cholecystokinin and Epilepsy

Recent evidence supports the hypothesis of a functional dichotomy of perisomatic inhibition in the cerebral cortex: the parvalbumin- and cholecystokinin-containing basket cells that are specialized to control rhythm (as a clockwork) and "mood" (as a fine-tuning device), respectively, of network oscillations. Pathology extends this conclusion further, as the former is implicated in epilepsy and the latter in anxiety. The well-balanced cooperation of the two inhibitory systems is required for the normal network operations underlying the cognitive functions of the cerebral cortex.

Topics: Animals; Anxiety; Cerebral Cortex; Cholecystokinin; Epilepsy; Humans; Models, Neurological; Nerve Net; Neural Inhibition; Neurons; Parvalbumins

Topics: Animals; Anticonvulsants; Cholecystokinin; Epilepsy; Humans; Seizures

Neuropeptides are sufficiently stable to allow valid radioimmunoassay of peptide concentrations in post-mortem human nervous tissue and in human cerebrospinal fluid. Studies have now documented abnormalities of peptide concentrations in degenerative diseases of the brain. Somatostatin concentration is reduced in the hippocampus and neocortex of patients dying with Alzheimer's type dementia. In Huntington's disease, there are reduced concentrations of substance P, met-enkephalin and cholecystokinin in the basal ganglia; in contrast the concentrations of somatostatin and TRH are increased. Immunocytochemical and experimental lesion studies are underway in an attempt to localize the peptide-containing cells affected by these disorders; and the potential role of alterations in neuropeptide function in the pathogenesis, clinical manifestations and therapy of these illnesses is of great interest. Although alterations of CSF peptide concentrations have been reported in a variety of human diseases, interpretation of these results requires knowledge of the origin and disposition of CSF peptides. Future research into the pathology of peptidergic systems will depend on the development of specific peptide antagonists to probe dynamic aspects of peptide function and on the application of the tools of molecular biology, such as specific mRNA assays, to human material.

Topics: Alzheimer Disease; Animals; Brain; Cholecystokinin; Choline O-Acetyltransferase; Endorphins; Epilepsy; Forecasting; Histocytochemistry; Humans; Huntington Disease; Migraine Disorders; Nerve Tissue Proteins; Nervous System Diseases; Pain; Parkinson Disease; Radioimmunoassay; Somatostatin; Substance P; Thyrotropin-Releasing Hormone; Tissue Distribution; Vasopressins

Inhibitory GABAergic interneurons are fundamental elements of cortical circuits and play critical roles in shaping network activity. Dysfunction of interneurons can lead to various brain disorders, including epilepsy, schizophrenia, and anxiety. Based on the electrophysiological properties, cell morphology, and molecular identity, interneurons could be classified into various subgroups. In this study, we investigated the density and laminar distribution of different interneuron types and the co-expression of molecular markers in epileptic human cortex. We found that parvalbumin (PV) and somatostatin (SST) neurons were distributed in all cortical layers except layer I, while tyrosine hydroxylase (TH) and neuropeptide Y (NPY) were abundant in the deep layers and white matter. Cholecystokinin (CCK) neurons showed a high density in layers IV and VI. Neurons with these markers constituted ~7.2% (PV), 2.6% (SST), 0.5% (TH), 0.5% (NPY), and 4.4% (CCK) of the gray-matter neuron population. Double- and triple-labeling revealed that NPY neurons were also SST-immunoreactive (97.7%), and TH neurons were more likely to express SST (34.2%) than PV (14.6%). A subpopulation of CCK neurons (28.0%) also expressed PV, but none contained SST. Together, these results revealed the density and distribution patterns of different interneuron populations and the overlap between molecular markers in epileptic human cortex.

Topics: Adolescent; Adult; Brain Chemistry; Cerebral Cortex; Child; Cholecystokinin; Epilepsy; Female; Gene Expression Regulation; Humans; Interneurons; Male; Middle Aged; Neuropeptide Y; Parvalbumins; Phosphopyruvate Hydratase; Somatostatin; Tyrosine 3-Monooxygenase; Young Adult

The neuropeptide cholecystokinin (CCK) is abundant in the CNS and is expressed in a subset of inhibitory interneurons, particularly in their axon terminals. The expression profile of CCK undergoes numerous changes in several models of temporal lobe epilepsy. Previous studies in the pilocarpine model of epilepsy have shown that CCK immunohistochemical labeling is substantially reduced in several regions of the hippocampal formation, consistent with decreased CCK expression as well as selective neuronal degeneration. However, in a mouse pilocarpine model of recurrent seizures, increases in CCK-labeling also occur and are especially striking in the hippocampal dendritic layers of strata oriens and radiatum. Characterizing these changes and determining the cellular basis of the increased labeling were the major goals of the current study. One possibility was that the enhanced CCK labeling could be associated with an increase in GABAergic terminals within these regions. However, in contrast to the marked increase in CCK-labeled structures, labeling of GABAergic axon terminals was decreased in the dendritic layers. Likewise, cannabinoid receptor 1-labeled axon terminals, many of which are CCK-containing GABAergic terminals, were also decreased. These findings suggested that the enhanced CCK labeling was not due to an increase in GABAergic axon terminals. The subcellular localization of CCK immunoreactivity was then examined using electron microscopy, and the identities of the structures that formed synaptic contacts were determined. In pilocarpine-treated mice, CCK was observed in dendritic spines and these were proportionally increased relative to controls, whereas the proportion of CCK-labeled terminals forming symmetric synapses was decreased. In addition, CCK-positive axon terminals forming asymmetric synapses were readily observed in these mice. Double labeling with vesicular glutamate transporter 1 and CCK revealed colocalization in numerous terminals forming asymmetric synapses, confirming the glutamatergic identity of these terminals. These data raise the possibility that expression of CCK is increased in hippocampal pyramidal cells in mice with recurrent, spontaneous seizures.

Topics: Animals; CA1 Region, Hippocampal; Cholecystokinin; Dendritic Spines; Epilepsy; Excitatory Postsynaptic Potentials; Fluorescent Antibody Technique; Glutamic Acid; Hippocampus; Immunoenzyme Techniques; Immunohistochemistry; Mice; Mice, Inbred C57BL; Microscopy, Confocal; Microscopy, Electron; Pilocarpine; Presynaptic Terminals; Receptor, Cannabinoid, CB1; Scopolamine

For the purpose of investigating the role of physical exercise in developmental seizure-induced cognitive deficit, hippocampal mossy fiber sprouting and related gene expression, a seizure was induced by penicillin every other day in Sprague-Dawley rats from postnatal day 24 (P24). The authors assigned ten rats each randomly into the control group (CONT1), the control plus exercise group (CONT2), the seizure group (EXP1) and the seizure plus exercise group (EXP2). Morris water maze test was used respectively during P39-P45 and P61-P66. Treadmill exercise was performed daily by CONT2 and EXP2 rats during P49-P54. On P66, mossy fiber sprouting and gene expression in hippocampus were assessed by Timm staining and real-time RT-PCR. EXP2 rats performed better than EXP1 rats in the second water maze navigation test. In the entire two spatial probe tests, both EXP1 and EXP2 rats performed worse than the two control rats. Physical exercise remarkably reduced the aberrant mossy fiber sprouting in the supragranular region of dentate gyrus and CA3 subfield of hippocampus. Both EXP1 and EXP2 rats had a higher amount of glutamate receptor 1 (GluR1) and lower amount of the ratio of GluR2/GluR1 in hippocampus when compared with CONT rats. In addition, there was long-term enhancement of both gamma-aminobutyric acid receptor A-alpha3 (GABA-Aalpha3) and cholecystokinin (CCK) of EXP2 rats compared with the other three groups. These results showed that physical exercise improved learning capacity by modulating hippocampal regenerative sprouting and related gene expression in a developmental rat model of penicillin-induced recurrent epilepticus.

Topics: Animals; Cholecystokinin; Coloring Agents; Epilepsy; gamma-Aminobutyric Acid; Gene Expression; Learning; Male; Maze Learning; Mossy Fibers, Hippocampal; Nerve Regeneration; Penicillins; Physical Conditioning, Animal; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction

Repeated brief seizures evoked by kindling progressively increase seizure susceptibility and eventually induce spontaneous seizures. Previous studies have demonstrated that the initial seizures evoked by kindling increase paired-pulse inhibition at 15-25 msec interpulse intervals in the dentate gyrus and also induce apoptosis, progressive neuronal loss, mossy fiber sprouting, and neurogenesis, which could potentially alter the balance of excitation and/or inhibition and modify functional properties of hippocampal circuits. In these experiments, paired-pulse inhibition in the dentate gyrus was reduced or lost after approximately 90-100 evoked seizures in association with emergence of spontaneous seizures. Evoked IPSCs examined by single electrode voltage-clamp methods in granule cells from kindled rats experiencing spontaneous seizures demonstrated altered kinetics (reductions of approximately 48% in 10-90% decay time, approximately 40% in tau, and approximately 65% in charge transfer) and confirmed that decreased inhibition contributed to the reduced paired-pulse inhibition. The loss of inhibition was accompanied by loss of subclasses of inhibitory interneurons labeled by cholecystokinin and the neuronal GABA transporter GAT-1, which project axo-somatic and axo-axonic GABAergic inhibitory terminals to granule cells and axon initial segments. Seizure-induced loss of interneurons providing axo-somatic and axo-axonic inhibition may regulate spike output to pyramidal neurons in CA3 and could play an important role in generation of spontaneous seizures. The sequence of progressive cellular alterations induced by repeated seizures, particularly loss of GABAergic interneurons providing axo-somatic and axo-axonic inhibition, may be important in the development of intractable epilepsy.

Topics: Animals; Axons; Carrier Proteins; Cells, Cultured; Cholecystokinin; Dentate Gyrus; Epilepsy; Evoked Potentials; GABA Plasma Membrane Transport Proteins; Humans; Interneurons; Kindling, Neurologic; Kinetics; Male; Membrane Proteins; Membrane Transport Proteins; Neural Inhibition; Organic Anion Transporters; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Seizures

The anterior part of the piriform cortex (the APC) has been the focus of cortical-level studies of olfactory coding and associative processes and has attracted considerable attention as a result of a unique capacity to initiate generalized tonic-clonic seizures. Based on analysis of cytoarchitecture, connections, and immunocytochemical markers, a new subdivision of the APC and an associated deep nucleus are distinguished in the rat. As a result of its ventrorostral location in the APC, the new subdivision is termed the APC(VR). The deep nucleus is termed the pre-endopiriform nucleus (pEn) based on location and certain parallels to the endopiriform nucleus. The APC(VR) has unique features of interest for normal function: immunostaining suggests that it receives input from tufted cells in the olfactory bulb in addition to mitral cells, and it provides a heavy, rather selective projection from the piriform cortex to the ventrolateral orbital cortex (VLO), a prefrontal area where chemosensory, visual, and spatial information converges. The APC(VR) also has di- and tri-synaptic projections to the VLO via the pEn and the submedial thalamic nucleus. The pEn is of particular interest from a pathological standpoint because it corresponds in location to the physiologically defined "deep piriform cortex" ("area tempestas") from which convulsants initiate temporal lobe seizures, and blockade reduces ischemic damage to the hippocampus. Immunostaining revealed novel features of the pEn and APC(VR) that could alter excitability, including a near-absence of gamma-aminobutyric acid (GABA)ergic "cartridge" endings on axon initial segments, few cholecystokinin (CCK)-positive basket cells, and very low gamma-aminobutyric acid transporter-1 (GAT1)-like immunoreactivity. Normal functions of the APC(VR)-pEn may require a shaping of neuronal activity by inhibitory processes in a fashion that renders this region susceptible to pathological behavior.

Topics: Animals; Axons; Biotin; Calbindin 2; Calbindins; Carrier Proteins; Cholecystokinin; Dextrans; Epilepsy; GABA Plasma Membrane Transport Proteins; gamma-Aminobutyric Acid; Glutamate Decarboxylase; Immunohistochemistry; Isoenzymes; Male; Membrane Proteins; Membrane Transport Proteins; Neural Pathways; Neurons; Olfactory Pathways; Organic Anion Transporters; Parvalbumins; Phytohemagglutinins; Prefrontal Cortex; Rats; Rats, Sprague-Dawley; S100 Calcium Binding Protein G; Smell; Vasoactive Intestinal Peptide

Basket cells, defined by axons that preferentially contact cell bodies, were studied in rat piriform (olfactory) cortex with antisera to gamma-aminobutyric acid (GABA)ergic markers (GABA, glutamate decarboxylase) and to peptides and calcium binding proteins that are expressed by basket cells. Detailed visualization of dendritic and axonal arbors was obtained by silver-gold enhancement of staining for vasoactive intestinal peptide (VIP), cholecystokinin (CCK), parvalbumin, and calbindin. Neuronal features were placed into five categories: soma-dendritic and axonal morphologies, laminar distributions of dendritic and axonal processes, and molecular phenotype. Although comparatively few forms were distinguished within each category, a highly varied co-expression of features from different categories produced a "combinatorial explosion" in the characteristics of individual neurons. Findings of particular functional interest include: dendritic distributions suggesting that somatic inhibition is mediated by feedforward as well as feedback pathways, axonal variations suggesting a differential shaping of the temporal aspects of somatic inhibition from different basket cells, evidence that different principal cell populations receive input from different combinations of basket cells, and a close association between axonal morphology and molecular phenotype. A finding of practical importance is that light microscopic measurements of boutons were diagnostic for the molecular phenotype and certain morphological attributes of basket cells. It is argued that the diversity in basket cell form in the piriform cortex, as in other areas of the cerebral cortex, reflects requirements for large numbers of specifically tailored inhibitory processes for optimal operation that cannot be met by a small number of rigidly defined neuronal populations.

Topics: Animals; Axons; Calbindins; Cell Size; Cholecystokinin; Dendrites; Epilepsy; gamma-Aminobutyric Acid; Glutamate Decarboxylase; Immunohistochemistry; Interneurons; Isoenzymes; Male; Neural Inhibition; Olfactory Pathways; Parvalbumins; Presynaptic Terminals; Rats; Rats, Sprague-Dawley; S100 Calcium Binding Protein G; Vasoactive Intestinal Peptide

We sought to describe quantitatively the morphological and functional changes that occur in the dentate gyrus of kainate-treated rats, an experimental model of temporal lobe epilepsy. Adult rats were treated systemically with kainic acid, and, months later, after displaying spontaneous recurrent motor seizures, their dentate gyri were examined. Histological, immunocytochemical, and quantitative stereological techniques were used to estimate numbers of neurons per dentate gyrus of various classes and to estimate the extent of granule cell axon reorganization along the septotemporal axis of the hippocampus in control rats and epileptic kainate-treated rats. Compared with control rats, epileptic kainate-treated rats had fewer Nissl-stained hilar neurons and fewer somatostatin-immunoreactive neurons. There was a correlation between the extent of hilar neuron loss and the extent of somatostatin-immunoreactive neuron loss. However, functional inhibition in the dentate gyrus, assessed with paired-pulse responses to perforant-pathway stimulation, revealed enhanced, and not the expected reduced, inhibition in epileptic kainate-treated rats. Numbers of parvalbumin- and cholecystokinin-immunoreactive neurons were similar in control rats and in most kainate-treated rats. A minority (36%) of the epileptic kainate-treated rats had fewer parvalbumin- and cholecystokinin-immunoreactive neurons than control rats, and those few (8%) with extreme loss in these interneuron classes showed markedly hyperexcitable dentate gyrus field-potential responses to orthodromic stimulation. Compared with control rats, epileptic kainate-treated rats had larger proportions of their granule cell and molecular layers infiltrated with Timm stain. There was a correlation between the extent of abnormal Timm staining and the extent of hilar neuron loss. Granule cell axon reorganization and dentate gyrus neuron loss were more severe in temporal vs. septal hippocampus. These findings from the dentate gyrus of epileptic kainate-treated rats are strikingly similar to those reported for human temporal lobe epilepsy, and they suggest that neuron loss and axon reorganization in the temporal hippocampus may be important in epileptogenesis.

Topics: Action Potentials; Animals; Axons; Behavior, Animal; Cholecystokinin; Coloring Agents; Dentate Gyrus; Epilepsy; Excitatory Amino Acid Agonists; Immunohistochemistry; Kainic Acid; Male; Neurons; Nissl Bodies; Parvalbumins; Rats; Somatostatin; Staining and Labeling

Whole-cell patch-clamp recordings and immunocytochemical experiments were performed to determine the short- and long-term effects of lateral fluid percussion head injury on the perisomatic inhibitory control of dentate granule cells in the adult rat, with special reference to the development of trauma-induced hyperexcitability. One week after the delivery of a single, moderate (2.0-2.2 atm) mechanical pressure wave to the neocortex, the feed-forward inhibitory control of dentate granule cell discharges was compromised, and the frequency of miniature IPSCs was decreased. Consistent with the electrophysiological data, the number of hilar parvalbumin (PV)- and cholecystokinin (CCK)-positive dentate interneurons supplying the inhibitory innervation of the perisomatic region of granule cells was decreased weeks and months after head injury. The initial injury to the hilar neurons took place instantaneously after the impact and did not require the recruitment of active physiological processes. Furthermore, the decrease in the number of PV- and CCK-positive hilar interneurons was similar to the decrease in the number of the AMPA-type glutamate receptor subunit 2/3-immunoreactive mossy cells, indicating that the pressure wave-transient causes injurious physical stretching and bending of most cells that are large and not tightly packed in a cell layer. These results reveal for the first time that moderate pressure wave-transients, triggered by traumatic head injury episodes, impact the dentate neuronal network in a unique temporal and spatial pattern, resulting in a net decrease in the perisomatic control of granule cell discharges.

Topics: Animals; Brain Injuries; Cholecystokinin; Dentate Gyrus; Down-Regulation; Epilepsy; gamma-Aminobutyric Acid; Interneurons; Male; Mossy Fibers, Hippocampal; Neocortex; Nerve Tissue Proteins; Neurons; Parvalbumins; Patch-Clamp Techniques; Pressure; Rats; Rats, Wistar; Receptors, AMPA; Wounds, Nonpenetrating

Northern Blot and hybrization in situ techniques were used to investigate the effect of electroacupuncture (EA) on the changes of cholecystokinin (CCK) mRAN levels of the hippocampus in rat penicillin-induced epilepsy model. Epilepsy can significantly increase CCK mRNA levels in dentate gyrus and CA3 areas of hippocampus in diencephalic sections after penicillin-induced seizure, whereas EA not only can attenuate the seizure behaviors and EEG changes, but also can decrease the increase of CCK mRNA contents induced by the seizure. However, in the subiculum, dentate gyrus and CA3 areas of mesencephalic sections of rat hippocampus, EA can further increase the enhancement of CCK mRNA concentration induced by penicillin-induced seizure. The results suggest that EA inhibitory effects on the seizure's behaviors and epileptiform activities may be related to the alteration of CCK gene expression in the different area of hippocampus.

Topics: Animals; Blotting, Northern; Cholecystokinin; Electroacupuncture; Electroencephalography; Epilepsy; Gene Expression; Hippocampus; In Situ Hybridization; Male; Penicillins; Rats; Rats, Wistar; RNA, Messenger

We studied the effects and the interactions of some candidate genes related to the pathogenesis of epilepsy using a domestic audiogenic epilepsy-prone rat, matched with the epilepsy-resistant Wistar rat, and primary fetal cerebral cortical neuronal cell cultures of both. The preliminary results showed that there was a possible abnormality of the CCK gene at the post-translational stage in the early postnatal period in P77PMC rat brain; the later rapidly increased rate of CCK-8 synthesis in the hippocampus and subcortical region may represent a compensatory response to the neuronal pathways involved in audiogenic seizures. CCK-8 can decrease the NMDA (1 microM)-induced free intracellular Ca2+ concentration, so it seems to be an inhibitory neuromodulator. In neuronal cell cultures, the NMDA (0.1 microM)-induced c-fos mRNA expression on culture day 18 in vitro was higher in P77PMC than Wistar rats (P < 0.05). Interleukin-1 (20 nM) can induce endogenous opioid mRNA expression and peptide release in neuronal cell cultures, which can be abolished by the addition of antisense oligos of c-fos/c-jun to cell cultures treated with interleukin-1. Both interleukin-1 and opioids can increase the free intracellular Ca2+ concentration, and their specific antagonists can reverse their effects, so they both seem to be excitatory neuromodulators in the CNS.

Topics: Animals; Cholecystokinin; Disease Models, Animal; Epilepsy; Genes, Immediate-Early; Mutation; Neurons; Pilot Projects; Rats; Rats, Mutant Strains; Rats, Wistar

Interruption of a chronic GABA infusion into the rat somatosensory cortex induces the appearance of focal epileptic manifestations, known as the 'GABA withdrawal syndrome' (GWS). The aim of the present study was to determine, by immunocytochemistry, if neurotransmitters other than GABA are involved in GWS, namely: noradrenaline (NA), serotonin, choline acetyltransferase (CAT), cholecystokinin, neuropeptide Y, somatostatin and glial fibrillary acid protein (GFAP). Immunocytochemical data were compared in three animal groups: GABA-, saline- and L-aspartate (L-Asp)-infused rats. Only GABA-infused rats presented epileptic manifestations after interruption of the infusion. Saline- and L-Asp-infused rats served as controls. Observations were limited to the region surrounding the cortical infusion site. GABA-infused rats showed in the zone of the epileptic focus a number of cell bodies strongly immunoreactive to NA antibodies much larger than control rats. In addition, NA-immunoreactive fibers formed a dense plexus and some of them were observed around perikarya. In saline- and L-Asp-infused rats, the NA-immunolabelled fibers were sparse and NA immunolabelling was rarely observed in cell bodies. These results contrast to those obtained for the serotonergic system, where no significant difference was observed among the three groups of rats. CAT immunolabelling was observed in cell bodies, but not in nerve terminals in rats of the three groups. The number of CAT-immunoreactive cell bodies was much greater in GABA-infused rats than in the control animals. GFAP immunolabelling showed an important number of astrocytes throughout the cortex of the GABA-infused hemisphere, whereas, astrocytic reaction was limited to the infusion site in controls. Immunocytochemical data concerning peptides revealed cortical neuronal elements labelled similarly in the three groups of rats. Noradrenergic, cholinergic and glial modifications observed mainly in GABA-infused rats can result from lesion and from a specific action of GABA in chronic infusion. These modifications may contribute to the epileptogenesis of GWS, as recently demonstrated by electrophysiological recordings that show a modulating action of NA on firing activity of neurons involved in the epileptic focus.

Topics: Animals; Cholecystokinin; Choline O-Acetyltransferase; Epilepsy; gamma-Aminobutyric Acid; Glial Fibrillary Acidic Protein; Gliosis; Immunohistochemistry; Male; Neuropeptide Y; Norepinephrine; Rats; Rats, Wistar; Serotonin; Somatosensory Cortex; Somatostatin

P77PMC rat is a breed of rat with congenital audiogenic seizure (AS). AS attacks could be suppressed by cholecystokinin octapeptide (CCK-8) injected intracerebroventricularly (i.c.v.). In the present study we made i.c.v. injection of plasmid pSV2-beta Gal or pSV2-CCK encapsulated with lipofectin. Expression of pSV2-beta Gal in brain occurred from d 1 to d 14, with maximal expression at d 3 and d 4. After i.c.v. injection of pSV2-CCK plasmid, the AS of the P77PMC rats was markedly reduced, which was most obvious at d 3 and d 4. The time course of the AS repression was almost identical with that of pSV2-beta Gal expression. The results suggest that the repression of the AS in P77PMC rats is accounted for by the expression of foreign CCK gene in brain tissue.

Topics: Acoustic Stimulation; Animals; beta-Galactosidase; Cerebral Ventricles; Cholecystokinin; DNA; Epilepsy; Genetic Therapy; Genetic Vectors; Plasmids; Rats; Rats, Mutant Strains; Recombinant Fusion Proteins; Seizures

The occurrence of seizure activity in human temporal lobe epilepsy or status epilepticus is often associated with a characteristic pattern of cell loss in the hippocampus. An experimental model that replicates this pattern of damage in normal animals by electrical stimulation of the afferent pathway to the hippocampus was developed to study changes in structure and function that occur as a result of repetitive seizures. Hippocampal granule cell seizure activity caused a persistent loss of recurrent inhibition and irreversibly damaged adjacent interneurons. Immunocytochemical staining revealed unexpectedly that gamma-aminobutyric acid (GABA)-containing neurons, thought to mediate inhibition in this region and predicted to be damaged by seizures, had survived. In contrast, there was a nearly complete loss of adjacent somatostatin-containing interneurons and mossy cells that may normally activate inhibitory neurons. These results suggest that the seizure-induced loss of a basket cell-activating system, rather than a loss of inhibitory basket cells themselves, may cause disinhibition and thereby play a role in the pathophysiology and pathology of the epileptic state.

Topics: Animals; Cholecystokinin; Disease Models, Animal; Electric Stimulation; Epilepsy; gamma-Aminobutyric Acid; Hippocampus; Immunologic Techniques; Interneurons; Male; Neural Inhibition; Rats; Somatostatin; Time Factors; Vasoactive Intestinal Peptide

Topics: Acupuncture Therapy; Animals; Body Temperature Regulation; Brain; Brain Diseases; Cerebrospinal Fluid; Cholecystokinin; Endorphins; Enkephalins; Epilepsy; Feeding Behavior; Humans; Learning; Memory; Nervous System Diseases; Neurotransmitter Agents; Pain; Peptides; Pituitary Hormones; Substance P; Synaptic Transmission