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We report a study on the relation between open-field behavior and electroencephalographic (EEG) changes during lindane-induced seizures in 2-month-old adult male Wistar rats. For chronic EEG recordings and power spectra analysis, 3 electrodes were implanted into the skull. Three groups of animals, (i) saline-injected control (n = 6), (ii) DMSO-treated (n = 6), and (iii) lindane intraperitoneally administered: L(4) (4 mg/kg, n = 10), L(6) (6 mg/kg, n = 11), and L(8) (8 mg/kg, n = 11), were observed for 30 min for the occurrence of convulsive behavior. It was assessed by incidence of motor seizures, and seizure severity grade was determined by a descriptive rating scale (0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus with full rearing; 3, progression to generalized clonic convulsions followed by tonic extension of fore and hind limbs and tail; 4, status epilepticus). EEG signal and spectral analyses were suitable to describe the dynamics of complex behavioral responses. Incidence and severity of epileptic manifestations, recorded as high voltage spike-wave complexes, polyspikes, sleep-like patterns in EEG, and power spectra changes, were greater in lindane-treated groups in a dose-dependent manner compared with control or DMSO-treated groups. Our results suggest good correlation between lindane-induced epileptiform activity and behavioral changes.

Chronic ethanol consumption is a major risk factor for epilepsy, and seizures frequently occur during the withdrawal period. The aim of our study was to investigate effects of ethanol on lindane-induced seizures in rats. Male Wistar rats were injected i.p. with one of the following 5 treatments: (i) saline, (ii) dimethylsulfoxide, (iii) lindane (8 mg/kg) (L), (iv) ethanol in doses of 0.5 g/kg (E(0.5)), 1 g/kg (E(1)), and 2 g/kg (E(2)), and (v) groups that received ethanol 30 min before lindane (LE(0.5), LE(1), and LE(2)). Behavioral changes were described by using a descriptive scale as follows: 0, no response; 1, head nodding, lower jaw twitching; 2, myoclonic body jerks, bilateral forelimb clonus; 3, generalized tonic-clonic convulsions; 4, status epilepticus. The incidence of convulsions in the LE(2) group was significantly lower than the incidence in the L (p < 0.01) and LE(0.5) groups (p < 0.05). The median grade of convulsive behavior was significantly lower in the LE(2) (p < 0.01) and LE(1) groups (p < 0.05) compared with the L group. Latencies to the first seizure response were not significantly different among groups. ED50 of ethanol was 1.40 (1.19-1.65). Our findings suggest that ethanol decreased severity and incidence of lindane-induced seizures in a dose-dependent manner.

We investigated the effects of hypothermia on the incidence and EEG signs of audiogenic seizures in rats treated with metaphit (1-[1(3isothiocyanatophenyl)-cyclohexyl] piperidine), an experimental model of generalized reflex epilepsy. After i.p. injection with metaphit (10 mg/kg) Wistar rats were exposed to audiogenic stimulation at hourly intervals during the time course of the experiment. After intermittent use of an ice pack 8 h after the metaphit treatment, when seizure was fully developed, the body temperature was reduced to 30 +/- 0.5 degrees C in one half of the rats, and maintained at 37 +/- 0.5 degrees C in the other half. Saline-injected rats served as a control group. In the hypothermia group, the incidence of audiogenic seizures induced by metaphit was completely suppressed during the 3 consecutive testing times, while no signs of epileptiform activity were noted in EEG tracings. The termination of hypothermic treatment resulted in the recovery of seizure susceptibility, and during audiogenic stimulation, bursts of spiking activity were recorded in the EEGs of metaphit-treated rats. These findings indicate that moderate body hypothermia is an effective anticonvulsant treatment for audiogenic seizures in metaphit-treated rats.