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

Acute hypertension increases the cerebrovascular permeability to protein to a higher extent in anesthetized than in conscious rats. When hypertension is combined with a pronounced cerebral vasodilatation, e.g. in bicuculline-induced seizures, the protein leakage is enhanced. Conscoius, unrestrained 2--3-months-old rats received adrenaline or bicuculline i.v. during continuous recording of the mean arterial pressure and were killed 3 minutes later. Rats, neonatally sympathectomized by 6-hydroxydopamine, had significantly increased extravasation of 125I serum albumin in the brain after adrenaline-induced hypertension than nonsympathectomized rats. Since transection of the cervical sympathettic trunk alone does not have the same effect, a protection of the blood-brain barrier in acute hypertension in conscious rats may, at least in part, be mediated via the central noradrenergic innervation of cerebral vessels. Bicuculline did not increase blood pressure in 6-OHDA treated rats; thus the blood-brain barrier remained intact.
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PMID:Neonatal 6-hydroxydopamine treatment increases the vulnerability of the blood-brain barrier to acute hypertension in conscious rats. 4 65

The effects of some GABAergic agents on seizures induced by quinine were studied in mice. Muscimol, AOAA, DABA and baclofen significantly protected mice against quinine-induced convulsions. Bicuculline effectively enhanced quinine-induced convulsions, and significantly attenuated the protective effects of muscimol, AOAA and DABA against convulsions induced by quinine. Diazepam and phenobarbitone significantly protected mice against convulsions induced by quinine. However, phenytoin did not affect quinine-induced seizures to any significant degree. These results indicate that the convulsant effect of quinine may be due to a disturbance in the status of the GABAergic system.
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PMID:Effects of some GABAergic agents on quinine-induced seizures in mice. 132 22

The binding of 3H-muscimol and 3H-diazepam to rat striatum membranes after picrotoxin- and bicuculline-induced seizures was characterized. No alteration in the maximal binding capacity (Bmax) of 3H-muscimol was observed. However, bicuculline produced a 27% decrease in Kd. Both picrotoxin and bicuculline increased the binding capacity of 3H-diazepam. Bicuculline produced a 86% increase in Kd. These results suggest that the GABA antagonists-induced seizures may modulate 3H-muscimol and 3H-diazepam binding in rat striatum.
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PMID:[Effects of GABA antagonist-induced seizures on 3H-muscimol and 3H-diazepam binding in the rat striatum]. 132 78

In mice, tonic convulsive seizure induced by intravenous administration of caffeine (adenosine A1, A2 receptors antagonist) was significantly potentiated by any one of L-PIA (adenosine A1 receptor agonist), NECA (adenosine A2 receptor agonist) and 2-ClAd (adenosine A1, A2 receptors agonist). The caffeine-induced seizure was unaffected by diazepam (benzodiazepine receptor agonist), but was inhibited by Ro 15-1788 (antagonist or partial agonist). beta-DMCM (antagonist or inverse agonist) increased the seizure. Muscimol (GABA-a receptor agonist), baclofen (GABA-b receptor agonist) and AOAA (GABA transaminase inhibitor) did not show significant effect on caffeine-induced convulsion. Bicuculline (GABA-a receptor antagonist) and picrotoxin (chloride channel blocker) significantly potentiated the convulsion at the doses which did not induce it. Caffeine-induced convulsion was potentiated by NMDA with its non-convulsive dose. CPP (competitive NMDA receptor antagonist) and MK-801 (non-competitive NMDA receptor antagonist) significantly inhibited the seizures. These results suggest that caffeine-induced seizure is not caused by blockade of adenosine receptors. Caffeine may act to beta-carboline sensitive benzodiazepine receptor (Type 1) which has no linkage with GABA-a receptor. Furthermore, it is implied that caffeine plays some role at NMDA receptor calcium ion channel complex.
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PMID:[Effects of agonists and antagonists of benzodiazepine, GABA and NMDA receptors, on caffeine-induced seizures in mice]. 132 1

Audiogenic seizures (AS) are a model of generalized tonic-clonic seizures. The inferior colliculus (IC) and the GABAergic neurotransmission seems to be the most critical site and neurotransmitter system, respectively, of the auditory midbrain involved in AS origin and development. Thus, audiogenic-like seizures are evoked by GABAA antagonists such as bicuculline (BIC). Wistar audiogenic AS resistant (R) rats were sham-transected through the midcollicular line and microinjected with IC bicuculline (BIC; 80 ng/0.2 microliters) (n = 8); transected through the midcollicular line and microinjected with IC saline 0.9% (n = 8); transected through the cortex above the midcollicular line and microinjected with IC BIC (n = 3); transected through the midcollicular line up to 6.0 mm depth and microinjected with IC BIC (80 ng/0.2 microliters or 120 ng/0.3 microliters (n = 8). Wistar AS susceptible (S) rats were submitted to cortical transections (n = 8) and midcollicular transections (n = 7). Animals were studied by means of an ethological method before and after microinjections and/or transections in order to evaluate possible pathways in the AS-like evoked seizures. Bicuculline-evoked seizures were very similar to those evoked by acoustic stimulation, but lacked the tonic-clonic component. No modification in animal behavior was observed in the presence of sound, once the AS-like behavior was initiated. A small percentage of the animals, however, presented procursive behavior which was increased by sound. The IC BIC-evoked patterns were almost totally blocked by midcollicular but not cortical transections. Furthermore, midcollicular but not cortical transections blocked the tonic-clonic component of AS in genetically S animals without modifying the wild running component. These data suggest that the inferior colliculus-superior colliculus connection may be involved in the sensorimotor transduction necessary for AS-like behaviors.
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PMID:Neuroethological evaluation of audiogenic seizures and audiogenic-like seizures induced by microinjection of bicuculline into the inferior colliculus. I. Effects of midcollicular knife cuts. 133 63

1. The effects of chemically induced convulsions, clinically similar to those elicited by electroconvulsive treatment (ECT), on brain regional distribution of neuropeptide Y-, neurokinin A-, substance P- and neurotensin-like immunoreactivities were studied in the rat. 2. Pentylenetetrazole (PTZ) and bicuculline (BIC) were used to induce grand mal seizures. Rats were divided into three groups receiving one of the following treatments: Saline, PTZ (45 mg/kg) or BIC (1.5 mg/kg). 3. After sacrifice by focused microwave irradiation, brains were dissected, peptides extracted and measured by specific radioimmunoassays. 4. Repeated grand mal convulsions induced by PTZ, in similarity to ECT, markedly increased NPY-LI concentrations in frontal cortex and hippocampus. In contrast to ECT, no changes in NKA- or SP-LI levels were seen. NT-LI was lowered in striatum. 5. Bicuculline effects were more circumscribed: some animals developed grand mal and died while convulsing (peptides not measured), others did not develop generalized seizures and were sacrificed after the fourth treatment. 6. The results demonstrate a similar effect of PTZ and ECT on regional NPY-LI concentrations and raise the possibility that grand mal, regardless of etiology, is necessary for effects on peptides.
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PMID:Brain neuropeptides: changes by treatment with the convulsants pentylenetetrazole and bicuculline. 149 30

Laminer analysis of the distribution of GABA and GAD in the superior colliculus has shown that the distribution pattern of GABA within the SC is similar in rabbit, cat, and guinea pig. The highest levels of GABA were found in the superficial gray layer (SGL), averaging 37-40 mmol/kg dry weight. The GABA concentrations in the deep layers were each only half that of the levels in the SGL. The concentrations of both GABA and GAD in the upper half of SGL are the same as those in the substantia nigra and medial forebrain bundle which have the highest amounts of GABA in the CNS. Denervation studies of the fibers projecting to SGL suggest that the GABA concentrated in the SGL is intrinsic to the layer. The results obtained from immunohistochemical and electron microscopic studies on the localization of GABA neurons corresponds well with the regional distribution pattern of GABA and GAD reported here. However, pharmacological and electrophysiological studies do not necessarily accord well with the GABA distribution studies because they indicate that there are many GABA sensitive neurons in both the SGL and DGL. To investigate the role of GABA in the SGL, the effect of GABA and its agonists and antagonists on neurotransmission in SGL has been studied in SC slices in a perfusion system. Bath applied GABA (100 microM to 1 mM) enhanced the amplitude of postsynaptic field potentials (PSP) in SGL in a dose-dependent fashion and at concentrations above 1 mM it depressed the PSP in a dose-dependent fashion. A similar response pattern was obtained with muscimol (0.1-10 microM excitation; greater than 10 microM inhibition). However (-)-baclofen only inhibited the PSP. Bicuculline (1 microM) shifted the dose-response inhibitory curve of GABA to the right, while the excitatory effect was enhanced. These results indicate that GABA has an excitatory and inhibitory action on neurotransmission in the SGL. The nigro-tectal GABAergic fibers terminate in the intermediate and deep layers of SC. Inhibition of GABAergic activity in the SC causes irrepressible saccades made toward the center of the movement field while GABA activation delays and slows saccadic eye movements. Thus, GABA in the SC plays an important role in the control of eye movements. The same GABAergic projection is also related to the propagation of generalized seizures. There exist collicular neurons which suppress the propagation of seizures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The distribution and function of gamma-aminobutyric acid (GABA) in the superior colliculus. 163 1

Rats were exposed for 24 min to bilateral clamping of the common carotid arteries (BCCA) in pentobarbital anaesthesia. The GABA content was measured 24 hours, 48 hours, 4 days, 14 days and 3 months after BCCA. In other groups of rats seizures were elicited by i.p. injection of (+)-bicuculline (3 mg/kg) 24 hours, 48 hours, 4 days, 14 days and 3 months after BCCA. Analysis of the GABA content revealed significant increase compared with controls in the hippocampus, frontal cortex and substantia nigra from 24 hours up to 3 months. Bicuculline treatment induced tonic/clonic seizures and status epilepticus in sham operated animals; these effects were drastically diminished at various time points after BCCA. The present results suggest that BCCA produces a longlasting increase in GABA content and as a consequence protection from bicuculline-induced seizures.
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PMID:Transient reduction of cerebral blood flow leads to longlasting increase in GABA content in vulnerable structures and decreased susceptibility to bicuculline induced seizures. 163 44

1. The influence of some GABAergic agents on tonic seizures elicited by chloroquine was investigated in mice. 2. Chloroquine (45-100 mg/kg) elicited seizures in mice in a dose related manner. 3. Muscimol (1-2 mg/kg), DABA (8-16 mg/kg) and baclofen (4-16 mg/kg) profoundly delayed the onset of chloroquine (65 mg/kg)-induced seizures. The incidence of the seizures was also significantly reduced by muscimol (1-2 mg/kg), DABA (8 mg/kg) and baclofen (4-8 mg/kg). 4. AOAA (10 mg/kg) profoundly reduced the proportion of mice that convulsed while AOAA (20 mg/kg) completely protected mice against chloroquine (65 mg/kg)-induced seizures. 5. Bicuculline (5 mg/kg) and picrotoxin (0.5-1 mg/kg) significantly potentiated chloroquine (50 mg/kg)-induced seizures. The onset of seizures and the number of mice that convulsed were shortened and increased respectively. The onset of chloroquine (65 mg/kg)-elicited seizures was also profoundly shortened. Bicuculline (5 mg/kg) and picrotoxin (0.5 mg/kg) effectively antagonised the protective effects of muscimol (2 mg/kg), AOAA (10 mg/kg) and DABA (8 mg/kg) against chloroquine (65 mg/kg)-elicited seizures. 6. Diazepam (1 mg/kg) and phenobarbitone (20 mg/kg) significantly antagonised chloroquine (65 mg/kg) seizures. The onset of seizures was significantly delayed by both diazepam (0.25-1 mg/kg) and phenobarbitone (10-20 mg/kg). 7. These data suggest that enhancement and inhibition of GABAergic neurotransmission respectively attenuate and potentiate chloroquine seizures in mice.
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PMID:Involvement of GABAergic mechanisms in chloroquine-induced seizures in mice. 163 37

We have investigated the pharmacological basis of CNS excitation that occurs in association with general anaesthesia in mice. Propofol produced sustained clonic movements during anaesthesia. Methohexitone produced intermittent non-rhythmic jerking during anaesthesia. Ethanol and pentobarbitone produced anaesthesia without associated clonic movements. Doses of all anaesthetic drugs were equipotent. Surface EEG recordings showed paroxysmal discharges consistent with interictal manifestations of cortical seizures with methohexitone or propofol, but not with ethanol or pentobarbitone. Strychnine, a glycine antagonist without effects on the cerebral cortex, and bicuculline, a GABAA antagonist with effects on the cerebral cortex, were used in doses that were equipotent-0.5 log units less than the ED10 for clonic convulsions. Strychnine potentiated both excitatory behaviour and EEG paroxysmal discharges when given with methohexitone or propofol, but not with ethanol or pentobarbitone. Bicuculline did not affect either behaviour or EEG with any of the anaesthetic drugs. Our data show that methohexitone and propofol produced CNS excitation, while pentobarbitone and ethanol did not. We propose that the pharmacological basis of this excitation may be glycine antagonism occurring in subcortical structures.
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PMID:Does glycine antagonism underlie the excitatory effects of methohexitone and propofol? 164 44


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