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PubMed2001

Consequences of hypothyroidism on auditory system function in Tshr mutant (hyt) mice.

The otological consequences of hypothyroidism and the outcome of thyroxin (T4) administration during the developmental period preceding the onset of hearing were examined in mice that express a point mutation in the gene encoding the thyrotropin receptor (Tshr), the so-called hyt mouse. Progeny of sires homozygous for the trait and heterozygous dams were injected with T4 or saline placebo from birth through the tenth postnatal day and auditory-evoked brainstem responses (ABRs) to acoustic clicks and tone bursts were recorded from young adults. Mutant (hyt/hyt) mice exhibited a distinctive pattern of sensory pathology that was characterized by their insensitivity to sound, prolonged response latencies, reduced peak amplitudes, and steep latency-intensity curves relative to the phenotypically normal, euthyroid, +/hyt littermates. Following thyroxin treatment, hyt/hyt mice responded to acoustic stimuli more frequently, were more sensitive to tone bursts throughout their audiometric range, and exhibited decreased latencies and increased amplitudes when compared with placebo-treated homozygous mutants. Although thresholds to acoustic stimuli were improved relative to the untreated group, T4-treated homozygotes were less sensitive than normal, euthyroid individuals. In addition, energy consumption by auditory brainstem nuclei, measured by 2-deoxyglucose (2-DG) uptake, was significantly lower in hyt/hyt mice compared with heterozygotes, and T4 treatment increased the level of 2-DG utilization. Moreover, mean ages for eye-opening and pinna-raising were delayed in animals that were homozygous for the hyt allele. When T4 was administered to hyt/hyt animals, pinna-raising occurred earlier than in untreated animals. A subset of homozygotes exhibited circling behavior, indicative of vestibular and/or motor dysfunction, even though all individuals assumed a normal righting reflex. These findings, including recruitment-like behavior and the restoration of response magnitude at high levels but not low, suggest that the cochlear amplifier is the primary locus of an enduring otological defect associated with hypothyroidism in the Tshr mouse.

Animals↗

PubMed2006

Effects of genetic and procedural variation on measurement of alcohol sensitivity in mouse inbred strains.

Mice from eight inbred strains were studied for their acute sensitivity to ethanol as indexed by the degree of hypothermia (HT), indexed as the reduction from pre-injection baseline of their body temperature. Two weeks later, mice were tested for their loss of righting reflex (LRR) after a higher dose of ethanol. The LRR was tested using the "classical" method of watching for recovery in animals placed on their backs in a V-shaped trough and recording duration of LRR. In a separate test, naive animals of the same strains were tested for HT repeatedly to assess the development of rapid (RTOL) and chronic tolerance (CTOL). We have recently developed a new method for testing LRR that leads to a substantial increase in the sensitivity of the test. Strains also have been found to differ in the new LRR test, as well as in the development of acute functional tolerance (AFT) to this response. In addition, our laboratory has periodically published strain difference data on the older versions of the HT and LRR responses. The earlier tests used some of the exact substrains tested currently, while for some strains, different substrains (usually, Nih versus Jax) were tested. We examined correlations of strain means to see whether patterns of strain differences were stable across time and across different test variants assessing the same behavioral construct. HT strain sensitivity scores were generally highly correlated across a 10-23 years period and test variants. The CTOL to HT was well-correlated across studies, and was also genetically similar to RTOL. The AFT, however, was related to neither RTOL nor CTOL, although this may be because different phenotypic end points were compared. The LRR data, which included a variant of the classical test, were not as stable. Measures of LRR onset were reasonably well correlated, as were those taken at recovery (e.g., duration). However, the two types of measures of LRR sensitivity to ethanol appear to be tapping traits that differ genetically. Also, the pattern of genetic correlation between HT and LRR initially reported in 1983 was not seen in current and contemporaneous studies. In certain instances, substrain seems to matter little, while in others, substrains differed a great deal. These data are generally encouraging about the stability of genetic differences.

Alcoholism↗

PubMed2006

Changes in expression of GABAA alpha4 subunit mRNA in the brain under anesthesia induced by volatile and intravenous anesthetics.

We investigated changes in levels of GABAA receptor alpha4 subunit mRNA in the mouse brain after administration of volatile or i.v. anesthetic, by performing quantitative RT-PCR. We also performed immunohistochemical assays for c-fos-like protein. During deep anesthesia (which was estimated by loss of righting reflex) after administration of propofol, levels of GABAA receptor alpha4 subunit mRNA in the hippocampus, striatum and diencephalons were significantly greater than those observed after administration of pentobarbital, midazolam or GOI (5.0% isoflurane and 70% nitrous oxide in oxygen). Under incomplete anesthesia, levels of GABAA receptor alpha4 subunit mRNA were significantly increased by midazolam in all brain regions, and were significantly increased by pentobarbital in the posterior cortex and striatum. Expression of GABAA receptor alpha4 subunit mRNA closely correlated with expression of c-fos-like protein. These results indicate that the GABAA receptor alpha4 subunit plays an important role in regulating the anesthetic stage of i.v. anesthetics.

Anesthesia↗

PubMed1988

Cardiovascular and central nervous system effects of rilmenidine (S 3341) in rats.

Rilmenidine (S 3341) is a new alpha 2 agonist, with antihypertensive properties. Pharmacologic data concerning its hemodynamic and central nervous system effects in the rat are described in this report. In the anesthetized or conscious spontaneously hypertensive rat, rilmenidine was found effective and potent as an antihypertensive agent, lowering blood pressure in a dose-dependent manner after intravenous and oral administration. These effects are related to a reduction in sympathetic tone as seen by the decrease in plasma catecholamines induced by rilmenidine in the spontaneously hypertensive rat. Studies in the normotensive pithed rat (electrical stimulation and adrenalectomization) confirmed the presynaptic alpha 2-stimulating properties of rilmenidine and suggested that a component of the antihypertensive activity of rilmenidine could be exerted through these peripheral receptors. A study of the central effects of rilmenidine was performed using classic neuropharmacologic tests. No effect was observed on the pentobarbitone-induced sleeping time in the rat. Rilmenidine caused only a minimal and non-dose-dependent inhibition of the righting reflex in the chick. In the rat, rilmenidine did not decrease the motor activity at concentrations up to 50 times higher than the antihypertensive dose. These results confirmed the contrast between rilmenidine and clonidine and suggest that a dissociation between sedative and antihypertensive effects could occur with rilmenidine.

Adrenalectomy↗

PubMed1982

Relationship of brain cyclic nucleotide levels and the interaction of ethanol with chlordiazepoxide.

The effects of combined administration of ethanol (4 g/kg) and chlordiazepoxide (CDP, 12.5 mg/kg) on mouse brain c-AMP and c-GMP levels were investigated in order to test the hypothesis that the supra-additive effect of CDP on ethanol sleep time may be related to a supra-additive alteration in brain cyclic nucleotide levels induced by the combined drugs. Ethanol alone or CDP by itself did not cause any change in brain c-AMP levels, except for a transient decrease in the cerebral cortex and midbrain at 0.5 hr after ethanol injection, as well as a transient increase in the cerebellum at 0.5 hr after CDP injection. The combined drug treatment did not result in a supra-additive effect on c-AMP levels. On the other hand, c-GMP levels were depressed significantly for 4 hr after ethanol injection especially in the cerebellum. The mice regained the righting reflex when the c-GMP levels were still about 30 per cent of control values. Ethanol and CDP together induced a supra-additive decrease of c-GMP concentrations in the cerebellum at 2 and 4 hr. This resulted in a lengthened period (about 2.5 hr) during which the cerebellar c-GMP levels were below 30 per cent of control values, and this interval coincided with the increase in sleep time, suggesting a possible relationship between these two factors. Injection of ethanol and N-demethyl-chlordiazepoxide (NDCDP) simultaneously (the latter being a metabolite of CDP) also elicited a more than additive depression of cerebellar c-GMP levels at 4 hr. These data suggest that NDCDP or its metabolite could be responsible for the supra-additive effect of CDP on the ethanol-induced decrease in cerebellar c-GMP levels.

Animals↗

PubMed1990

Lack of effect of halofantrine on hepatic drug metabolism in the rat in vivo and in vitro.

The effect of the antimalarial drug halofantrine (Hf) on hepatic drug metabolism in the rat has been studied in vivo and in vitro using different model drug substrates. Hf in vitro produced no significant effect on the values of Km and Vmax for aminopyrine N-demethylation or 7-ethoxycoumarin O-dealkylation in microsomes incubated with Hf (0.01-0.1 mM) or on the rate of N-demethylation of aminopyrine or O-dealkylation of Ec in microsomes produced from rats dosed chronically with Hf (200 mg/kg) for 4 days. The disposition of antipyrine (Ap) was investigated in the isolated perfused rat liver preparation (IPRL). Following the administration of bolus doses of Hf (0.5, 2.5 and 5.0 mg) no significant changes were observed in the half-life (t1/2), clearance (Cl) or apparent volume of distribution (Vd) for Ap compared with controls. Pentobarbitone induced sleeping time was also assessed in mice. No significant difference was determined in time to recovery of the righting reflex for mice receiving Hf as single oral doses or chronically over 4 days when compared with appropriate controls. The potential for selective isoenzyme effects was studied in vivo. The three principal urinary metabolites of Ap, norantipyrine (Np), 3-OH and 4-OH Ap were measured in rat urine, with no significant change in urinary recovery of Ap or any of the metabolites in the presence of Hf (1.25 mg/kg i.p.) compared with controls. These results suggest that Hf is not, in contrast to many commonly used quinoline antimalarials, a potent or specific inhibitor of drug metabolism in vitro or in vivo.

Animals↗

PubMed1990

Chrysin (5,7-di-OH-flavone), a naturally-occurring ligand for benzodiazepine receptors, with anticonvulsant properties.

Chrysin (5,7-di-OH-flavone) was identified in Passiflora coerulea L., a plant used as a sedative in folkloric medicine. Chrysin was found to be a ligand for the benzodiazepine receptors, both central (Ki = 3 microM, competitive mechanism) and peripheral (Ki = 13 microM, mixed-type mechanism). Administered to mice by the intracerebroventricular route, chrysin was able to prevent the expression of tonic-clonic seizures induced by pentylenetertrazol. Ro 15-1788, a central benzodiazepine receptor antagonist, abolished this effect. In addition, all of the treated mice lose the normal righting reflex which suggests a myorelaxant action of the flavonoid. The presence in P. coerulea of benzodiazepine-like compounds was also confirmed.

Animals↗

PubMed1979

Endogenous phosphorylation in vitro: differential effects of brain state (anesthesia, post-mortem) on electrophoretically separated brain proteins.

In vitro phosphorylation of rat cerebral cortex synaptosomes was measured in animals that had been acutely treated with sodium pentobarbital. [32P]Labelled phosphoproteins were separated by SDS-slab gel electrophoresis, and the autoradiographs were analyzed by densitometry. We report here that Band F of our previous reports can be separated into two components, F1 and F2, using an improved gel system. This separation is particularly relevant in this report since these components appear to be differentially sensitive to the manipulations used. Specifically, we found that while F1 phosphorylation was markedly diminished by deep barbiturate anesthesia, F2 was relatively stable. While phosphorylation of F2 was also stable 24 h post-mortem, Band F1 phosphorylation was no longer detectable. Finally, while osmotic shock treatment of synaptosomes reduced phosphorylation of F2 somewhat, it eliminated the in vitro phosphorylation of Band F1. We found that under light barbiturate anesthesia, just at the time when the animals lost the righting reflex, the in vitro phosphorylation of Bands D (MR 78,000--80,000 daltons), F1 (MR 47,000--49,000) and F2 (MR 40,000--45,000) increased relative to unanesthetized controls. The in vitro labelling of Bands D and F1 was depressed in tissue prepared from animals that were deeply comatose. These effects of pentobarbital were more pronounced when animals were sacrificed by liquid nitrogen immersion, rather than by decapitation. Cyclic AMP-dependent phosphorylation of Band D exhibited remarkable stability 24 h post-morten (7 days in one case), even when brain tissue was left at room temperature (21--23 degrees C). Phosphorylation of Band F1, however, was not detectable in post-mortem tissue. The results of these studies indicate that phosphorylation of Band F1 is: (1) sensitive to pentobarbital, and (2) unstable post-mortem. Previous findings from our laboratory suggest that Band F1 is: (3) increased in phosphorylation in liquid nitrogen P2 preparations, and may be (4) cAMP-independent, (5) rapidly turning over its phosphate in vivo, and (6) altered by a training experience. Other evidence suggests that: (7) Band F1 phosphorylation may be Ca2+-dependent and that: (8) its phosphorylation is sensitive to osmotic lysis of synaptosomes. The results suggest an important and perhaps unique role for Band F1 in neuronal function.

Animals↗

PubMed1985

Changes in the local cerebral metabolic rate for glucose in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) primate model of Parkinson's disease.

Nine adult monkeys (Macaca fascicularis) were used in this study. Five animals were used as controls. Three animals were injected intravenously daily with 0.5 mg/kg of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) over a 4-day period; one animal was injected weekly over a 4-week period. Neurological examination of the MPTP-treated animals revealed a flexed posture of trunk and extremities, bradykinesia, increased tone without cogwheel rigidity, loss of vestibular righting reflexes, decreased vocalization and swallowing, failure of upgaze and abnormal pursuit eye movements. Reflexes were hyperactive. The compound 2-deoxy-D-[14C]glucose (2-DG) was utilized for the determination of the local cerebral metabolic rate for glucose (lCMRg). A generalized decrease in lCMRg was noted in all cerebral cortical areas as compared to control values. The cerebellar cortex demonstrated no change in lCMRg. Areas that demonstrated a significant increase in lCMRg were: the internal and external segments of the globus pallidus (P less than 0.01), the pars compacta and the pars reticulata of the substantia nigra (P less than 0.05). Areas that demonstrated a significant decrease in lCMRg were: the head of the caudate nucleus (P less than 0.05), the anterior dorsomedial putamen (P less than 0.05) and the anterior segment of the subthalamic nucleus (P less than 0.05). The 2-DG analysis of the MPTP primate model of Parkinson's disease is particularly suited to demonstrate areas in the central nervous system that are affected by this neurotoxin. Further studies of these areas may lead to a better understanding of the mechanisms that underlie the clinical symptomatology of Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1987

Tetrodotoxin-insensitive central depression by grayanotoxin-III in mice.

The effect of systemic administration of grayanotoxin (GTX)-III, a constituent in leaves of Pieris japonica D. Don with an ability to activate the voltage-sensitive sodium channels in excitable tissues, on general behaviors of animals was studied using Std-ddy mice. Intraperitoneal administration of the toxin (0.1-0.25 mg/kg b. wt.) resulted in a dose-dependent manner in a significant and reversible muscle relaxation, and a profound and long lasting (greater than or equal to 60 min) depression of locomotor activity. Pretreatment with GTX-III caused a profound potentiation of the duration of loss of righting reflex by pentobarbital with a concomitant delay of the onset of convulsive seizures by various convulsants such as strychnine, picrotoxin and pentetrazol. Neither tetrodotoxin (1-5 micrograms/kg, i.p.) nor Ro15-1788 (1-5 mg/kg, i.p.) prevented the GTX-III-induced suppression of locomotor activity. These results suggest that GTX-III may elicit a central depressant action in mice through a molecular mechanism other than activation of the voltage-sensitive sodium channels in the brain.

Animals↗

PubMed1987

The effect of neurotensin, TRH and the delta-opioid receptor antagonist ICI 174864 on alcohol-induced narcosis in rats.

The effects of microinjections of thyrotropin-releasing hormone (TRH), neurotensin and ICI 174864 into the nucleus accumbens, nucleus caudatus, septum and mesencephalic periaqueductal grey were studied on ethanol-induced narcosis in the rat. Levels of narcosis were assessed by alterations in ethanol-induced hypothermia and sleep time. Ethanol produces a 2 degree C fall in body temperature over the first hour which then recovered over the next 2 h. Sedation was produced to the extent that the righting reflex was lost for between 80 and 90 min. In the nucleus caudatus all 3 peptides were ineffective at altering narcosis. In the periaqueductal grey, septum and accumbens, TRH (5 micrograms) and ICI 174864 (1 microgram) microinjections significantly reduced the sleep time by between 50 and 70%. ICI 174864 was approximately 10 times more potent that TRH at reducing the sleep time. In addition, both these peptides significantly accelerated the recovery from the ethanol-induced hypothermia in the periaqueductal grey, septum and accumbens. ICI 174864 prevented the ethanol-induced fall in body temperature. Neurotensin (5 micrograms) significantly increased the sleep time by up to 50% and potentiated the ethanol-induced hypothermia. These results suggest that the administration of TRH or the blockade of delta-opioid receptors, resulting in an inhibition of endogenous enkephalin transmission, may significantly inhibit ethanol narcosis in the rat. Opposing this, the application of neurotensin appears to potentiate ethanol narcosis. These results also indicate that endogenous enkephalin release plays an important role in ethanol narcosis.

Animals↗

PubMed1991

Evidence that sensitivity to steroid anesthetics appears late in evolution.

The effects of pregnanolone, a steroid anesthetic, were compared with diethyl ether and short chain alkanols in 21 aquatic species from 7 phyla. Loss of righting reflex and escape response were used as indicators of anesthesia. All organisms were anesthetized by diethyl ether and short chain alkanols, but pregnanolone affected only organisms belonging to the phylum Chordata. It is probable that pregnanolone exerts its effect on the gamma-aminobutyric acid (GABA) receptor. Because many invertebrates do possess GABA receptors, our results suggest that a binding site at which steroid binding causes organismal anesthesia appeared early in chordate evolution on a previously existing GABA receptor. The results also appear to exclude a primary lipid bilayer site for steroid anesthetic action.

Alcohols↗

PubMed1991

Effects of non-competitive NMDA receptor antagonists on reproductive and motor behaviors in female rats.

MK-801 and dextrorphan, selective non-competitive antagonists at N-methyl-D-aspartate (NMDA) receptors, were used to evaluate the effect of NMDA receptor blockade on sexual and motor behaviors in female rats. Ovariectomized rats were treated with estradiol benzoate (EB) for 48 or 72 h followed by progesterone (P) 3.5-4 h before testing the animals for sexual receptivity. After testing for estrous responsiveness, the effect of NMDA antagonists on several motor behaviors was also assessed. Lordosis frequency and intensity were inhibited in animals that received 0.5 mg/kg MK-801 30 min before EB; the same dose of MK-801 was relatively ineffective when administered 24 h after EB. In neither case did MK-801-treated females differ from controls when motor behaviors were assessed after mating tests. When 30 mg/kg dextrorphan, a short-acting NMDA antagonist, was administered 15 min before P, sexual behavior was not blocked. However, both 0.05 mg/kg MK-801 and 30 mg/kg dextrorphan suppressed ongoing female sexual behavior within 30 min in animals made receptive with EB and P. These deficits in sexual behavior were associated with changes in motor performance. MK-801 (0.1 mg/kg) and dextrorphan (30 mg/kg) abolished movement in the vertical dimension (e.g. jumping and rearing). By contrast, the drugs increased movement in the longitudinal (locomotion) and lateral (circling) dimensions. At 0.2 mg/kg, MK-801 blocked movement in both the vertical and longitudinal dimensions; however, it failed to block circling. Only at 0.4 mg/kg did MK-801 inhibit lateral movements and righting reflexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Regional catecholamine levels in brains of normal and ethanol-tolerant long-sleep and short-sleep mice.

The objective of this study was to further investigate neurochemicals which might modulate congenital differences in sensitivity to the acute and chronic effects of ethanol. Catecholamine levels were measured in the cortex, hippocampus, midbrain and cerebellum of long-sleep (LS) and short-sleep (SS) mice. These measurements revealed that norepinephrine (NE) levels were equivalent in all these brain regions of both strains except for a significantly greater concentration in the midbrain of LS mice. The hippocampus, cortex and cerebellum of SS mice contained more epinephrine (E) than for LS mice. Likewise, the hippocampus and cerebellum of SS mice had higher levels of dopamine (DA), while in the midbrain this amine was more abundant in LS mice. Following 7-10 days of ethanol ingestion, both LS and SS mice exhibited a significant reduction in the duration of ethanol-induced loss of righting reflex. This tolerant state was associated with a depletion of NE in the hippocampus and cortex of both strains. NE was also significantly reduced in the midbrain of LS and the cerebellum of SS mice. On the other hand, E levels were unaltered except for a reduction in the hippocampus of tolerant SS mice. DA levels declined in all brain regions of tolerant mice except for the cerebellum of LS mice and the midbrain of SS mice where a significant increase and no change in DA concentration was detected, respectively. Interestingly, the brain levels of 3-methoxy-4-hydroxyphenylglycol were uniformly increased during the tolerant state for both strains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Antinociceptive actions of cannabinoids following intraventricular administration in rats.

Intraventricular administration of 5 or 20 micrograms of the cannabinoids WIN55,212-2 and CP-55,940 markedly reduced rat's responses to noxious thermal stimuli in the tail-flick test; no significant effect was found at 1 micrograms. The dose-response curves were steep and monotonic, the onset was rapid, and the effect lasted about an hour at the highest dose. In contrast to their antinociceptive actions, WIN55,212-2 and CP-55,940 failed to alter the latency of righting reflexes at the highest dose, suggesting that motor impairment did not cause the decreased responsiveness to the thermal stimulus. Finally, an assessment of the biodistribution of intraventricularly administered [3H]WIN55,212-2 in brain and spinal cord at the time of maximal antinociception revealed that the drug was confined to the brain. The levels of [3H]WIN55,212-2 found in S3-S4, the location of the spinal mechanisms for tail-flick, were below the limit of detectability. Together, these findings provide direct evidence that the antinociceptive effects of cannabinoids are mediated, at least in part, by their actions in the brain.

Analgesics↗

PubMed1994

Lesions of the pedunculopontine tegmental nucleus abolish catalepsy and locomotor depression induced by morphine.

The cataleptic and locomotor depressant effects of morphine are mediated by a series of neural structures, all of which project to the pedunculopontine tegmental nucleus (PPTg). To test the idea that the PPTg is also involved in mediating morphine's effect on these behaviours, we examined catalepsy and spontaneous motor activity following bilateral lesions of the PPTg (0.5 microliters of 0.1 M N-methyl-D-aspartate infused over 10 min). We also examined the effect of PPTg lesions on motor functioning by observing sensorimotor responses, limb use, muscle tone and locomotion. PPTg lesions completely abolished the catalepsy and decreased activity that normally follows morphine administration. In addition lesioned animals exhibited increased muscle tone, and impairments in limb use and righting reflexes. Although the deficits were subtle, these results confirm that damage to the PPTg is associated with motor abnormalities.

Acoustic Stimulation↗

PubMed1996

Sleep and nitric oxide: effects of 7-nitro indazole, inhibitor of brain nitric oxide synthase.

We examined the effect of 7-nitro indazole (7-NI, 2.5-50 mg/kg, i.p.), an inhibitor of central nitric oxide (NO) synthesis, on general behaviour and sleep. The results show that 7-NI induces ptosis, a loss of the righting reflex and decrease of the EEG amplitudes. Furthermore, a duration of slow wave sleep (SWS) and REM sleep decreased, while the latencies of SWS and REM sleep increased. The effects of 7-NI on general behaviour and sleep were partially antagonized by intraventricular administration of the NO precursor, L-arginine (600 micrograms). These findings indicate that 7-NI induces a state of prominent central depression associated with motor deficit and decrease in sleep stages and wakefulness. It further suggests that NO exerts a significant excitatory effect on the neuronal structure involved in the regulation of locomotion and vigilance.

Animals↗

PubMed1976

On the possible role of brain protein synthesis in functional barbiturate tolerance.

Pentobarbital pellet implantation increased more than 200% the ED50 dose of pentobarbital required to induce loss of the righting reflex within 2 min of i.p. injection and increased the onset of barbital-induced sleep. Both tests of functional barbiturate tolerance were blocked by the intraventricular injection of cycloheximide. The effects of acute (45 mg/kg i.p.) and chronic (pellet implantation) pentobarbital treatment on the incorporation of 3/-lysine into the protein of various subcellular fractions of the cortex and subcortex were studied. In the subcortex, chronic pentobarbital treatment significantly stimulated protein synthesis 40-50% in the microsomal, soluble and mitochondrial fractions. Both acute and chronic pentobarbital treatments significantly increased (3H-lys)-protein accumulation in a fraction of synaptic plasma membranes derived from a population of nerve ending particles (NEP) enriched in gamma-aminobutyric acid (GABA). The possible significance of these data to pentobarbital tolerance and dependence development is discussed.

Animals↗