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L D Calder

Publications and source records attributed to L D Calder.

28 records · Page 2Linked to original sources
PubMed1989

Blockade of "reverse tolerance" to cocaine and amphetamine by MK-801.

"Reverse tolerance" was produced in rats and mice by repeated exposure to either cocaine or amphetamine. The locomotorstimulant effect was studied in mice; stereotypy and convulsions in rats. MK-801, the NMDA antagonist, blocked the development of "reverse tolerance" to all three effects. In contrast, haloperidol selectively blocked "reverse tolerance" to cocaine-induced stereotypy but not to convulsions. The data suggest that the glutamate system participates in the mechanism of "reverse tolerance" to the dopaminergic effects of cocaine and amphetamine, as well as to the convulsant effect of cocaine.

Amphetamine↗
PubMed1989

Pentylenetetrazol kindling in mice.

Kindling with pentylenetetrazol to produce minimal and maximal convulsions was investigated in CF-1 mice. Like electrical kindling, the kindling effect was directly proportional to the dose or the intensity of the kindling stimulus. Similarly, the kindling effect was persistent, as was emphasized by the ability to kindle with an interdose interval of 3 days and by the convulsions produced by a challenge with pentylenetetrazol 30 days after withdrawal from the kindling treatment. The changes in excitability, associated with the kindling state, appeared to be relatively selective for pentylenetetrazol, because no changes in thresholds to either electroshock or administration of picrotoxin or N-methyl-DL-aspartate correlated temporally with the persistence of kindling. The influence of two anticonvulsant drugs, ethosuximide and cannabidiol, on kindling was also investigated. Both drugs blocked the development of kindling to pentylenetetrazol-induced minimal convulsions. Of these drugs, only ethosuximide raised the minimal convulsive threshold to pentylenetetrazol. Against pentylenetetrazol-induced kindling to maximal convulsions, only cannabidiol blocked kindling and only cannabidiol raised the maximal seizure threshold for pentylenetetrazol. Although the drugs modified the kindling effect, the mechanism of the interaction is not clear.

Animals↗
PubMed1986

Prolonged CNS hyperexcitability in mice after a single exposure to delta-9-tetrahydrocannabinol.

A single exposure to delta-9-tetrahydrocannabinol (THC) resulted in a "rebound" hyperexcitability in the CNS in mice, which was assessed in terms of the susceptibility of the CNS to electrically-induced convulsions. The magnitude of the hyperexcitability was dose-related (25-150 mg/kg, i.p.), as measured 24 hr after treatment. The time-course study of the effect indicated a peak-effect at 24 hr after administration of the drug, with a duration of the effect for as long as 196 hr. The time course of the rebound hyperexcitability to THC was compared to that for phenobarbital, which peaked at 48 hr after administration of the drug and returned to the control value by 96 hr. Tolerance developed rapidly to the motor-toxic effect of THC, but after 23 days of daily treatment there was no evidence of tolerance to the rebound hyperexcitability. The functional significance of the hyperexcitable state was assessed in two tests; electrical kindling to minimal convulsions was enhanced, even when the kindling procedure was initiated 120 hr after exposure to the drug; and the anticonvulsant activity of phenytoin was blocked when mice were treated with the anticonvulsant 96 hr after a single exposure to THC. The results suggest that the rebound response from a single exposure to THC represents a functionally significant prolonged increase in excitability of the CNS.

Animals↗
PubMed1984

Interaction between delta-9-tetrahydrocannabinol and kindling by electrical and chemical stimuli in mice.

Mice were kindled to produce minimal convulsions by repeated application of either electrical or chemical stimuli. Electrical kindling involved the use of corneal electrodes; chemical kindling involved the use of pentylenetetrazol or picrotoxin. Delta-9-tetrahydrocannabinol (delta-9-THC) appeared to be capable of enhancing kindling to all three stimuli. In the studies with electroshock and pentylenetetrazol, in contrast to those with picrotoxin, a single exposure to delta-9-THC sufficed to facilitate the subsequent kindling, and the enhancement of kindling persisted after withdrawal of the cannabinoid. In the case of electrical kindling, the cannabinoid may promote the phenomenon by decreasing the convulsion threshold. Because the threshold was not lowered to all kindling stimuli, however, other mechanisms must be involved. In general, the data indicate that even a single dose of delta-9-THC can promote the development of long-lasting elevations of CNS excitability.

Animals↗
PubMed1984

Naloxone-induced augmentation of the photically evoked afterdischarge in conscious rats.

Naloxone, at subconvulsive dose levels, from 1 to 15 mg/kg were administered to conscious rats. Significant increases in photically evoked afterdischarge occurrence were seen at naloxone dose levels above 5 mg/kg with no clinical evidence of seizure activity being observed. Typically photically evoked afterdischarge augmentation is only observed following the administration of convulsive drugs.

Animals↗
PubMed1983

Posttrial electrical stimulation of the dorsal hippocampus facilitates acquisition of the nictitating membrane response.

Rabbits with electrodes implanted in the dorsal hippocampus were trained on the acquisition of the nictitating membrane response. Posttrial application of subseizure-level electrical stimulation within a single session resulted in a facilitation of nictitating membrane response conditioning. In contrast, seizure-level stimulation within a single session and subseizure-level stimulation in multiple sessions had no facilitatory or deleterious effects on conditioning. It is suggested that dorsal hippocampus stimulation facilitates conditioning by activation of midbrain and cerebellar circuits.

Animals↗
PubMed1982

Naloxone-induced epileptogenesis has brain-site specificity in rats.

Naloxone injected into the lateral septum caused intense electrocortical seizures which did not occur following callosal or periaqueductal gray (PAG) injections. Conversely, injections into periaqueductal gray caused a characteristic and pronounced backward circling with only moderate electrocortical changes. Intracerebral injection of naloxone had effects, including epileptogenesis, which appeared to be site-specific. These effects are in some ways similar to the effects of enkephalin and morphine.

Animals↗
PubMed1981

Phencyclidine and behavior: I. Sensory-motor function, activity level, taste aversion and water intake.

Phencyclidine (PCP) injections in rats at doses of 4 mg/kh increased activity level, which might have been a function of impaired habituation. At doses of 8 mg/kg PCP produced a marked reduction in activity level. At doses of 12 mg/kg and above there were profound disruptive effects in detection of odors, visual square and touch measures, and performance of placing reflexes requiring visuo-motor coordination, righting, grasping reflexes, and equilibrium. Decreases in water intake occurred only at higher dose levels of PCP (16 and 24 mg/kg). On a qualitative basis the changes observed in rats are similar to changes described for humans.

Animals↗