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Biomedical subjects

T L Ripley

Publications and source records attributed to T L Ripley.

7 recordsLinked to original sources
PubMed1995

Nitrendipine prevents the decrease caused by chronic ethanol intake in the maintenance of tetanic long-term potentiation.

Prolonged ethanol consumption has previously been reported to decrease long-term potentiation (LTP) in isolated hippocampal slices. Dihydropyridine calcium channel antagonists, such as nitrendipine, have been previously found to prevent some of the adaptive responses to chronic ethanol intake. The present study investigated the effects of concurrent in vivo administration of nitrendipine and ethanol on LTP in isolated mouse hippocampal slices. LTP was produced by either one or two tetanic stimuli or by increased calcium. When one tetanus was used, although the potentiation of the population spike height was less after the ethanol treatment, the difference was not quite significant. However, the potentiation after in vivo administration of ethanol plus nitrendipine was significantly greater than after ethanol alone. When two tetanic stimuli were applied, the maintenance of the potentiation of the population spike height was significantly decreased by the chronic ethanol treatment. This decrease was not seen when nitrendipine was given with the ethanol. When LTP was produced by a transient increase in the calcium concentration in the bathing medium, the chronic ethanol treatment did not alter the potentiation of the population spike height, but in vivo treatment with ethanol plus nitrendipine decreased the potentiation.

Alcohol Drinking↗
PubMed1995

Effects on ethanol withdrawal hyperexcitability of chronic treatment with a competitive N-methyl-D-aspartate receptor antagonist.

The effects of the competitive N-methyl-D-aspartate receptor antagonist DL-(E)-2-amino-4-methyl-5-phosphonopentanoate carboxy-ethylester (CGP39551) on the hyperexcitability produced by withdrawal from chronic ethanol treatment were studied in mice, to which CGP39551 was given chronically with the ethanol. When an interval of 72 or 96 hr was left between the last of the repeated CGP39551 injections and withdrawal from ethanol, the severity of the ethanol withdrawal syndrome was increased. When shorter time intervals were left between the end of the CGP39551 treatment and the ethanol withdrawal, the chronic CGP39551 treatment protected against the withdrawal hyperexcitability. When a single low dose of CGP39551 was given immediately after ethanol withdrawal, the compound protected against the withdrawal hyperexcitability. It is therefore suggested that the protective effects of concurrent chronic treatment with CGP39551, seen when the shorter intervals were allowed, were caused by residual compound. The increased severity of withdrawal, when sufficient time was left for washout of CGP39551, suggests that chronic administration of CGP39551 increased the adaptive changes that cause or contribute to ethanol withdrawal hyperexcitability. The results differ from the previously reported effects of N-methyl-D-aspartate antagonists on ethanol tolerance, because this was reduced by concurrent chronic treatment. They are also in contrast with the effects of chronic dihydropyridine calcium channel antagonists, which decreased both the development of tolerance and the ethanol withdrawal syndrome, when given chronically, concurrently with the ethanol. Cessation of prolonged ethanol intake results in a period of neuronal hyperexcitability, described as the withdrawal or abstinence syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1992

Evidence that changes in hippocampal excitability in vitro are caused by withdrawal from chronic in vivo ethanol administration.

A complex pattern of changes in the field potentials recorded from mouse hippocampal slices, prepared after chronic ethanol treatment in vivo, has previously been demonstrated in this laboratory. In the present study, recordings from slices prepared immediately after 2 weeks of ethanol treatment, showed only an increase in paired pulse potentiation, compared with controls, whereas recordings made immediately after 16 weeks of ethanol administration showed decreases in the thresholds for single and multiple population spikes, increases in paired pulse potentiation and epileptiform activity. In hippocampal slices prepared after 24 hr withdrawal, following 16 weeks of ethanol treatment, there were no signs of hyperexcitability in the field potentials. Ratings of convulsive behaviour were increased in mice during a 12-hr period after withdrawal from 16 weeks of ethanol treatment. Corresponding behaviour ratings for the mice given ethanol for 2 weeks, or those withdrawn for 24 hr after 16 weeks ethanol treatment, were not significantly different from control values. It was concluded that epileptiform activity seen in hippocampal slices after prolonged ethanol administration may contribute to the ethanol withdrawal hyperexcitability seen in vivo.

Alcohol Withdrawal Delirium↗
PubMed1991

Anticonvulsant activity of the imidazoline 6,7-benzoidazoxan.

The effects of the imidazoline 6,7-benzoidazoxan on seizure threshold were assessed using standard tests of anticonvulsant activity. Benzoidazoxan (10-30 mg/kg i.p.; 100 mg/kg p.o.) prevented tonic, but not clonic, convulsions induced by electroshock in mice. The increase in seizure threshold was of rapid onset, and, although of short duration, was comparable with that obtained using phenytoin and sodium valproate. Moreover, unlike sodium valproate, benzoidazoxan was an efficacious anticonvulsant at doses (20, 30 mg/kg i.p.) which did not impair rotarod performance. The anticonvulsant effects of benzoidazoxan were confirmed using the maximal electroshock test in mice (median effective dose, 13.2 mg/kg i.p.) and rats (anticonvulsant at 30 mg/kg i.p.). In addition, benzoidazoxan (10, 30 mg/kg i.p.) prevented tonic, but not clonic, seizures induced by bicuculline in mice. Thus, the imidazoline benzoidazoxan was found to be a novel anticonvulsant agent against electrically and chemically induced seizures in mice and rats with a profile of action similar to that of phenytoin.

Animals↗
PubMed1989

Exploring delta-receptor function using the selective opioid antagonist naltrindole.

Until recently the only pharmacological probes for delta-receptors have been peptide enkephalin analogues. These suffer from a number of limitations including high cost, partial agonist effects and a propensity for neurotoxicity. A stable non-peptide antagonist, naltrindole, has recently become available. We have explored its intrinsic actions and found that it attenuated swim stress-induced antinociception, a model for endogenous delta-receptor activation. Naltrindole may therefore be a useful alternative to presently available delta-receptor antagonists.

Animals↗
PubMed1989

Self-induced water intoxication and alcohol abuse.

According to Feighner criteria, alcohol abuse was significantly more common among 17 schizophrenic male inpatients with self-induced water intoxication than among 17 matched schizophrenic control inpatients. The alcohol abuse had begun 8-22 years before the diagnosis of water intoxication.

Adult↗