis and neuron densities for neuropeptide Y, somatostatin, and glutamate decarboxylase immunoreactivity in the epileptogenic human fascia dentata
GW Mathern, TL Babb, JK Pretorius and JP Leite
Division of Neurosurgery, UCLA School of Medicine 90024-8461, USA.
This study determined differences of fascia dentata (FD) peptide and
inhibitory neuroanatomy between patients with epileptogenic hippocampal
sclerosis (HS), those with extrahippocampal seizure pathologies, and
autopsy comparisons. Surgically treated temporal lobe epilepsy patients
were clinically classified into two pathogenic categories: (1) HS with
focal mesial temporal neuroimaging and histories of initial precipitating
injuries to the brain (n = 18) and (2) non-HS patients with
extrahippocampal mass lesions or idiopathic seizures (i.e., without lesions
or HS; mass lesion/idiopathic; n = 9). The hippocampal sections were
studied for (1) granule cell, hilar, CA4, and CA3 neuron densities; (2)
hilar densities and the percentage of neurons immunoreactive (IR) for
neuropeptide Y (NPY), somatostatin (SS), and glutamate decarboxylase (GAD);
(3) densities of GAD neurons in the lower granule cell and infragranular
zone (basket-like cells); (4) the semiquantitative pattern of IR
peptides/GAD FD molecular layer axon sprouting; (5) IR gray values (GV) of
the FD molecular layers; and (6) the thickness of the supragranular
molecular layer. Results showed the following. (1) Compared to autopsies,
both HS and mass lesion/idiopathic patients showed less granule cell and
CA3 neuron densities, but there were no statistical differences between the
latter two pathogenic categories. (2) By contrast, compared to autopsies
and mass lesion/idiopathic cases, HS patients showed less hilar and CA4
neuron densities, and there were no differences between autopsies and mass
lesion/idiopathic. (3) Compared to autopsies, the NPY and SS hilar neuron
densities in HS patients, but not mass lesion/idiopathic cases, were less.
(4) Compared to autopsies, the hilar GAD neuron densities for HS and mass
lesion/idiopathic patients were not less. (5) In HS patients the averaged
percentages of hilar SS neurons were less than autopsies, and no other
differences of IR hilar percentages were found. (6) The densities of GAD
basket-like neurons and the thickness of the supragranular molecular layer
were not different between any combination of pathogenic categories and
autopsies. (7) By semiquantitative visual assessments, peptides/GAD axon
sprouting into the FD was greater in HS compared to mass lesion/idiopathic
or autopsies. (8) Compared to mass lesion/idiopathic cases, in HS NPY outer
molecular layer GVs were lower, SS GVs were not different, and GAD inner
molecular layer GVs were higher. (9) Analyses comparing the two pathogenic
categories and neuron densities with peptides/GAD axon sprouting found six
comparisons that correlated sprouting with hilar and CA4 neuron losses, and
four comparisons showing greater sprouting in HS compared to mass
lesion/idiopathic.(ABSTRACT TRUNCATED AT 400 WORDS)
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