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Query: UMLS:C0036572 (
seizures
)
80,221
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The properties of [3H]clonazepam, [3H]diazepam and [3H]zolpidem (N,N,6[trimethyl-2-(4-methyl-phenyl)imidazo[1,2-a]pyridine-3-acetamide hemitratrate) binding to synaptic membranes of cerebellum, cortex,
olfactory
bulb, striatum and spinal cord of rat were compared to the binding properties of [3H]flunitrazepam, [3H]flumazenil and [3H]midazolam. In the cerebellar, cortical and
olfactory
bulb membranes, the density of high-affinity binding sites of all these tritiated benzodiazepine (BZ) ligands is almost identical. In contrast, in the striatum, the density of [3H]clonazepam and [3H]zolpidem binding sites is approximately 60 and 30%, respectively, of the density of [3H]diazepam, [3H]flunitrazepam or [3H]flumazenil sites. In spinal cord membranes, the number of high-affinity binding sites of [3H]clonazepam and [3H]zolpidem is less than 20% of the number of binding sites for [3H]diazepam, [3H]flunitrazepam, [3H]flumazenil and [3H]midazolam. Moreover, the displacement of [3H]flunitrazepam from spinal cord membranes by clonazepam and zolpidem was characterized by high IC50 values and Hill slopes significantly less than 1. Because [3H]BZ ligand binding in the spinal cord is enhanced by gamma-aminobutyric acid (GABA), these data suggest that different regions of the rat central nervous system may contain different GABA-BZ receptor subtypes. The different pharmacological properties of clonazepam, diazepam and zolpidem (i.e., regarding their ability to enhance bicuculline
seizure
threshold, to decrease locomotor activity, to induce ataxia or to elicit anticonflict action) further support the concept that in the rat central nervous system preferential occupancy of heterogeneous GABAA receptors by these drugs can be related to their effects on behavior.
...
PMID:gamma-Aminobutyric acidA receptor heterogeneity in rat central nervous system: studies with clonazepam and other benzodiazepine ligands. 184 29
Recent studies have revealed that mossy fiber axons of granule cells in the dentate gyrus undergo reorganization of their terminal projections in both animal models of epilepsy and human epilepsy. This synaptic reorganization has been demonstrated by the Timm method, a histochemical technique that selectively labels synaptic terminals of mossy fibers because of their high zinc content. It has been generally presumed that the reorganization of the terminal projections of the mossy fiber pathway is a consequence of axonal sprouting and synaptogenesis by mossy fibers. To evaluate this possibility further, the time course for development of Timm granules, which correspond ultrastructurally to mossy fiber synaptic terminals, was examined in the supragranular layer of the dentate gyrus at the initiation of kindling stimulation with an improved scoring method for assessment of alterations in Timm histochemistry. The progression and permanence of this histological alteration were similarly evaluated during the behavioral and electrographic evolution of kindling evoked by perforant path, amygdala, or
olfactory
bulb stimulation. Mossy fiber synaptic terminals developed in the supragranular region of the dentate gyrus by 4 d after initiation of kindling stimulation in a time course compatible with axon sprouting. The induced alterations in the terminal projections of the mossy fiber pathway progressed with the evolution of behavioral kindled
seizures
, became permanent in parallel with the development of longlasting susceptibility to evoked
seizures
, and were observed as long as 8 months after the last evoked kindled
seizure
. The results demonstrated a strong correlation between mossy fiber synaptic reorganization and the development, progression, and permanence of the kindling phenomenon.
...
PMID:Mossy fiber synaptic reorganization induced by kindling: time course of development, progression, and permanence. 188 May 49
The levels of inhibitory amino acids (Tau, Gly), or excitatory amino acids (Glu, Asp) and Gln, precursor of GABA, have been determined, under resting conditions, in 17 brain areas of 3 sublines of inbred Rb mice displaying different responses to an acoustic stimulus. Rb1 mice were clonictonic
seizure
-prone, Rb2 mice were clonic
seizure
-prone and Rb3 mice were
seizure
resistant. Profile of distribution in the brain of each one of these amino acids differed. Maximum to minimum level ratio was higher for Tau (3.8) than for Glu or Asp or Gln (2). The level of Gly was similar in 13 out of the 17 areas examined. Multiple inter-subline differences were recorded for each amino acid. These differences have been analyzed considering the
seizure
susceptibility or severity of the three Rb sublines. Common lower levels (approximately -20%: Rb1/Rb3, Rb2/Rb3) of Gln in Temporal Cortex may be implicated in
seizure
susceptibility.
Seizure
severity (Rb1/Rb2) seems to correlate, in some areas, with additional lower amounts of GABA already reported and, to a lower extent, of Asp (-19% in striatum, inferior colliculus and cerebellum), of Tau and Gly; a tendency for a rise in Gln content was observed in certain others (10-20% in
olfactory
bulb, thalamus, hypothalamus, substantia nigra, and frontal, temporal and occipital cortex). The data and correlations recorded provide guidelines for further investigations for synaptosomal and metabolic alterations in the three sublines of the same strain of Rb mice.
...
PMID:Amino acid neurotransmitter alterations in three sublines of Rb mice differing by their susceptibility to audiogenic seizures. 197 52
Norepinephrine (NE) concentrations were measured in 15 discrete areas of the central nervous system of two types of genetically epilepsy-prone rats (GEPRs) and in nonepileptic controls. Both moderate-
seizure
(GEPR-3) and severe-
seizure
(GEPR-9) animals had extensive abnormalities in brain NE concentration. Deficits of equal magnitude in GEPR-3s and GEPR-9s were found in the spinal cord, midbrain minus the inferior colliculus, inferior colliculus, hypothalamus, amygdala, hippocampus, occipital + parietal cortex, frontal cortex, and
olfactory
septum. Because both types of GEPRs share these deficits and share
seizure
susceptibility, we hypothesize that these areas are candidates for regulation of
seizure
susceptibility in GEPRs. In addition, because GEPR-9s have more severe
seizures
than GEPR-3s and because GEPR-9s had greater NE deficits in several brain areas (cerebellum, pons-medulla, thalamus, and possibly the temporal cortex and
olfactory
bulbs), we hypothesize that these areas may be important in regulation of
seizure
severity in GEPRs. All animals used in these experiments had been protected from
seizure
-provoking stimuli and were naive to
seizures
. Because the abnormalities in NE concentration were present in
seizure
-predisposed animals that were protected from
seizures
, we conclude that these abnormalities are important components of the
seizure
-predisposition characteristic of GEPRs and do not result from
seizure
experience.
...
PMID:Noradrenergic abnormalities in the central nervous system of seizure-naive genetically epilepsy-prone rats. 200 21
The piriform cortex, especially its deep anterior part, has been recently suggested to be a crucial epileptogenic site in the rat brain. We investigated the susceptibility of different parts of the piriform cortex to the development of electrical kindling as compared to that of the basolateral amygdala. A locus in the deep cell layer (layer III) of the rostral portion of the posterior piriform cortex (PPC) is described, which is considerably more sensitive to electrical stimulation than adjacent areas of the PPC, including the deep prepiriform cortex or the amygdala. The sensitive locus in the PPC can be readily kindled, and focal
seizure
thresholds in fully kindled rats are 60-90% lower than respective thresholds in rats kindled from other loci. Treatment of fully kindled rats with antiepileptic drugs diazepam, carbamazepine, phenobarbital, and valproate showed that anticonvulsant effects of these drugs in animals kindled from stimulation of the PPC were comparable to respective effects in animals kindled from stimulation of the basolateral amygdala, although the locus in the PPC tended to be more resistant. The data support the idea that the piriform area may contain the most sensitive neuronal tissue responsible for the generation of
seizures
during kindling. It remains to be determined if the described locus in the PPC is critical to the kindling process when kindling is induced from other structures within the
olfactory
-limbic system.
...
PMID:Kindling from stimulation of a highly sensitive locus in the posterior part of the piriform cortex. Comparison with amygdala kindling and effects of antiepileptic drugs. 201 64
We have localized brain-derived neurotrophic factor (BDNF) mRNA in rat brain and examined its regulation by
seizure
activity. In situ hybridization of BDNF 35S-cRNA most prominently labeled neurons in hippocampal stratum pyramidale and stratum granulosum, superficial
olfactory
cortex, pyramidal cell layers of neocortex, amygdala, claustrum, endopiriform nucleus, anterior
olfactory
nucleus, and ventromedial hypothalamus. Hybridization to BDNF mRNA was markedly increased in all of these regions after lesion-induced recurrent limbic
seizures
and within dentate gyrus granule cells following one electrically stimulated epileptiform afterdischarge. In contrast to
seizure
-elicited changes in nerve growth factor (NGF) mRNA expression, increases in BDNF mRNA occur in a greater number of different neuronal populations and develop several hours more rapidly in extrahippocampal loci. These results indicate that regulation by physiological activity may be an intrinsic property of this class of neurotrophic factor but that, in the recurrent
seizure
paradigm, different mechanisms mediate increased expression of mRNAs for BDNF and NGF outside hippocampus.
...
PMID:BDNF mRNA expression is increased in adult rat forebrain after limbic seizures: temporal patterns of induction distinct from NGF. 205 88
Mongolian gerbils were subjected to different environmental and specific sensory stimuli to determine the ability of these stimuli to provoke
seizures
. None of the specific sensory stimuli, somatosensory,
olfactory
, auditory or visual, were effective in inducing convulsions. This finding does not implicate dysfunctions of the specific sensory pathways in
seizure
genesis in gerbils. In contrast, several novel environmental stimuli that exposed the animals to a difficult exploratory task (i.e., Y-maze, disk rack, etc.) could trigger
seizures
, and this suggests that the pathophysiology of epileptiform events in gerbils may have a unique association with exploratory behavior. However, the frequency, latency and severity of the
seizures
showed no correlation with each other, indicating that these parameters are probably determined by independent factors. Taken together with previous studies on the electrophysiology of the dentate gyrus during exposure to novel experiences, and the anatomical abnormalities found in the hippocampus of the
seizure
-sensitive gerbil, these behavioral data provide further support for a significant role of the hippocampus in the pathophysiology of
seizures
in this model of genetic epilepsy.
...
PMID:An analysis of various environmental and specific sensory stimuli on the seizure activity of the Mongolian gerbil. 206 May 1
A tenth case (a subtype of complex partial seizures) is proposed as a Limbic (?) Psychotic Trigger Reaction. Upon crying, an infant girl was hit fatally by her devoted father while he was off anticonvulsants prescribed for Jacksonian and petit mal (?)
seizures
with "porencephalic cyst involving motor cortex and limbic system." Crying revived traumatic memories of frequently repeated ("kindling") experiences of his mother crying when hit by his father, in turn sometimes hit by patient while helping the mother. Hitting also had been helpful (cognitive mismatch between helpful and harmful hitting) during the victim's accidental choking 11 days earlier. This had occurred on the same day his distant mother died. Two days later he attempted suicide with anticonvulsants. Symptoms of the well remembered, unmotivated infanticide included flat affect,
olfactory
and command hallucinations, and delusions of grandeur (his mother leaving him millions and power).
...
PMID:Infanticide in Limbic (?) Psychotic Trigger Reaction in a man with jacksonian and petit mal (?) seizures: "kindling" by traumatic experiences. 212 78
Pilocarpine-induced status epilepticus leads to widespread limbic forebrain damage in rats and provides a model for studying intractable epilepsy. Noradrenergic neurons in suspension, prepared from the locus coeruleus region of donors on the 13th or 14th gestational day, were microinjected bilaterally into the hippocampus (8 rats) and into the cerebellum (4 rats) or the
olfactory
bulb (4 rats) of epileptic rats. Three microliters of suspension was deposited at the rate of 1 microliter/min. Control animals were not submitted to surgery (4 rats). After six weeks a marked reduction of suppression of spontaneous
seizures
was observed in intrahippocampally grafted rats. From these preliminary results we suggest that grafts can be used to suppress spontaneous recurrent epileptic
seizures
.
...
PMID:Some evidence that intrahippocampal grafting of noradrenergic neurons suppresses spontaneous seizures in epileptic rats. 213 60
Kindling phenomenon provides an experimental model of limbic secondarily generalized epilepsy. It can be easily obtained by stimulation of the
olfactory
bulb (OB) which is strongly connected to limbic structures. The after-discharge induced by subconvulsant electrical stimulations, is followed by a behavioral phenomenon, named Wet Dog Shakes (WDS). In the course of the Rat OB kindling, the development of WDS is biphasic: 1) an ascendant phase during the first three stages, and 2) a descendant phase in the stages 4 and 5, that may give evidence of the installation and the intensification of the kindling process. The significance of this behavior in
seizure
generalization is discussed.
...
PMID:["Wet dog shakes" during olfactory bulb kindling]. 215 Jul 86
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