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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The basket cells are an important cell type in the dentate gyrus because their axon terminals form a prominent plexus with the somata of the principal cells, the granule cells. The basket cells consist of five morphological types that have different dendritic arborizations and somal positions. All five types of basket cell display immunoreactivity for glutamate decarboxylase, the synthesizing enzyme for the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Electron microscopy has shown that basket cells have similar ultrastructural features including smooth dendrites, infolded nuclei, intranuclear rods, prominent Nissl bodies, and a thick rim of perikaryal cytoplasm. The axon terminals of basket cells form symmetric synapses with the somata and proximal dendrites of granule cells. Since the somata, basal dendrites and proximal apical dendrites of basket cells are postsynaptic to granule cell axon collaterals, the basket cells are linked to granule cells in a powerful feedback inhibitory circuit. The basket cells are also involved in feedforward inhibition as a result of being postsynaptic to perforant path and commissural axons. The calcium-binding protein, parvalbumin, is found in each type of basket cell but less than 40% of the basket endings display parvalbumin-immunoreactivity. In contrast, virtually all cortical basket cells contain parvalbumin, and this difference for basket cells between neocortex and hippocampus may contribute to the lower seizure threshold for the hippocampal formation as compared to the neocortex. Studies show that basket cells play a role in at least two experimental models of epilepsy.
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PMID:Local circuitry of GABAergic basket cells in the dentate gyrus. 133 68

The pattern of hippocampal cell death has been studied following hippocampal seizure activity and status epilepticus induced by 110-min stimulation of the perforant pathway in awake rats. The order of vulnerability of principal cells in the different hippocampal subfields--as determined by silver impregnation--was found to be very similar to the pattern found in ischemia; i.e., dentate hilus greater than CA1, subiculum greater than CA3c greater than CA3a,b greater than dentate granule cells. The hilar somatostatin-containing cells were the most vulnerable cell type, whereas all other subpopulations of nonprincipal neurons--visualized by immunocytochemistry for the calcium binding proteins parvalbumin and calbindin--were remarkably resistant. Pyramidal cells in the CA3 region containing neither of the examined calcium binding proteins were more resistant to overexcitation than CA1 pyramidal cells, most of which do contain calbindin. This indicates that no simple relationship exists between vulnerability in status epilepticus and neuronal calcium binding protein content, and that local and/or systemic hypoxia during status epilepticus may be responsible for the ischemic pattern of cell death.
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PMID:Pattern of neuronal death in the rat hippocampus after status epilepticus. Relationship to calcium binding protein content and ischemic vulnerability. 134 49

The expression of the protein products of the immediate-early genes c-fos, Fos B, Fos-related proteins (FRAs), c-jun, jun B, jun D and krox-24 was investigated in the rat hippocampus at various times after electrically-induced hippocampal seizures. Hippocampal seizures induced all the immediate-early gene proteins in dentate granule cells with differing time-courses. In addition, Krox-24, Fos and Jun D were also induced in somatostatin-containing interneurons throughout the hippocampus and also in a small percentage of parvalbumin-containing interneurons. Thus, hippocampal seizures induce waves of immediate-early gene protein expression in dentate granule cells and a selective expression of krox-24, Fos and Jun D in hippocampal somatostatin interneurons. These results suggest that biochemical and/or morphological changes occurring in dentate granule cells and somatostatin interneurons after seizures may be regulated by immediate-early gene expression, and that these immediate-early gene proteins may be involved in seizure development in the nervous system.
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PMID:Induction of immediate-early gene proteins in dentate granule cells and somatostatin interneurons after hippocampal seizures. 134 20

Autopsy study of a patient who died after an episode of prolonged unilateral status epilepticus revealed neuronal loss in the hippocampus on the epileptic side, with gliosis confined to the CA1 and CA3 fields. There was loss of the parvalbumin-immunoreactive gamma-aminobutyric acid (GABA)-ergic interneurons in the hippocampus on that side. There was also loss of the normal laminar pattern of substance P staining with increased substance P immunoreactivity in the supragranular plexus on that side. Met-enkephalin immunoreactivity was also increased in the outer molecular layer of the dentate gyrus on the epileptic side. Mossy fibers on the epileptic side stained more strongly with the Hicks' silver stain and with antibodies against glutamate and taurine, but less intensely with antibodies against calbindin. In the contralateral cerebellum, there was Purkinje cell loss, injury to the remaining Purkinje cells, and increased prominence of the Bergmann glia. Our observations show that prolonged unilateral seizure activity can be associated with specific histochemical changes in the human hippocampus.
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PMID:Neuropathologic asymmetries in the brain of a patient with a unilateral status epilepticus. 171 86

The substantia nigra has a gating function controlling the spread of epileptic seizure activity. Additionally, in models of prolonged status epilepticus the pars reticulata of substantia nigra (SNR) suffers from a massive lesion which may arise from a massive metabolic derangement and hyperexcitation developing in the activated SNR. In this study, status epilepticus was induced by systemic injection of pilocarpine in rats. The neuropathology of SNR was investigated using immunohistochemical techniques with the major emphasis on the time-course of changes in neurons and astrocytes. Animals surviving 20, 30, 40, 60 min, 2, 3, 6 hours, 1, 2, and 3 days after induction of status epilepticus were perfusion-fixed, and brains processed for immunohistochemical staining of SNR. Nissl-staining and antibodies against the neuron-specific calcium-binding protein, parvalbumin, served to detect neuronal damage in SNR. Antibodies against the astroglia-specific cytoskeletal protein, glial fibrillary acidic protein (GFAP), and against the glial calcium-binding protein, S-100 protein, were used to assess the status of astrocytes. Immunohistochemical staining for serum-albumin and immunoglobulins in brain tissue was taken as indicator of blood-brain barrier disturbances and vasogenic edema formation. Immunohistochemical staining indicated loss of GFAP-staining already at 30 min after induction of seizures in an oval focus situated in the center of SNR while sparing medial and lateral aspects. At 1 h there was additional vacuolation in S-100 protein staining. By 2 hours, parvalbumin-staining changed in the central SNR indicating neuronal damage, and Nissl-staining visualized some neuronal distortion. Staining for serum-proteins occurred in a patchy manner throughout the forebrain during the first hours. By 6 h, vasogenic edema covered the lesioned SNR. By 24 h, glial and neuronal markers indicated a massive lesion in the center of SNR. By 48-72 h, astrocytes surrounding the lesion increased in size, and polymorphic phagocytotic cells invaded the damaged area. In a further group of animals surviving 1 to 5 days, conventional paraffin-sections confirmed the neuronal and glial damage of SNR. Additional pathology of similar quality was found in the globus pallidus. Since astrocytes were always damaged in parallel with neurons in SNR it is proposed that the anatomical and functional interrelationship between neurons and astrocytes is particularly tight in SNR. Both cell elements may suffer in common from metabolic disturbance and neurotransmitter dysfunction as occur during massive status epilepticus.
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PMID:Damage of substantia nigra pars reticulata during pilocarpine-induced status epilepticus in the rat: immunohistochemical study of neurons, astrocytes and serum-protein extravasation. 175 84

The Mongolian gerbil (Meriones unguiculatus) is used as a model in epilepsy studies. Structural abnormalities in the hippocampus and in its GABAergic system have been correlated with this affliction. A reliable marker of a subpopulation of GABAergic neurons is the Ca2+ binding protein parvalbumin (PV). Here we show that, whereas PV is present in the same population of hippocampal interneurons in gerbil as described in the rat, in the gerbil, PV-immunoreactivity is also found in the outer molecular layer of the hippocampus. Ultrastructural analysis revealed that it is located there in axospinous boutons with asymmetric synaptic junctions, i.e. the terminals of the entorhinal perforant path. Upon ablation of the intensely PV-immunoreactive entorhinal cortex, PV-staining is completely absent in its hippocampal termination zones. Thus, in gerbil hippocampus (but not in the rat, mouse, cat and man) PV is contained in a presumably excitatory projection. This outstanding feature of the limbic system of the gerbil implies different functional properties related to Ca2+ mediated processes, and could be of relevance for the seizure sensitivity of this animal species.
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PMID:The perforant path in the seizure sensitive gerbil contains the Ca(2+)-binding protein parvalbumin. 188 54

A selective loss of somatostatin (SS)-containing neurons in the hilar region has been reported in patients suffering from temporal lobe epilepsy. Conversely, neurons containing calcium-binding proteins such as parvalbumin (PARV) are known to be very resistant under experimental seizure conditions. In this study, we analyzed the coexistence of SS and PARV in neurons of the rat fascia dentata by using serial semi-thin cryostat sections for pre-embedding immunocytochemistry. Our results show that only 5.7% of the SS-immunoreactive hilar neurons contain PARV. The data suggest that SS-containing hilar neurons are less protected against seizure-induced calcium overload than other neurons containing calcium-binding proteins.
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PMID:Most somatostatin-immunoreactive neurons in the rat fascia dentata do not contain the calcium-binding protein parvalbumin. 198 Feb 25

The calcium-binding protein parvalbumin (PARV) is supposed to have a protective function under conditions of experimental seizure and hypoxia in a subgroup of GABAergic inhibitory neurons in the adult rat hippocampus. Here we studied the appearance of PARV immunoreactivity in rat hippocampal non-pyramidal cells during postnatal development in comparison to glutamate decarboxylase (GAD) immunoreactivity. PARV-immunoreactive neurons were not observed before postnatal day 7 whereas GAD-positive neurons and terminal-like puncta were present at postnatal day 2 (P2) and were frequent around P5. From other studies it is known that all GABAergic neurons are formed prenatally. Our data thus indicate that in the early postnatal period GABAergic non-pyramidal cells are poorly protected by calcium-binding proteins against a pathological calcium influx.
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PMID:Late appearance of parvalbumin-immunoreactivity in the development of GABAergic neurons in the rat hippocampus. 227 61

The immunoreactivity of parvalbumin (PV), a Ca2+-binding protein present in a subpopulation of interneurons, was studied in the hippocampal CA1 region during kindling epileptogenesis, induced by tetanic stimulation of the Schaffer collateral/commissural fibers. PV-immunoreactivity was increased in comparison to controls after 13 afterdischarges and after the induction of generalized seizures. A quantification of the number of PV-immunoreactive somata showed an increase of 20% in both stages of kindling. This level had returned to baseline level 31 days after the last seizure. These results imply that changes in PV-immunoreactivity are related to seizure activity rather than to the long-term increase in seizure sensitivity in kindled animals. Co-localization study in controls showed that 32% of PV-immunoreactive somata were also immunopositive for GABA. A colocalization study in stratum oriens and pyramidale on the stimulated side of kindled animals 31 days after the last generalized seizure showed neither a reduction in the number of PV-immunoreactive somata nor in the number of GABA-immunopositive cell bodies that co-localized with PV. In contrast, the number of GABA-immunoreactive somata that did not co-localize with PV was reduced by 50%. It has been shown that a large influx of Ca2+ plays a crucial role in epileptogenesis. Here we demonstrate that the presence of the calcium-binding protein parvalbumin seems to exert a protective effect against the process that leads to a decrease in GABA content.
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PMID:Kindling induced changes in parvalbumin immunoreactivity in rat hippocampus and its relation to long-term decrease in GABA-immunoreactivity. 292 51

Two neuronal calcium-binding proteins, calbindin-D28k (CaBP) and parvalbumin (PV), were localized in the normal rat hippocampus by using immunocytochemical methods to determine 1) their location and 2) whether a correlation exists between the presence of these two calcium-binding proteins and the selective vulnerability of different hippocampal neuronal populations to experimental seizure activity. CaBP-like immunoreactivity (CaBP-LI) is present in all dentate granule cells and some, but not all, CA1 and CA2 pyramidal cells. Some CA1 pyramidal cells lack CaBP-LI, and those that do are lightly stained compared to the dentate granule cells. CA3 pyramidal cells appear to contain neither CaBP- nor PV-LI, and no granule or pyramidal cells exhibit PV-LI. CaBP-LI is present in distinct populations of dentate and hippocampal interneurons but absent from others. In area dentata, CaBP-LI is present in a small number of interneurons of the molecular and granule cell layers and in a small population of presumed basket cells in or below the granule cell layer. Conversely, more presumed dentate basket cells exhibit PV-LI than CaBP-LI. In the hilus of area dentata, few cells are CaBP- or PV-immunoreactive. The hilar somatostatin/neuropeptide Y (NPY)-immunoreactive cells and hilar mossy cells, two distinct and large populations, lack CaBP- and PV-LI. In the CA3 region, CaBP-LI is present in a relatively small number of interneurons in each stratum. PV-immunoreactive interneurons in area CA3 are more numerous. In area CA1, CaBP-LI is present in many interneurons in strata radiatum and lacunosum-moleculare. Some, but relatively fewer, CaBP-positive interneurons are present in strata pyramidale and oriens. Conversely, PV-immunoreactive interneurons are numerous in strata pyramidale and oriens but rare in strata radiatum and lacunosum-moleculare. Staining with the particulate chromagen benzidine hydrochloride revealed a previously undescribed dense band of CaBP-LI in the inner dentate molecular layer, a lamina enriched with kainate-displaceable glutamate-binding sites and innervated by the apparently excitatory ipsilateral associational/commissural (IAC) pathway that originates in the CaBP-negative hilar mossy cells. Bilateral electrical stimulation of the perforant path was performed in order to destroy the hilar mossy cells and to determine if this band of CaBP-LI is normally present within the mossy cell terminals. Perforant path stimulation that destroyed hilar mossy cells throughout the dorsal portions of both hippocampi did not abolish the dense CaBP-like immunoreactivity in the inner molecular layer.
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PMID:Calcium-binding protein (calbindin-D28k) and parvalbumin immunocytochemistry: localization in the rat hippocampus with specific reference to the selective vulnerability of hippocampal neurons to seizure activity. 292 92


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