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R M Vardaris

Publications and source records attributed to R M Vardaris.

17 recordsLinked to original sources
PubMed1987

The modulation of long-term potentiation by delta-9-tetrahydrocannabinol in the rat hippocampus, in vitro.

The duration of long-term potentiation (LTP) of the CA1 evoked field potential in rat hippocampal slices was significantly modulated by pre-treatment of slices with delta-9-tetrahydrocannabinol (THC) added to the incubation media. The three THC doses tested: 10 picomolar (pM), 100 pM, and 1000 pM, resulted in a biphasic change in population spike amplitude, such that 10 pM resulted in an increase, while 100 and 1000 pM resulted in dose-related decreases as compared to the control treatment. Upon subsequent induction of LTP by tetanizing stimulation, the THC treatments resulted in significant changes in the duration but not magnitude of potentiation. The early component of potentiation, post-tetanic potentiation, or PTP, was not affected by the THC treatments. LTP was seen to decay in an exponential manner over the 121 mini post-tetanus monitoring period. For comparisons of LTP duration, therefore, the half-life (t1/2) of LTP was extrapolated from linear regression analysis. The t1/2 values were determined for each treatment group from the slopes of the linear regression analysis of the logarithmically transformed time course data. While the control group t1/2 was determined as 280 min, the t1/2 for the THC groups were: 350 min (10 pM); 91 min (100 pM); and 33 min (1000 pM) doses, respectively. In context with previous reports of the disruptive action of marihuana intoxication on learning and memory, these results suggest that one possible action of THC may be in modulating hippocampal electrophysiology and its role in short-term memory processes.

Animals↗
PubMed1984

Effects of corticosterone on the electrophysiology of hippocampal CA1 pyramidal cells in vitro.

Modulation of CA1 field potential amplitudes by normal and stress concentrations of corticosterone (CT) was observed in hippocampal slice preparations from adrenalectomized rats. Slices exposed to CT levels characteristic of a morning (4 nM) or evening (7 nM) resting state showed increased population spike amplitudes in the CA1 pyramidal cell field within 10 min. A stress concentration (15 nM) also increased spike amplitudes, but only at the higher stimulus intensities. The effects of these doses were essentially the same 10 and 60 min after administration. The hormone facilitated responding more in morning resting concentrations than in concentrations characteristic of the evening resting state. This occurred, however, only for relatively low intensity stimuli. The data provide some support for the suggestion that circadian fluctuations in magnitude of long-term potentiation result from corresponding changes in CT level. The rapid onset of the observed changes is difficult to account for in terms of generally accepted mechanisms of receptor binding.

Adrenalectomy↗
PubMed1982

Changes in hippocampal CA1 population spikes following administration of delta-9-THC.

The effects of delta-9-tetrahydrocannabinol (delta-9-THC) on monosynaptic population responses in hippocampal CA1 pyramidal cells were examined in acute rats for several doses and at several post injection time periods. Delta-9-THC enhanced paired pulse inhibition in a dose-dependent manner; however biphasic dose effects were observed on cell responses during low frequency potentiation and on population spikes elicited by a conditioning stimulus. The biphasic responses were such that 2--4 mg/kg THC (IP) excited while 16 mg/kg depressed the stimulus elicited CA1 response. For low doses of THC slight biphasic time effects were observed. Evidence presented suggests that some of THC's actions on hippocampus may be due to direct or indirect actions on GABA-mediated activity.

Analysis of Variance↗
PubMed1982

delta 9-THC and 17-beta-estradiol in hippocampus.

Electrophysiological field potentials recorded from in vitro hippocampal slice preparations show dose-dependent differences in response to 17-beta-estradiol (E2) and delta-9-tetrahydrocannabinol (THC) added to the incubation medium. Using a wide range of doses (1 pM-10 nM), it was found that mid-range concentrations of estradiol (100 pM) and THC (10 pM) tended to increase field potentials in CA1 of rodents. Higher dose levels of each agent were found to depress neuronal activity. In the context of prior findings, these results suggest that the two compounds share a common mechanism of action in the hippocampus.

Animals↗
PubMed1981

The origin of the hippocampal commissure in the rat.

The present study was designated to determine the origin of commissural axons in the hippocampus. One hippocampus of 94 rats was pressure injected with 40% horseradish peroxidase (Sigma VI), or with 2-4% wheat germ agglutinin HRP (E-Y Labs). Injections (0.001 to 0.1 microliter) were made through glass micropipettes with fitted plungers. Pipettes were positioned stereotaxically, and by electrophysiological monitoring through the injection syringe. An ipsilateral stimulating electrode activated CA3 and CA1 cells via Schaffer collaterals. Population potentials were monitored as the recording pipette was advanced from the cortical surface into the hippocampus. Wave forms of monosynaptically elicited field potentials provided an accurate indicator of its position. Following survival periods of 24 hours, the brains were processed according to the Mesulam method. Forty-micron sections were serially mounted and counterstained. Injection sites and filled cells were plotted manually on a standard set of coronal sections. Our results indicate that field CA1 receives input from contralateral subfields CA1a and c, as well as from all CA3 subfields. In addition, rostral CA1 injections resulted in labeling of cells in the contralateral subiculum and entorhinal cortex. Homotopic connections exist between subfields CA3a and b; it appears that a major input to CA3c is from the contralateral polymorph cells of the dentate hilus. Commissural input to the dentate granule cells appears to be the giant polymorph and CA3c cells of the contralateral dentate hilus. With respect to the question of homotopicity, our results suggest that commissural connections are predominantly homotopic in the mediolateral plane, although CA1 and CA3 injections also resulted in contralateral labeling of hippocampal cells caudal to the levels of injection.

Animals↗
PubMed1980

Gonadal steroids: effects on excitability of hippocampal pyramidal cells.

Electrophysiological field potentials from hippocampal slices of rat brain show sex-linked differences in response to 1 X 10(-10)M concentrations of estradiol and testosterone added to the incubation medium. Slices from male rats show increased excitability to estradiol and not to testosterone. Slices from female rats are not affected by estradiol, but slices from female rats in diestrus show increased excitability in response to testosterone whereas slices from females in proestrus show decreased excitability.

Action Potentials↗
PubMed1977

Competition of delta 9-tetrahydrocannabinol with estrogen in rat uterine estrogen receptor binding.

Direct competition experiments with delta 9 -tetrahydrocannibinol (delta 9-THC) and estradiol in binding assays with rat uterine cytosol estrogen receptors showed that delta 9-THC was a weak, but nevertheless significant, competitor for binding to cytoplasmic estrogen receptors. These data support, at the molecular level, the observations that delta 9-THC has a weak estrogenic activity (at least the ability to bind to estrogen receptors). Moreover, estrogen-like binding suggests that delta 9-THC, acting at the level of estrogen receptor, causes a primary estrogenic effect rather than an indirect or secondary phenomenon.

Animals↗
PubMed1976

Chronic administration of delta-9-tetrahydrocannabinol to pregnant rats: studies of pup behavior and placental transfer.

Tritiated delta-9-tetrahydrocannabinol was administered orally to female rats throughout pregnancy at a dose level of 2 mg/kg/day. Chemical analysis of rat pup tissues indicated an average drug level near 20 ng/gm was attained via placental transfer. Although there was no teratogenicity, the pups showed both transient and relatively permanent behavioral effects. A deficit in acquisition of a passive avoidance response at 21 days of age was observed. This effect was not apparent during retraining and testing at 90 days of age. Rats whose dams had received the drug forced control animals to back out of a push tube in 67% of the tests at 21 days of age and 94% of the tests at 90 days of age.

Aggression↗
PubMed1975

Technique for chronic electrode or cannula implantation in decorticate animals.

A surgical technique is described which enables chronic recording of electrophysiological activity and chemical or electrical stimulation in the decorticated animal. This procedure circumvents the problems of inadequate electrode/cannula patency and of the short-term debilitating consequences of cortical ablation. These features make it possible to analyze the relationships between neuroelectrophysiology, behavior and the central mechanisms underlying the restitution of function following brain damage. The procedure appears to be suitable for a wide range of mature laboratory animals and offers several advantages over the few techniques currently available.

Animals↗
PubMedDate not supplied

delta9-tetrahydrocannabinol and the hippocampus: effects on CA1 field potentials in rats.

The effects of delta9-tetrahydrocannabinol (THC) on ortho- and antidromically elicited CA1 field potentials were observed in locally anesthetized rats and in anesthetized with urethane. THC augmented amplitudes of population EPSP's as well as orthodromic and antidromic population spikes from pyramidal cells in locally anesthetized animals. Latencies to peak amplitude of these response were increased. Conditioning-test shock experiments revealed taht THC also depressed recurrent inhibition probably mediated by basket cells. In animals under urethane anesthesia THC enhanced test responses, but failed to augment population response to the conditioning stimulus. It was concluded that THC enhanced postsynaptic excitatory processes but attenuated recurrent inhibition. Urethane anesthesia completely blocked the postsynaptic excitatory effect of THC but had little apparent influence on THC's disinhibitory action.

Animals↗