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PubMed1987

Ethanol enhances recurrent inhibition in the dentate gyrus of the hippocampus.

Intraperitoneal injection of ethanol (2 g/kg) substantially augmented recurrent inhibition in the dentate gyrus, as measured by population responses to paired-pulse stimulation of the perforant path. In contrast, this dose of ethanol had no significant effect on singly evoked (or conditioning) population spikes. These data indicate that the increased recurrent inhibition by ethanol was not due to a generalized depressant effect, and suggests that at these doses and time points ethanol can selectively alter synaptic transmission in the hippocampus.

Action Potentials↗

PubMed1988

Antagonist action of imidazobenzodiazepine Ro 15-4513 on ethanol-induced alterations of saccadic eye movements in the pigmented rat.

Following an intraperitoneal injection of ethanol (1 g/kg), spontaneous saccades performed by pigmented rats showed a backward post-saccadic drift which was still present 45 min after the administration. When 5 mg/kg of Ro 15-4513 were injected, 15 min after ethanol, there was an immediate remarkable reduction in post-saccadic drift amplitude, with a full recovery in about 30 min after Ro 15-4513 administration. This drug is thus able to reverse the effect of ethanol and to restore effectively a mechanism of motor integration.

Animals↗

PubMed1990

Phencyclidine increases extracellular dopamine metabolites in rat medial frontal cortex as measured by in vivo dialysis.

An acute intraperitoneal injection of phencyclidine (PCP) caused a tetrodotoxin-reversible increase in extracellular release of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the dialysates from the medial frontal cortex of the rat. Moreover, there was an increase in the tissue content of DOPAC and HVA with acceleration of dopamine (DA), but not noradrenaline, utilization in the cortical area after systemic administration of PCP. These results suggest that PCP facilitates DA metabolism in the medial frontal cortex by increasing impulse flow in the DA neurons projecting to the prefrontal region.

Animals↗

PubMed1994

The endogenous cofactors, thioctic acid and dihydrolipoic acid, are neuroprotective against NMDA and malonic acid lesions of striatum.

Thioctic acid (alpha-lipoic acid) and dihydrolipoic acid are endogenous, interconvertible cofactors of the mitochondrial pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes. These compounds help to maintain glutathione and alpha-tocopherol in their reduced states, and they possess intrinsic free radical scavenging properties. We examined whether systemic treatment with thioctic acid or dihydrolipoic acid is protective against direct- and indirect-acting excitotoxins. Adult rats were treated for 10 days with intraperitoneal injections of vehicle, thioctic acid or dihydrolipoic acid, and on day 7 of treatment animals received unilateral stereotaxic injections of NMDA or malonic acid into the striatum. Histological assessment 3 days after the stereotaxic injections revealed a marked reduction in lesion volume in animals treated with thioctic acid or dihydrolipoic acid. We conclude that thioctic acid and dihydrolipoic acid are neuroprotective against direct and indirect excitotoxic insults.

Animals↗

PubMed1994

Expression of c-fos immunoreactivity in the hypothalamic magnocellular neurons during chronic osmotic stimulations.

The immunoreactivity of c-fos protein was transiently detected in magnocellular neurons of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the rat hypothalamus after intraperitoneal injection of hypertonic NaCl solution. In contrast, c-fos-positive magnocellular neurons were persistently observed in the SON and PVN of the rats which were chronically stimulated by the drinking of hypertonic NaCl solution instead of water or by water deprivation. c-fos immunoreactivity was eliminated in the animals which were allowed to drink tap water for 24 h following the chronic osmotic stimulations. These results suggest that persistent expression of c-fos protein is closely associated with the neural plasticity of the hypothalamic magnocellular neuron.

Administration, Oral↗

PubMed1989

Alternated delta and mu receptor activation: a stratagem for limiting opioid tolerance.

The development of tolerance to the antinociceptive effects of chronically administered delta (delta) and mu (mu) agonists was examined in vivo in rats using a protocol of alternated preferential activations of delta and mu receptors. This was accomplished by alternated chronic administrations of the relatively delta- and mu-selective agonists DADLE ([D-Ala2, D-Leu5]-enkephalin) and morphine sulfate (MSO4), respectively. Specifically, the agonists were given as 3 sequential 6 day cycles: (1) osmotic pump infusions of DADLE into the lumbar intrathecal space; (2) followed by intraperitoneal injections of MSO4; (3) followed again by intrathecal DADLE infusions. Following each cycle, the agonists' antinociceptive activities were measured using the tail-flick test of nociception. These were compared to their baseline (i.e., drug-naive) activities as a measure of tolerances. In a separate experiment the same total intrathecal dose of DADLE was infused chronically over twelve days without an interposed dose of MSO4. In the alternated agonist experiment, DADLE's antinociceptive ED50 value was increased by 10.4-fold, then reverted to only a 1.5-fold change from baseline and was subsequently shifted to a 13.7-fold increase over baseline. After cycle 2 with MSO4 a significant recovery from DADLE tolerance was noted as compared to that following cycle 1: 1.5- versus 10.4-fold, respectively. Furthermore, the interposition of a cycle of MSO4 between two cycles of DADLE resulted in a much lesser degree of tolerance for DADLE following cycle 3 (12 days of non-continuous DADLE infusion) than was noted after the 12 day continuous DADLE intrathecal infusion (13.7- versus 25.0-fold tolerance, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Age and sex dependence of the effects of an aqueous extract of Physalis alkekengi fruits on rat hepatic glucose 6-P dehydrogenase activity.

Intraperitoneal injections of an aqueous extract of winter cherry fruits (Physalis alkekengi) to new-born, weanling and adult female rats and to weanling and adult male rats had no effect on body weight, liver weight and liver cytosol protein content. The specific activities of hepatic glucose 6-P dehydrogenase (an estrogen induced protein) in rats of different age and sex groups in terms of mU/mg protein were: treated new-born females, 15.9 +/- 0.5; control, 29.1 +/- 0.6; treated weanling females, 14.9 +/- 0.3; control, 24.8 +/- 0.7; treated adult females, 25.7 +/- 0.5; control, 26.1 +/- 0.5; treated weanling males, 7.9 +/- 0.2; control, 7.9 +/- 0.1; treated adult males, 9.6 +/- 0.4; and control, 9.7 +/- 0.3. Treatment of new-born and weanling female rats with the extract resulted in 40-45% reduction in hepatic G6PD activity. However, treatment of adult females, and weanling and adult males produced no significant change in the activity of this enzyme. The data are discussed both in terms of the increase in the capacity of rodent liver to metabolize steroidal compounds with age and the presence of low levels of circulating estradiol necessary for enzyme induction in male rats.

Age Factors↗

PubMed1988

Effects of anticonvulsants on responses to excitatory amino acids applied topically to rat cerebral cortex.

1. Five clinically used anticonvulsants were examined to find out if they block the effects of excitatory amino acids in the cerebral cortex of urethane anaesthetised rats. 2. Compounds were tested by topical application to the cortical surface and following their intraperitoneal injection at anticonvulsant doses. 3. Pentobarbital and diphenylhydantoin blocked the effect of quisqualic acid but only at concentrations higher than the therapeutically relevant levels. 4. Pentobarbital and diphenylhydantoin did not alter the effects of N-methyl-D,L-aspartic acid (NMDLA) or kainic acid. 5. Diazepam prevented the kainic acid-induced development of distorted somatosensory evoked potentials (SEPs) at therapeutically relevant levels. 6. Diazepam had no effect on NMDLA or quisqualic acid. 7. Carbamazepine and chlormethiazole had no effect on NMDLA, kainic acid or quisqualic acid. 8. The anticonvulsive effects of these drugs, with the exception of diazepam, probably do not involve antagonism of endogenous EAAs.

Administration, Topical↗

PubMed1991

The effect of U-50,488H, a kappa-opiate receptor agonist on tolerance to the analgesic and hyperthermic effects of morphine in the rat.

1. The effect of intraperitoneal injections of U-50,488H, a kappa-opiate receptor agonist, on the development of tolerance to the analgesic and hyperthermic effects of morphine was determined in male Sprague-Dawley rats. 2. Tolerance was induced by implantation of four morphine pellets during a 3-day period (4/3 schedule) or six morphine pellets during a 7-day period (6/7 schedule). 3. Administration of U-50,488H (25 mg/kg, twice a day for 3 days in 4/3 schedule) or (5, 10 and 20 mg/kg twice a day for 7 days in 6/7 schedule) did not affect the development of tolerance to the pharmacological actions of morphine. 4. It is concluded that activation of kappa-opiate receptors does not modify the development of tolerance to morphine in the rat.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1995

Lipid peroxidation and antioxidant enzyme activity in aspirin-treated rats.

1. Malondialdehyde formation and antioxidant enzyme activity after oral or intraperitoneal treatment of rats with various doses of aspirin was studied. 2. Aspirin, orally, had no effect on spontaneous, Fe(II)- or Fe(II)/ascorbate-induced malondialdehyde formation in liver homogenates; orally, ascorbate-induced malondialdehyde production was inhibited but only after 5-day treatment with 500 mg/kg aspirin; after intraperitoneal injection, the drug inhibited ascorbate- and Fe(II)/ascorbate-induced production of malondialdehyde. 3. Aspirin had no effect on malondialdehyde formation in erythrocytes, irrespective of the dose and route of drug administration. 4. Aspirin increased glutathione peroxidase activity in liver after 5-day treatment with an oral dose of 500 mg/kg and decreased enzyme activity in both liver and erythrocytes, 24 hr after a single injection of the same dose. 5. Aspirin, in vivo slightly affected lipid peroxidation and antioxidant enzyme activity.

Administration, Oral↗

PubMed1987

An immunohistochemical study of the acute and long-term effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the marmoset.

Administration of the drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine induces a parkinsonian syndrome in primates. Intraperitoneal injections of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the common marmoset (Callithrix jacchus) produced symptoms of rigidity, akinesia and tremor which persisted for at least one month. However, after this time, considerable behavioural recovery occurred, although animals were still severely bradykinetic compared with controls. Marmosets were allowed to survive for 1, 3 1/2 or 7 months prior to histological and immunocytochemical analysis. Detection of catecholaminergic neurons using antibodies directed against the enzyme tyrosine hydroxylase revealed a profound (80%) loss of dopaminergic cells from the substantia nigra one month after initiation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment. This was accompanied by a severe gliosis. Fewer cells were lost from the adjacent ventral tegmental area (45%), but dopamine-containing cells in other brain areas were not obviously affected. At longer survival times the substantia nigra was less damaged, with a proliferation of glia in the pars compacta and a loss of approximately 20% of the dopaminergic perikarya. Using immunohistochemical techniques, the distribution of neuropeptides substance P, [Met]enkephalin and dynorphin 1-17-like immunoreactivity were examined and found to exhibit distinctive patterns in the marmoset substantia nigra. The integrity of these systems appeared intact at all times after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment. These results support the hypothesis that the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine produces a clinical syndrome, indistinguishable from Parkinson's disease, via a selective destruction only of neurons with perikarya in the substantia nigra pars compacta and the ventral tegmental area. The findings that the peptidergic input to these cells together with most non-nigral dopaminergic cell groups are not damaged, indicate that the selectivity of the lesion produced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine appears greater than that seen in idiopathic Parkinson's disease. The neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the marmoset may not be permanent since both behavioural and biochemical recovery were observed after several months.

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

PubMed1988

Effect of simultaneous administration of bleomycin on the acute skin reactions of mice after single and fractionated doses of radiation.

The effect of bleomycin on the acute mouse foot skin reactions, occurring after irradiation, was investigated. Bleomycin was delivered simultaneously with the irradiation treatment, either by intraperitoneal injection or by subcutaneous continuous infusion. Experiments were carried out to investigate (a) the modification by bleomycin of the response to single doses of radiation (b) the effect of total drug dose on this modification (c) the influence of the drug on repair of sublethal radiation damage and (d) the interference by the drug with compensatory repopulation after irradiation. In none of the experiments could any influence of the drug on these radiation induced reactions and recovery processes be demonstrated. These results are in direct contrast to what we have observed previously for similar types of experiments in another epithelial system, the mouse lip mucosa.

Animals↗

PubMed1990

Paradoxical sleep-promoting effects of brain extract from paradoxical sleep-deprived rats.

Brain extract was obtained from whole brains of donor rats following four days of paradoxical sleep deprivation (PSD). Intraperitoneal injection of this brain extract in normal (i.e., not pretreated) recipient rats led to a significant increase of paradoxical sleep (PS) which was beginning at the third hour postinjection and still present on the day after treatment. Both PS episode number and PS episode duration were increased by the PSD extract, whereas slow-wave sleep was not influenced. Brain extract of nondeprived control rats, on the other hand, had no significant effects. In the present experiments, an extract volume obtained from two donor brains was transferred to one recipient. Compared to our earlier investigations (one donor brain/one recipient) this higher "dose" of PSD extract exerted a more pronounced and prolonged effect. These results support the idea that some PS-inducing factor(s) accumulating in the brain during PS deprivation may be involved in the regulation of paradoxical sleep.

Animals↗

PubMed1989

Endogenous and heavy-metal-ion-induced metallothionein gene expression in salmonid tissues and cell lines.

Endogenous levels of metallothionein (MT) mRNA were detected by RNA probes in several somatic and germ-line tissues of rainbow trout, such as eggs, ovaries and immature testis. These levels may be related to metal-ion homeostasis in the observed tissues. The induction kinetics of trout MT isoform B (MT-B) mRNA were studied after single intraperitoneal injections of CdCl2, CuCl2 and ZnCl2. MT-B mRNA was induced within 12 h in liver, kidney, spleen and gills. However, over the 48-h experimental period, the kinetics of MT-B mRNA accumulation differed in response to the three metal salts, possibly due to differential handling of the salts by these tissues. Multiple metal-salt injections induced high levels of MT-B mRNA in the four tissues studied. In the rainbow trout hepatoma cell line, ZnCl2 was a better inducer of the MT-B gene, as compared to CdCl2 and CuCl2. The expression of the exogenous trout MT-B promoter in Chinook salmon embryonic cell line indicates the presence of MT regulatory factors. In contrast, the endogenous MT genes in these cells are quiescent, possibly due to the methylation of their promoter region.

Animals↗

PubMed1987

Acetone effects on N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity.

Acetone has been shown to potentiate the toxicity of many halogenated hydrocarbons. The purpose of this study was to determine if acetone could alter the acute nephrotoxicity produced by the experimental fungicide N-(3,5-dichlorophenyl)succinimide (NDPS). Male Fischer 344 rats were administered acetone (1, 5 or 10 mmol/kg) or acetone vehicle (corn oil, 10 mg/kg) orally followed 16 h later by a single intraperitoneal injection of NDPS (0.2 or 0.4 mmol/kg) or NDPS vehicle (sesame oil, 2.5 ml/kg) and renal function was monitored at 24 and 48 h. Acetone (1 or 5 mmol/kg) did not alter NDPS (0.2 mmol/kg)-induced renal effects while acetone (10 mmol/kg) pretreatment attenuated NDPS (0.4 mmol/kg)-induced increases in blood urea nitrogen (BUN) concentration and kidney weight but had no effect on NDPS (0.4 mol/kg)-induced changes in urine volume or content, organic ion accumulation by renal cortical slices or renal morphology. These results suggest that acetone weakly attenuates NDPS-induced nephrotoxicity.

Acetone↗

PubMed1987

Effect of repeated administration of manganese on the striatal cholinergic and dopaminergic receptors in the rat.

Previous studies suggest that chronic administration of manganese produces symptoms akin to Parkinson's disease, which is believed to be due to derangement in the central cholinergic and dopaminergic system. In the present study the effect of repeated administration of manganese chloride to male Sprague-Dawley rats on the binding of [3H]spiroperidol and [3H]quinuclidinyl benzilate to striatal dopaminergic and cholinergic receptors, respectively, was determined. Daily intraperitoneal injections of manganese chloride (15 mg/kg) for 15 days followed by a 24 h drug-free period did not alter the receptor density (Bmax) or the apparent dissociation constant (Kd) of either [3H]spiroperidol or [3H]quinuclidinyl benzilate to the rat striatal membranes. It is concluded that chronic treatment with manganese does not change the plasticity of post-synaptic dopaminergic or cholinergic receptors in the rat striatum.

Animals↗

PubMed1990

Effect of almond and anis oils on mouse liver alcohol dehydrogenase, aldehyde dehydrogenase and heart lactate dehydrogenase isoenzymes.

The effects of short-term intraperitoneal injection of diluted almond or anis oil on heart lactate dehydrogenase isoenzymes, liver alcohol dehydrogenase and subcellular aldehyde dehydrogenase were studied in the female mouse. Hepatic alcohol dehydrogenase was induced from control by administration of almond oil 3.2 g/kg/d for 7 days, or anis oil 1.6 g/kg/d for 7 days. Treatment with almond but not anis oil inhibited both cytoplasmic and mitochondrial liver aldehyde dehydrogenase. The mitochondrial isoenzyme with an apparently low Km was also inhibited by the almond oil trial. No significant changes occurred in heart lactate dehydrogenase isoenzymes by the treatments used. The enzymatic inhibition kinetics were found to be non-competitive. The apparent Km for almond-treated mouse aldehyde dehydrogenase was greater than the controls. This indicates lower substrate affinity for almond oil than for acetaldehyde. The results suggest adverse hepatic metabolic interaction between almond oil and alcohol.

Alcohol Dehydrogenase↗

PubMed1991

Mobilization of cadmium by liposome-encapsulated meso-2,3-dimercaptosuccinic acid in pre-exposed mice.

meso-2,3-Dimercaptosuccinic acid (DMSA) treatment in free of liposome-encapsulated form was given to mice pre-exposed to cadmium as CdCl2 (2 intraperitoneal injections; 0.5 mg Cd/kg along with 5 microCi 109CdCl2 in 4 ml volume within 24 h). Both treatments removed cadmium from liver, spleen, testis and blood with liposomal DMSA exhibiting higher efficacy in mobilizing cadmium not only from whole organs but also from liver proteins. It also resulted in higher excretion of cadmium via urine as compared with free DMSA or saline treatment. Whereas this treatment eliminated significantly higher amounts of cadmium via the fecal route throughout the period examined, free DMSA responded only 48 h after treatment and was less effective. The results suggest mobilization of cadmium from intracellular sites of deposition. However, DMSA in the dose administered (24 mumol/kg i.v.) in either form was ineffective in decorporating cadmium from the kidney, the critical organ in cadmium intoxication.

Animals↗