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At least 19 recordsLinked to original sources

PubMed1976

Specific and nonspecific multiple unit activities during the onset of pentylenetetrazol seizures. II. Acute lesions interrupting nonspecific system connections.

Nonspecific cortical, thalamic, mesencephalic, and pontine multiple unit activities (MUA) and changes in EEG and MUS of the sciatic nerve after threshold pentylenetetrazol activation were studied in three groups of animals in which neuronal connections were interrupted at three different levels of the central nervous system: spinal, mesencephalic, and prethalamic. Maximal increments of nonspecific MUA and maximal increments and maximal decrements of sciatic MUA after pentylenetetrazol from each group of lesioned animals were statistically compared with tose observed in intact animals. 1. Pentylenetetrazol threshold for producing cortical tonic-clonic EEG discharges was increased in animals with nesencephaic and prethalamic lesions but was not modified in animals with spinal transection. 2. Cortical MUA maximal increment was significantly decreased in mesencephalic and prethalamic lesioned animals, whereas thalamic MUA maximal increment was significantly decreased in mesencephalic and significantly increased in prethalamic lesioned animals. Pontine MUA maximal increment was significantly increased in spinal, mesencephalic, and prethalamic lesioned animals, and mesencephalic M-A maximal increment was not significantly modified in either prethalamic lesioned or in spinal transected animals. 3. Sciatic MUA maximal increment and maximal decrement were significatly decreased in spinal transected animals, whereas only maximal increment was significantly decreased in mesencephalic and only maximal decrement was significantly decreased in prethalamic lesioned animals. These results based on lesion experiments permit us to infer than under normal cinditions the development of generalized seizures induced by threshold pentylenetetrazol injection is highly dependent upon the neuronal interactions between nonspecific structures at different levels of the central nervous system. The possible nature of these neuronal interactions in the intact animals is discussed.

Animals↗

PubMed1977

Comparison of effects of bicuculline, strychnine, and picrotoxin with those of pentylenetetrazol on photically evoked afterdischarges.

The effects of bicuculline, strychnine, and picrotoxin on photically evoked afterdischarges (PhADs) in rat visual cortex were compared with those of pentylenetetrazol (a known PhAD potentiator) and a diazepam (a known PhAD suppressor) challenge. Bicuculline was found to augment PhADs in a manner similar to that found with pentylenetetrazol, with the exception that potentiation only occurred at convulsive levels whereas pentylenetetrazol augmentation occurred at both subconvulsive and convulsive levels. Diazepam suppressed bicuculline-potentiated PhADs. Picrotoxin was found to have some limited augmenting effect on PhAD activity but in a manner unlike that observed with either bicuculline or pentylenetetrazol. Strychnine had no systematic augmenting effect on PhADs. These results were discussed in terms of the possible role of GABA in thalamic systems responsible for PhAD production.

Animals↗

PubMed1976

Pentylenetetrazol-induced amnesia: a case for overt seizures.

In this study, the possible role of overt convulsions following pentylenetetrazol (PTZ) in retrograde amnesia was investigated. Following a single passive avoidance conditioning, when overt convulsions were blocked with sodium pentobarbital (Nem), the amnesic effect of pentylenetetrazol was also blocked. Subconvulsive doses of the drug did not produce amnesia. Animals that received a typically convulsive dose of the drug but failed to convulse were not amnesic; only animals with overt convulsions were different from saline controls. The data suggest that overt convulsions may be necessary for the development of pentylenetetrazol-induced retrograde amnesia.

Amnesia↗

PubMed1979

Inosine, an endogenous ligand of the brain benzodiazepine receptor, antagonizes pentylenetetrazole-evoked seizures.

Partially purified extracts of bovine brain were previously found to inhibit competitively the binding of [3H]-diazepam to rat brain synaptosomal membranes. The purines inosine and hypoxanthine were subsequently identified as the compounds responsible for this inhibitory activity. Intracerebroventricular administration of inosine to mice of the C3H/HEN and NIH general purpose strains caused a dose- and time-dependent increase in the latency to clonicotonic seizures produced by intraperitoneal administration of the convulsant pentylenetetrazole. Intracerebroventricular administration of equimolar doses of 2'-deoxyinosine, which is more potent than inosine in inhibiting the binding of [3H]diazepam in vitro, significantly increased pentylenetetrazole-evoked seizure latency. In contrast, both 7-methylinosine and thymidine were ineffective in inhibiting the in vitro binding of [3H]diazepam and increasing the latency to pentylenetetrazole-induced seizures in vivo. These results suggest that endogenously occurring purines such as inosine exhibit diazepam like effects when administered intracerebroventricularly, and these effects may be related to the interaction of inosine and related compounds with benzodiazepine receptors in the central nervous system.

Animals↗

PubMed1979

Effects of ischemia on the removal of extracellular potassium in cat cortex during pentylenetetrazol seizures.

Changes in cortical extracellular potassium activity ([K+]0), NADH fluorescence, and oxygen consumption were studied in anesthetized cats during pentylenetetrazol seizures. The effects of partial ischemia induced by either hypotension or intermittent carotid artery occlusion on these parameters were investigated. Nonischemic seizures were characterized by gradual generalized decreases in cortical NADH fluorescence and increases in O2 consumption, along with rapid increases in [K+]0, which then usually fell slightly as the ictal discharge continued. Ischemic seizures, on the other hand, were accompanied by complex changes in NADH fluorescence, by smaller delayed maximal increases in O2 consumption that lasted beyond the end of ictal activity, and by more sustained increases in [K+]0. The decay of [K+]0 after the termination of seizures in both nonischemic and moderately ischemic animals was not a monoexponential function: plots of ln delta [K+]0 versus time showed an initial linear decline (of slope M1) that rather abruptly slowed (to slope M2) after 2 to 5 sec and then often increased to the original rate. Both M1 and M2 were proportionately decreased by ischemia. In addition, the rate of [K+]0 removal could be slowed by acute ischemia induced either during or after the end of ictal activity. The initial rate of postictal [K+]0 removal (M1) was found to be linearly and inversely related to the level of cortical NADH fluorescence at the time of seizure termination. The results of this study suggest that an O2-dependent transport mechanism plays a major role in the removal of [K+]0 during and following the termination of generalized pentylenetetrazol seizures in the cat.

Animals↗

PubMed1977

Synaptic mechanism of pentylenetetrazole: selectivity for chloride conductance.

In the neurons of Aplysia californica pentylenetetrazole (2 millimolar) greatly reduced chloride-dependent responses to the iontophoresis of putative transmitters. At the same concentration, pentylenetetrazole caused less attenuation of the other iontophoretic responses and had minimal membrane effects. Several convulsants have been observed to have a similar selectivity for the chloride conductance. A common mechanism of convulsant action--reduction of transmitter-induced chloride conductances--is hypothesized.

Acetylcholine↗

PubMed1977

Photic and pentylenetetrazol-induced seizure susceptibility in Macaca mulatta.

Ninety-five out of 100 male Macaca mulatta of varying ages from a restricted habitat in N. India showed no abnormal seizure susceptibility or EEG response to photic stimulation and no electro-clinical features of epilepsy after pentylenetetrazol, 40 mg/kg sc.c. Autopsy studies on the remaining five monkeys with increased seizure proneness revealed depressed skull fractures with cortical trauma in four and a neoplasm in one. Presumably, these factors were responsible for the lowered seizure susceptibility to photic stimulation and pentylenetetrazol activation.

Animals↗

PubMed1979

Effects of pentylenetetrazol, pentobarbital and lidocaine on pallidal unit activities in rats.

In anesthetized immobilized rats, pallidal unit activities were recorded extracellularly through glass microelectrodes. Spontaneous activities were converted to an interspike interval histogram and an autocorrelogram by a medical computer and a correlator. Following pentylenetetrazol injection (20 mg/kg i.v.), burst discharges increased remarkably and the bursts tended to synchronize with repetitive spikes in electrocardiogram. Following administration of liocaine (5 mg/kg i.v.) the bursts increased by pentylenetetrazol were facilitated in approximately 70% neurons, whereas pentobarbital showed obvious reduction of the bursts in 80% neurons, although both drugs reduced the firing rate. Facilitation of burst discharges was also observed with high doses of lidocaine alone. These results indicate that lidocaine, as compared with pentobarbital, may block more easily inhibitory rather than excitatory neurons.

Action Potentials↗

PubMed1979

On some relationships between dopaminergic and serotoninergic mechanisms in pentylenetetrazol convulsions in albino mice.

Experiments with pentylenetetrazol convulsion model in albino mice--80 mg/kg subcutaneously--have revealed the following. The inhibitory effect of 5-HT, introduced intracerebroventricularly in a dose of 100 micrograms per mouse is eliminated by 500 mg/kg L-DOPA, 100 mg/kg amantadine, 5 mg/kg amphetamine and apomorphine, while for lower doses of the dopaminergic agent only a tendency towards antagonism is observed. The inhibitory effect of 50HTP in a dose of 200 mg/kg i. p. is eliminated by 500 mg/kg L-DOPA, 50 mg/kg amantadine and 5 mg/kg amphetamine, but it is not influenced by these drugs in doses of 250 mg/kg L-DOPA, 25 mg/kg amantadine and 5 mg/kg apomorphine, although when applied independently L-DOPA and amantadine in these lower doses potentiate convulsive reactions. The results obtained show that the dopaminergic and 5-HT-ergic systems have an antagonist effect on the convulsive reactivity in the case of pentylenetetrazol convulsion model. These results are in agreement with our views about the determining role of the balance between the various neurotransmitter systems in convulsive-seizure reactions.

5-Hydroxytryptophan↗

PubMedDate not supplied

The convulsive action of pentylenetetrazol and electroshock in irradiated rats.

Convulsive activity of pentylenetetrazol and electroshock was measured in rats irradiated 24 hr earlier with 800 R of X rays. At this time the content of "free" acetylcholine (ACh) was increased in the cerebral cortex, and the content of "bound" ACh was depressed in the brain stem. Irradiation facilitated the action of convulsogenic agents. Atropine did not prevent convulsions but facilitated them. An increase in the endogenous pool of ACh by eserine similarly to atropine facilitated the action of convulsogenic agents in control rats. In irradiated rats eserine shortened the duration of electrogenic convulsions, but it did not change significantly the latency of pentylenetetrazol convulsions. A causal relationship between the effects observed and post-irradiation modification of the content of "free" and "bound" ACh in the cerebral cortex and brain stem is discussed.

Acetylcholine↗

PubMed1976

Pharmacokinetic studies of pentylenetetrazol in dogs.

Pharmacokinetic profiles of pentylenetetrazol in the dog were studied following rapid intravenous and oral administrations of a convulsant dose (15-20 mg/kg). Plasma level-time curves after a rapid intravenous injection showed biexponential decline, indicating that the disposition of this drug in the dog follows a two-compartment body model. Pharmacokinetic parameters were calculated from the intravenous data. After oral administration of the solution dose, the peak plasma level appeared at about 30 min postdose, indicating that the absorption occurs rapidly. Areas under the oral plasma level-time curves s howed that the drug was absorbed completely and that the first-pass metabolism effect was minimal. The ligation studies of the kidney and the liver suggested that the main elimination pathway of this drug was biotransformation in the liver. The average plasma half-life was 1.4 hr. At steady state, the volume of distribution was approximately equivalent to the volume of the total body water.

Administration, Oral↗

PubMed1979

Discriminative stimulus properties of pentylenetetrazol and bemegride: some generalization and antagonism tests.

In an operant procedure of lever pressing on a FR 10 schedule of food reinforcement, male hooded rats were trained to respond with a lever on one side of a food cup following a drug injection, and to respond with a lever on the alternate side following a 1 ml/kg saline injection. All of 14 subjects learned to discriminate reliably between the effects of 20 mg/kg pentylenetetrazol (PTZ) and saline. Seven of eight rats learned to discriminate between the effects of bemegride (5 mg/kg) and saline. None of 14 rats learned to discriminate between 5mg/kg PTZ and saline. The bemegride discriminative stimulus generalized to PTZ (20mg/kg) and was antagonized by chlordiazepoxide (10 mg/kg). Chlordiazepoxide, diazepam, flurazepam, clobazam, and meprobamate were all effective antagonist of PTZ in a dose-dependent manner. Bemegride and cocaine generalized to the PTZ discriminative stimulus in a dose-dependent manner, but d-amphetamine, methylphenidate, and nicotine did not. Since bemegride and PTZ are convulsants at higher doses, the discriminative stimulus properties of these drugs might be based on a subtle convulsive brain state. The anxiolytic properties of benzodiazepines and meprobamate suggest that the discriminative stimulus produced by these convulsants is related to an "anxiety-inducing" action.

Animals↗

PubMed1979

Disruption of taste aversion learning by pentylenetetrazol.

Rats were taught an aversion to a sucrose taste cue (CS) by pairing it with lithium chloride-induced toxicosis (UCS). The CS-UCS interval was 30 min. Animals were injected with pentylenetetrazol (PTZ) (50 mg/kg at 0, 15, 25, 28 or 30 min after the CS in an attempt to disrupt taste aversion learning. Only animals given PTZ 30 min after the CS (simultaneously with the UCS) showed a significant learning deficit. However, learning deficits were also observed in individual animals in groups given PTZ at 15, 25 and 28 min. As lithium salts may produce seizures and abnormal electroencephalographic activity, it is suggested that the neurophysiological consequences of PTZ administration may interact with those of LiCl, causing a greater amnesic effect than PTZ by itself. The resulting interference with the memory trace is probably affecting either the neural engram underlying the CS or the associative bond between the CS and UCS. Evidence was also found that PTZ could act as a UCS with which to establish a mild taste aversion.

Animals↗

PubMed1978

Inhibition of pentylenetetrazol-induced convulsions in rats by prostaglandin E1: role of brain monoamines.

Prostaglandin E1-(PGE1-) induced inhibition of pentylenetetrazol (PTZ) convulsions in rats were significantly antagonized after pretreatment with drugs known to reduce brain serotonin activity, but not by pharmacological agents that decrease brain catecholamine activity. PGF2alpha also significantly inhibited PGE1 action. The results suggest that PGE1-induced inhibition of PTZ convulsions is not a direct effect, but an indirect one mediated through increase in brain serotonin activity.

Animals↗

PubMed1976

The effects of pentylenetetrazol on molluscan neurons. I. Intracellular recording and stimulation.

The effects of the convulsant drug pentylenetetrazol (PTZ) were studied in neurons from isolated ganglia of the nudibranch molluscs, Archidoris montereyensis and Anisodoris nobilis, using conventional techniques of intracellular recording and constant current stimulation. PTZ was selected because it causes changes in the intracellularly recorded responses similar to the depolarization shifts recorded in mammalian epileptic neurons. When perfusate containing 120-140 mM PTZ is introduced, the intracellular recording is characterized by an initial silent period followed by small oscillations in membrane potential and irregular firing of spikes. Within 5-15 min, bursts of 2-3 spikes occurred followed by the appearance of episodic prolonged depolarizations with superimposed high-frequency spikes. In the presence of PTZ the prolonged depolarizations were evoked by intracellular stimulation and at the termination of conditioning hyperpolarizations. The prolonged depolarizations were also recorded in neurons isolated from all synpatic input by axonal ligation. Prolonged depolarizations showed threshold behavior since they can be terminated early by an intracellularly applied hyperpolarizing current.

Animals↗

PubMed1976

The effects of pentylenetetrazol on molluscan neurons. II. Voltage clamp studies.

The effects of pentylenetetrazol (PTZ) upon the steady and transient outward ionic currents during PTZ-induced prolonged depolarizations were investigated using voltage clamp techniques. PTZ causes a 5-35% reduction in gL and a 40-60% reduction in steady-state gK. There is also a marked reduction in the activation of gA of Connor and Stevens6 at all clamp potentials; a shortening of the time constant for the inactivation of gA; and a 10-15 mV shift in the depolarizing direction of the curve relating the steady-state inactivation of gA to membrane potential. The equilibrium potentials for both gA and gK are depolarized by 20 mV in PTZ solution. Equation and voltage clamp data for normal repetitive firing were integrated with the normal and PTZ-alered data. Solution to these equations demonstrated: (1) normal repetitive firing in response to a constant current stimulus; and (2) PTZ-altered repetitive firing that was in the direction of, and for the most part, similar to the observed behavior.

Animals↗

PubMed1976

The anticonvulsant activity of ketamine agains siezures induced by pentylenetetrazol and mercaptopropionic acid.

The activity of the dissociative anaesthetics ketamine and gamma-hydroxybutyrate against seizures induced by mercaptopropionate and pentylenetetrazol have been determined. Ketamine (90 mg/kg) prevented the seizures induced by both convulsants, but gamma-hydroxybutyrate had negligible anticonvulsant activity. Mercaptopropionate (150 mg/kg) produced a rapid fall in whole brain glutamate decarboxylase activity which correlated with the onset of convulsions. Ketamine given prior to the mercaptopropionate prevented the convulsions, but had no effect on the reduction of enzyme activity. It was concluded that although ketamine was an anticonvulsant it did not act by preventing the inhibition of glutamate decarboxylase responsible for mercaptopropionate-induced convulsions.

Animals↗

PubMed1977

Effect of lysine vasopressin on pentylenetetrazol-induced retrograde amnesia in rats.

Lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial facilitated passive avoidance retention. Amnesia was produced when a single 50 mg/kg (IP) injection of pentylenetetrazol was given immediately following the passive avoidance acquisition trial. A single injection of lysine vasopressin (1 microgram/rat SC) administered 1 hr prior to either the acquisition trial or 24 hr retention trial antagonized the amnesia.

Amnesia↗