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PubMed1995

Analysis of the results of routine lumbar puncture after a first febrile convulsion in Hofuf, Al-Hassa, Saudi Arabia.

Cerebrospinal fluid (CSF) was analysed to determine a lumbar puncture (LP) yield for meningitis in 95 children who presented with their first febrile convulsions between July 1993 and June 1994. There were 52 males and 43 females aged six months to six years with a mean age of 21.9 +/- 13.0 months at presentation. 87(91.6%) had simple febrile convulsions (SFC) while the remaining 8(8.4%) had complex febrile convulsions (CFC). The majority of the subjects presented with a sudden onset of convulsions that were preceded by a day or two history of fever, coryza, cough and respiratory distress while others had their convulsions preceded by fever and passage of bloody stools. The LP yield for meningitis in this series was 6.3%. The CSF analysis revealed six cases of meningitis comprising an eight month old infant with Haemophilus influenzae type B (HIB) meningitis, two partially treated pyogenic meningitis and three aseptic meningitis. All of them had presented with febrile convulsions without signs of meningeal irritation. Excluding aseptic meningitis from this series, a 3.1% LP yield for pyogenic meningitis is significant enough to recommend continued performance of LP in children with first febrile convulsions, especially if under the age of eighteen months.

Cerebrospinal Fluid↗
PubMed1978

On certain effects of dopaminergic agents in pentylenetetrazol convulsions.

In experiments with pentylenetetrazol convulsion model it has been found that L-DOPA in a dose of 50 mg/kg has no influence, while 500 mg/kg potentiate convulsions. Amantadine in a dose of 25 mg/kg and particularly markedly in a dose of 100 mg/kg potentaites convulsive seizures. Amphetamine in a dose of 0.5 mg/kg has no effect, while 5 mg/kg potentiate convulsive seizures, which is particularly pronounced in mice. Apomorphine in doses of 0.5 and 5 mg/kg has no marked effect on convulsions. Haloperidol in doses of 0.2 and 2 mg/kg does not have a pronounced effect on convulsive-seizure reactions and does not influence the effect of L-DOPA and amantadine on these reactions. The results obtained suggested a rather indirect effect of the dopaminergic system on convulsive-seizure reactivity. It is possible that the effects of some of the dopaminergic agents studied are realized through influencing the relationships between the dopaminergic system and other neurotransmitter systems (especially cholinergic, GABA-ergic and serotonin-ergic).

Amantadine↗
PubMed1994

Mineralocorticoid receptors mediate the enhancing effects of corticosterone on convulsion susceptibility in mice.

With hippocampal slice electrophysiology, direct evidence that mineralocorticoid receptors (MR) mediate excitatory effects of corticosteroids on neuronal activity was found. The present experiments extended this hypothesis to a whole animal model. The effects of manipulations of MR binding on convulsions produced by pentylenetetrazol (PTZ), strychnine and kainic acid were examined. Moderate increases in plasma corticosterone levels resulted in enhanced susceptibility to several convulsion types; decreased levels attenuated the susceptibility. The proconvulsant effects of corticosterone were inhibited by the MR antagonist, spironolactone. Convulsions typically affected by these manipulations were PTZ-induced myoclonic jerk and face and forelimb clonus and kainic acid-induced convulsions. Other convulsion types, e.g., PTZ-induced running bouncing clonus and tonic hindlimb extension and strychnine-induced convulsions, were generally unaffected by these manipulations, which suggests that central MR effects are not global. The convulsions that were sensitive to MR manipulations are believed to originate in limbic structures. These results provide the first direct evidence for a role of central MRs in the modulation of central nervous system excitability in a whole animal. Furthermore, they suggest that central MR action may be important in disruptions of excitability, such as epilepsy, drug withdrawal syndromes and arousal states in healthy animals.

Animals↗
PubMed1993

Convulsive effects of systemic administration of the delta opioid agonist BW373U86 in mice.

A systemically active, nonpeptidic delta receptor-selective agonist, (+-)-4-((alpha-R*)-alpha-((2S*,5R*)-4-allyl-2,5-dimethyl-1-piperazinyl) -3- hydroxybenzyl)-N,N-diethylbenzamide (BW373U86), produced a brief, nonlethal convulsion in mice. The behavioral pattern of convulsion produced by pentylenetetrazol was similar to that produced by systemic administration of BW373U86. Although several episodes of convulsion occurred with pentylenetetrazol, BWB373U86 produced a single, brief episode. Naltrexone (10.0 and 100 mg/kg) and naltrindole (1.0, 3.2 and 10.0 mg/kg), but not midazolam (0.32 mg/kg), produced dose-dependent rightward shifts in the potency of BW373U86 to induce a convulsion. A dose of 3.2 mg/kg of midazolam completely eliminated convulsions induced by BW373U86. Midazolam (0.32 and 3.2 mg/kg), but not naltrindole (3.2 and 32.0 mg/kg), produced parallel rightward shifts in the pentylenetrazol dose-effect curve. Pretreatment with a single injection of BW373U86 (3.2, 10.0, 32.0 or 100 mg/kg) produced a dose-related reduction in the capacity of BW373U86 to induce a second convulsion. Recovery of sensitivity to BW373U86 did not return to control levels for up to 2 weeks after pretreatment with a single injection of 32.0 mg/kg of BW373U86. Naltrindole (3.2 mg/kg) administered within 1 hr, but not at 2 hr, after a pretreatment dose of 10.0 mg/kg of BW373U86 prevented the refractoriness (tolerance) induced by the single dose of BW373U86. These data suggest that the convulsions as well as the tolerance induced by BW373U86 were initiated through delta opioid receptors.

Amino Acid Sequence↗
PubMed1993

Role of phenobarbitone in preventing recurrence of febrile convulsions.

A randomized double blind placebo controlled trial was carried out to study the effect of phenobarbitone (PB) in preventing recurrences of simple and atypical febrile convulsions among children in the age group 6 months to 6 years. Children with simple febrile convulsions were randomly allocated to receive either phenobarbitone or placebo. Children with atypical convulsions were treated with phenobarbitone, as a third group. Thirty children were admitted in each group. All the children were followed up for a period of twelve months. Recurrence of convulsions and side effects of PB were recorded. Recurrence occurred in only 7% (95% confidence interval: 1-22) of children on Phenobarbitone, suffering from either simple or atypical febrile convulsions, compared to 53% (95% confidence interval: 34-72) of children on placebo, suffering from simple febrile convulsions. With Phenobarbitone, 5% of children had intolerable side effects. These results suggest that long term prophylaxis with phenobarbitone, even in simple febrile convulsions will be useful.

Child↗
PubMed1997

Convulsant effects of some xanthine derivatives in genetically epilepsy-prone rats.

The behavioural and electrocorticographic (ECoG) convulsant effects of several xanthine derivatives injected intraperitoneally (i.p.) were studied in genetically-epilepsy prone rats. The aim of the study was to evaluate the relationship among convulsant potency, molecular structure and lipophilicity of some xanthines. Animals were injected i.p. with various doses (250-1000 micromol/kg) and a different convulsant potency was observed among the various xanthines tested. IBMX (3-isobutyl-1-methylxanthine), theophylline (1,3-dimethylxanthine) and caffeine (1,3,7-trimethylxanthine) induced an epileptogenic pattern that consisted in an initial phase characterized by wet-dog shakes followed by head tremor, nodding, clonic convulsion and they appeared to be the most potent xanthines among those studied. During seizures, the electrocortical activity was usually characterized by single or multiple sharp- or spike-wave episodes followed by polyspike discharges. After the highest doses of IBMX, theophylline and caffeine, the animals react with falling down, transient tonic clonic seizures, escape response and generalized seizures followed by post-ictal period. Equimolar doses of 8-chlorotheophylline and theobromine (3,7-dimethylxanthine) produced less evident epileptic responses in comparison to previous compounds, whereas no epileptic signs were observed following the administration of enprofylline (3-propylxanthine), etofylline [7-(2-hydroxyethyl)theophylline], diprophylline [7-(2,3-dihydroxy-propyl)theophylline] and doxofylline [7-(1,3-dioxolan-2-ylmethyl) theophylline]. Lipophylicity of the compounds was determined, but no convincing correlations were found between the rank order of lipophilicities and the convulsant potencies of the compounds studied. On the other hand, structure-activity relationship was also investigated. We suggest that the substitution pattern on the xanthine nucleus may explain, in part, the different convulsant potency of the compounds studied. Furthermore, a selective antagonism of adenosine subtype receptors should be considered.

1-Methyl-3-isobutylxanthine↗
PubMed1999

Effects of adrenalectomy and gonadectomy on sex and stress-induced differences in bicuculline-induced convulsions.

The effects of adrenalectomy, gonadectomy and combined adrenalectomy plus gonadectomy on the previously described sex-dependent anticonvulsive effect of swim stress were studied in rats. The convulsive signs (myoclonic twitch, generalized convulsions, tonic hindlimb extension) were produced by constant i.v. infusion of gamma-aminobutyric acid(A) (GABA(A)) antagonist bicuculline, which started 15 min after termination of swim stress (10-min swim at 18-19 degrees C). Adrenalectomy decreased the threshold doses of bicuculline producing the first myoclonic twitch and the onset of generalized convulsions only in females. In adrenalectomized females, but not in males, swim stress enhanced the threshold dose of bicuculline producing generalized convulsions, but, unlike in adrenal-intact animals, it failed to enhance the dose of bicuculline producing tonic hindlimb extension. In gonadectomized stressed and unstressed animals all sex differences disappeared, and swim stress enhanced in both sexes only the threshold doses of bicuculline producing tonic hindlimb extension. Adrenalectomized plus gonadectomized animals displayed clear sex differences in doses of bicuculline necessary to produce all the convulsive signs. In the same animals swim stress postponed, especially in females, the onset of the first myoclonic twitch and generalized convulsions, but not the onset of tonic hindlimb extension. In summary, our results suggest that hormones of the adrenal and gonadal glands are only partly responsible for decreased susceptibility, especially of female rats, to the GABA(A) antagonist bicuculline. Moreover, they have demonstrated that stress produces a gender-specific anticonvulsive effect even in the animals completely deprived of steroid hormones of peripheral origin.

Adrenalectomy↗
PubMed2003

Effects of anti-inflammatory drugs on convulsant activity of quinolones: a comparative study of drug interaction between quinolones and anti-inflammatory drugs.

Quinolones have been reported to possess potent convulsant activity, which is enhanced when they are administered concurrently with anti-inflammatory drugs. To define the individual drug interactions of quinolones with anti-inflammatory drugs, we studied the convulsant activity of six quinolones with or without 13 anti-inflammatory drugs and 3 analgesic/antipyretic drugs in mice. Intraventricular injections of norfloxacin (NFLX), enoxacin (ENX), ciprofloxacin, lomefloxacin (LFLX), levofloxacin, and gatifloxacin induced convulsions in mice in a dose-dependent manner. Concurrent administration of biphenylacetic acid strongly enhanced the convulsant activity of NFLX, ENX, and LFLX. Flurbiprofen also strongly enhanced the activity of NFLX and ENX, and ketoprofen strongly enhanced the activity of ENX. However, mefenamic acid, piroxicam, tenoxicam, meloxicam, etodolac, sulpyrine, isopropylantipyrine, and acetaminophen had no effect on the convulsant activity of quinolones. These results suggest that each quinolone has an individual drug interaction with each anti-inflammatory drug. It was suggested that we should know which anti-inflammatory drugs enhance the convulsant activity of individual quinolones, and which quinolone has no/weak drug interaction with different anti-inflammatory drugs when these drugs are used concurrently for the treatment of patients with infectious diseases.

Animals↗
PubMed1992

The uremic guanidino compound guanidinosuccinic acid induces behavioral convulsions and concomitant epileptiform electrocorticographic discharges in mice.

As yet, the in vivo epileptogenic properties of guanidinosuccinic acid (GSA) remained highly conjectural, still requiring the demonstration of GSA-induced behavioral convulsions accompanied by epileptiform electrographic discharges. Therefore, Swiss mice were injected intraperitoneally (i.p.) with increasing doses of GSA. Full-blown clonic or clonic-tonic convulsions appeared in a dose-dependent manner, with a median latency of about 25 min. CD50 (convulsive dose of the drug in 50% of the animals), the LD50 (lethal dose in 50%), and their 95% confidence limits for GSA suspensions in i.p. administration were 363 (287-458) mg/kg and 579 (445-756) mg/kg, respectively. In addition, four-channel electrocorticographic (ECoG) recordings were made in freely moving mice following the injection of 700 mg/kg (CD97). Epileptiform ECoG discharges coincided with the behavioral manifestation of the GSA-induced convulsions starting with initial decrease in amplitude, occasional spike-waves (10-20 min after injection), eventually leading to sustained spiking and spike-wave activity (30-50 min after injection). Clonic convulsions induced by a CD97 dose of GSA were only moderately attenuated by high doses of i.p. phenobarbital (20, 40 and 80 mg/kg), while tonic extension and lethal effects were dose-dependently blocked. A dose of 1000 mg/kg (CD97 for tonic extension) induced tonic extension in 100% of the animals, following treatment with 20 mg/kg of phenytoin none of the animals displayed tonic extension, and following 10 mg/kg only 30% of the animals displayed tonic extension, while the occurrence of clonic convulsions was not significantly attenuated.

Animals↗
PubMed1992

Lindane-induced convulsions in NMRI and OF1 mice: antagonism with (+)MK-801 and voltage-dependent calcium channel blockers.

The convulsant profile of lindane was investigated in OF1 and NMRI mice lines in relation to other convulsants acting at the GABAA and NMDA receptor complexes. Thus, a specific GABA-gated chloride channel blocker, PTX, a GABAA receptor antagonist, PTZ, and an excitatory amino acid receptor agonist, NMDA, were used. Antagonism of the convulsant effects of each of these drugs was investigated with (+)MK-801, a blocker of the NMDA-operated cation channel, and with nifedipine, a voltage-dependent calcium channel antagonist. While no differences in potency for PTX or PTZ to induce seizures were observed between OF1 and NMRI mice, lindane was approximately 80 and 90% more potent in its ability to induce seizures and lethality, respectively, in OF1 than in NMRI mice. Brain lindane concentrations at the moment of convulsion, measured after ED100 doses of lindane (400 and 200 mg/kg for NMRI and OF1 mice, respectively), did not differ between OF1 and NMRI mice, suggesting that the different potency of lindane between these mouse lines is a consequence of pharmacokinetic factors. Furthermore, (+)MK-801 antagonized seizures induced by either lindane, PTX or PTZ with similar potencies in both mouse lines. These results, coupled with the different pharmacokinetics of lindane in OF1 and NMRI mice, suggest that the distinct effects of lindane in these mice are not mediated by different activities at either NMDA or GABAA receptor complexes. Nonetheless, nifedipine antagonized lindane-induced seizures with a three-fold higher potency in NMRI than in OF1 mice. In contrast, nifedipine failed to antagonize PTX and PTZ convulsions in both OF1 and NMRI mice. These results suggest that besides the GABAA receptor complex other mechanisms related to calcium mobilization may be involved in the convulsant action of lindane.

Animals↗
PubMed1978

Alteration in pattern of EEG activities and convulsant effect of cocaine following chronic adminsitration in the rhesus monkey.

The effects of chronic administration of high doses of cocaine were studied in monkeys (Ss) with electrodes implanted in the brain. The Ss were injected daily with cocaine at a minimal convulsant dose (MCD) during polygraphic recording of EEGs, eye movement, respiratory and heart rates. The initial cocaine MCDs ranged from 3.2 to 6.5 mg/kg i.v. in ten Ss and markedly increased on each successive day following repeated daily injection (75--100% increase within 5--12 days). The elevated daily cocaine MCD was maintained for 1.5--2 months, and thereafter it gradually decreased and stabilized at levels between 20 and 30% above baseline within 2 months. During this period, the duration of daily convulsions evoked by cocaine MCD markedly decreased and stabilized at a constant level (30--35 sec) along with the latency of convulsions. The pattern of daily convulsions evoked by cocaine MCD changed from multiple episodes of intermittent tonic-clonic convulsions, which occurred during the earlier stage (1--2 months) of chronic treatment, to a single episode of sustained tonic-clonic convulsion. The Ss became extremely placid and tame or were profoundly depressed in their overall behavior most of the time. Simultaneously, the Ss continuously showed persistent rhythmic slow waves (5--6 c/sec) predominantly in the neocortex and limbic system structures. The results strongly suggested that chronic cocaine administration at high doses caused relatively permanent alteration of EEGs and behavior in the Ss, and the limbic system structures played an important role in the effect.

Animals↗
PubMed1982

Effects of cannabidiol on behavioral seizures caused by convulsant drugs or current in mice.

In mice, running, clonic and tonic convulsions and lethality were assessed following transcorneal (electroshock) current or convulsant drugs, each administered alone and after cannabidiol (CBD) pretreatment. CBD prevented tonic convulsions caused by a convulsant current (CC) 99.99, and by the convulsant dose (CD) 99.99 values of gamma-aminobutyric acid (GABA) inhibitors, 3-mercaptoproprionic acid (3MPA), picrotoxin (PIC), isonicotinic acid hydrazine (INH), pentylenetetrazol (PTZ) and bicuculline (BIC). Rankorder potencies, based on the antitonic ED50 of CBD, were: 3MPA greater than PIC = current = PTZ = BIC. Further, CBD prevented 3MPA-induced lethality, but failed to prevent the occurrence of the other behavioral endpoints of the above treatments. CBD also failed to prevent convulsions and lethality caused by the CD 99.99 of strychnine, a glycine antagonist. The differential effects of CBD suggest that the cannabinoid acts to inhibit seizure spread in the CNS by an action on GABA, but not glycine, mechanisms.

Animals↗
PubMed1982

Convulsant, anticonvulsant and anaesthetic barbiturates. In vivo activities of oxo- and thiobarbiturates related to pentobarbitone.

The convulsant, anticonvulsant and anaesthetic activities of a series of 6 barbiturates related to pentobarbitone have been qualitatively and quantitatively determined in mice. The presence or absence of convulsant activity was strongly dependent on molecular structure and there were marked variations in potency among the convulsant barbiturates. Anticonvulsant and anaesthetic activities were less dependent on structure and even the convulsant barbiturates had some underlying anticonvulsant action. Qualitative activities are also reported for a series of 8 thiobarbiturates. Convulsant activities were reduced in the thiobarbiturates, but some excitant activity remained in the thio analogue of each convulsant oxobarbiturate.

Anesthetics↗
PubMed1983

Effect of different convulsant drugs on some seizure parameters in morphine-dependent mice.

An investigation was made of the effect of morphine dependence on the characteristics of seizures induced in mice by convulsant drugs with differing mechanisms of action. Morphine dependence was induced in 90-day-old mice (weighing 29 to 32 g) by a 6-day schedule of twice daily i.p. injections of increasing doses of morphine (5, 32.5, 58, 82.5, 100, and 135 mg kg-1). Thirty minutes after the last morphine administration, convulsant drugs (4-aminopyridine 8 mg kg-1, pentylenetetrazol 50 mg kg-1, bicuculline 2.5 mg kg-1, strychnine 2.0 mg kg-1, and beta-mercaptopropionic acid 50 mg kg-1) were injected. 4-Aminopyridine (4-AP) and pentylenetetrazol (PTZ) increased both the number of animals with convulsions and death and in the case of 4-AP the period of convulsion latency was also increased. Naloxone at 1.0 mg kg-1 blocked the 4-AP effects, indicating that this action was mediated through an opioid receptor. Strychnine and beta-mercaptopropionic acid had an effect opposite 4-AP and PTZ in the number of animals with convulsions and death. On the other hand bicuculline had an effect more like 4-AP and PTZ than other inhibitory synapse-blocking drugs. We conclude that chronic morphine treatment modified the response of convulsant drugs depending on their mechanisms of action.

3-Mercaptopropionic Acid↗
PubMed1984

Convulsant potencies of tetrazoles are highly correlated with actions on GABA/benzodiazepine/picrotoxin receptor complexes in brain.

A series of tetrazole convulsants were examined for their potencies in displacing [35S]-t-butylbicyclophosphorothionate (TBPS) from the picrotoxin site on the benzodiazepine-GABA-chloride ionophore receptor complex. All of the tetrazole derivatives tested inhibited [35S]-TBPS binding from rat forebrain membranes, and except for one (undecamethylenetetrazole), had Hill coefficients near unity. Similar to other chemically unrelated convulsants the inhibition of [35S]-TBPS binding by the various tetrazole derivatives was unaffected by the addition of the bicucculine-like GABA antagonist, R 5135. To ascertain whether the inhibition of specific [35S]-TBPS binding by the tetrazole derivatives was related to their convulsant properties, we compared their in vitro potencies in displacing [35S]-TBPS binding with their minimum convulsant potencies in mice. A very good correlation was observed (r = 0.96, p less than 0.001) between their relative affinities for the [35S]-TBPS binding site and their convulsant potencies, indicating that pentamethylenetetrazol and related tetrazoles may produce their convulsant and anxiogenic actions via the GABA-benzodiazepine-chloride ionophore receptor complex.

Animals↗
PubMed1989

Potent convulsant actions of the adenosine receptor antagonist, xanthine amine congener (XAC).

The convulsant properties of xanthine amine congener (XAC, 8-(4-(2-aminoethyl)-aminocarboxylmethyloxy)phenyl-1,3-dipropylxant hine) are compared to those of caffeine. Male Swiss albino mice were infused with convulsants through a lateral tail vein. Convulsion thresholds (i.e. the amount of convulsants required to elicit convulsions) of 39.8 +/- 2.0 mg/kg (n = 10) and 109.8 +/- 2.3 mg/kg (n = 10) were calculated for XAC and caffeine respectively. Pretreatment of animals with the adenosine receptor agonists 2-chloroadenosine, N6-cyclohexyladenosine or 5'-N-ethylcarboxamido-adenosine (1 mg/kg, i.p., 20 minutes prior to infusion) significantly decreased the seizure threshold of both XAC and caffeine. The adenosine uptake blockers, 6-nitrobenzylthioinosine or dipyridamole (0.25 mg/kg, i.p., 20 minutes prior to infusion) did not significantly affect the seizure threshold to either XAC or caffeine. The benzodiazepine agonist diazepam (5 mg/kg, i.p., 20 minutes prior to infusion) significantly increased the seizure threshold to both XAC (p less than 0.05) and caffeine (p less than 0.01), whereas the benzodiazepine antagonist Ro 15-1788 (10 mg/kg, i.p., 20 minutes prior to infusion) significantly increased the seizure threshold to caffeine (p less than 0.01), but not XAC. The results suggest that actions at benzodiazepine receptors may be a tenable hypothesis to explain the convulsant actions of caffeine, but not those of XAC.

Animals↗
PubMed1988

Convulsant versus typical barbiturates: effects on conflict behavior in the rat.

Typical barbiturates produce a spectrum of behavioral effects, including anti-convulsant, muscle relaxant, sedative hypnotic and anti-anxiety actions. In contrast to these typical barbiturates, there exists a group of barbiturates which are pro-, rather than anti-convulsant. The effects of these convulsant barbiturates on anxiety-related behaviors have not been examined. Therefore, the present studies were designed to compare the effects of the convulsant barbiturate CHEB to those of a number of typical barbiturates in the Conditioned Suppression of Drinking (CSD) paradigm, an "animal model" for the study of anxiety and anti-anxiety agents. In daily 10-minute sessions, water-deprived rats were trained to drink from a tube which was occasionally electrified (0.5 mA), electrification being signalled by a tone. Within 3-4 weeks control responding had stabilized (10-15 shocks and 10-15 ml water/session); drug tests were then conducted at weekly intervals. Consistent with previous reports, typical barbiturates (pentobarbital, secobarbital, phenobarbital) produced dose-dependent increases in the number of shocks received at doses which did not depress background responding (water intake). In contrast, sub-convulsant doses of CHEB (0.3-2.5 mg/kg) produced a dose-dependent depression of both punished responding and background responding. Finally, it was found that pre-treatment with 1.25 mg/kg CHEB did not alter the anti-conflict effects of pentobarbital. These results suggest that (1) convulsant and typical barbiturates have markedly different effects on conflict behavior in the rat and (2) CHEB appears not to possess any "barbiturate antagonist" qualities.

Animals↗
PubMed1989

Patterns of convulsive susceptibility in the long-sleep and short-sleep selected mouse lines.

It has been hypothesized that the Long-Sleep and Short-Sleep mouse lines were bidirectionally selected for high and low brain excitability, and further, that these differences are mediated by the benzodiazepine/gamma-aminobutyric acid (GABA) receptor-chloride channel complex. Hence, mice from both lines were administered seven convulsants (bicuculline, pentylenetetrazol, 3-carbomethoxy-beta-carboline, picrotoxin, caffeine, flurothyl and strychnine) and myoclonic and clonic seizure latencies recorded. Supporting the original hypothesis, the results show that the two lines were differentiated by all of the convulsants and that in response to the drugs, three distinct convulsive patterns were found. Nevertheless, a simple genetic model accounting for these results was not evident. To further clarify these susceptibility patterns, a convulsant representing each of these patterns (bicuculline, pentylenetetrazol or caffeine) was administered in conjunction with the anticonvulsant-barbiturate phenobarbital or the benzodiazepine antagonist Ro 15-1788. Irrespective of the convulsant given, phenobarbital attenuated both myoclonus and clonus subsequent to all convulsants, while Ro 15-1788 had a more discrete anticonvulsant profile.

Animals↗