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Biomedical subjects

J S MacDonall

Publications and source records attributed to J S MacDonall.

7 recordsLinked to original sources
PubMed2000

Synthesizing concurrent interval performances.

Concurrent schedules may be viewed as consisting of two pairs of stay and switch schedules, each pair associated with one of the alternatives. A stay schedule arranges reinforcers for staying and responding at one alternative, whereas the associated switch schedule arranges reinforcers for switching to the other alternative. In standard concurrent schedules, the stay schedule at each alternative is equivalent to the switch schedule at the other alternative. MacDonall (1999) exposed rats to one pair of stay and switch variable-ratio schedules and varied the response requirements across conditions. Combining results from symmetric pairs produced composite performances that were described by the generalized matching law. This outcome was noteworthy because the data were obtained from performances at two alternatives with contingencies that were functionally unrelated to each other. This result suggests that concurrent performances may consist of two unrelated performances that alternate as behavior moves between alternatives. The purpose of the present experiment was to extend those results to interval schedules. Rats were exposed to pairs of random-interval schedules, and across conditions their mean intervals were varied. When data from appropriately paired conditions were combined, the composite performances were consistent with the generalized matching law. In addition, the results supported two models of concurrent performances that were based on local variables at an alternative (behavior, and stay and switch reinforcers): a modified version of the contingency discrimination model (Davison & Jenkins, 1985) and the local model (MacDonall, 1999).

Animals↗
PubMed1997

Effects of nitric oxide synthase inhibitors on cocaine sensitization.

Behavioral sensitization to cocaine was tested for in rats pretreated with a nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME) or 7-nitro indazole (7-NI). A 5-day pre-exposure to once daily cocaine (15 mg/kg, i.p.) injections yielded sensitization to cocaine (15 mg/kg)-induced behavioral activation. Pretreatment injections of L-NAME (100 mg/kg) or 7-NI (30 mg/kg), administered 30 min before each cocaine pre-exposure injection, acutely inhibited cocaine-induced behavioral activation. No sensitization was found after L-NAME pretreatment in a protocol with a 3-day withdrawal between pre-exposure and test cocaine injections. With a 10-day withdrawal period, cocaine sensitization was prevented by L-NAME or 7-NI pretreatment. These results after a 10-day withdrawal are unlikely to arise from deficient brain NO synthase activity on the test day. Instead, these findings suggest a role for NO in mechanisms underlying the development of cocaine sensitization. We conclude that NO participates in both the development of sensitization as well as the expression of cocaine-induced behavior in previously drug-naive animals.

Analysis of Variance↗
PubMed1995

Antagonist of N-methyl-D-aspartate receptors partially prevent the development of cocaine sensitization.

Behavioral sensitization to cocaine was tested for in rats pretreated with MK-801, a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, or D-3-(2-carboxypiperazin-4-yl)-1-propenyl-1-phosphonic acid (D-CPPene), a competitive NMDA antagonist. A 5-day regimen of once-daily cocaine (15 mg/kg) injections yielded sensitization to cocaine (15 mg/kg)-induced behavioral activation. Cocaine sensitization was partially prevented by MK-801 (0.25 mg/kg) or D-CPPene (20 mg/kg) pretreatment. These results differ from previous reports that NMDA receptor antagonists completely prevented the development of stimulant sensitization. While raising questions about methodological differences among laboratories studying this issue, our findings suggest that sensitization may involve mechanisms dependent on NMDA-receptor function as well as NMDA receptor-independent mechanisms.

Animals↗
PubMed1994

GM1 ganglioside treatment of spontaneously hypertensive stroke prone rats.

Many reports indicate that GM1 ganglioside is effective in reducing CNS ischemic injury in animal models. These models employ invasive surgery to induce ischemic damage in otherwise healthy animals. The purpose of this study was to determine if the beneficial effects of GM1 could be generalized to Spontaneously Hypertensive Rats-Stroke Prone (SHRSP). The SHRSP strain develops a pathology similar to those observed in patients with stroke. The SHRSP have "risk" factors that include hypertension, fibrinoid necrosis, and sensitivity to diet. Female SHRSP were randomly assigned to GM1- or saline-treatment conditions. Rats were fed a stroke-inducing diet. Daily body weights, weekly blood pressure, time of stroke onset, and age at death were recorded. Spontaneous activity and performance on a tail-hang test were assessed thrice weekly. The results indicate that GM1 treatment did not delay the time of stroke onset or death. GM1 did reduce hyperactivity in the initial stages of the ischemic pathology, but did not prevent the marked decline in behavioral activity observed at later time points. There were no differences in weight loss, performance on the tail-hang test, or number of CNS injury-related symptoms observed. These findings suggest that GM1 was not as effective in decreasing mortality, weight loss, or behavioral deficits in SHRSP as previously reported using other animal models of ischemia. Distinguishing between those animal models in which GM1 is more and less effective may be useful in determining under which clinical situations GM1 is likely to be most suitable.

Aging↗
PubMed1990

GM1 ganglioside reduces cognitive dysfunction after focal cortical ischemia.

The functional consequences of cortical focal ischemia and the effect of monosialoganglioside (GM1) treatment on learning/performance of a spatial reversal task were investigated. Cortical focal ischemia was induced by a permanent occlusion of the left common carotid artery and the ipsilateral middle cerebral artery, with a 1-h clamping of the contralateral carotid artery. Twenty-six rats were randomly assigned to three groups: sham controls, a saline-treated ischemic group, and a GM1 ganglioside-treated ischemic group (10 mg/kg/day: IM). Fifteen days after surgery rats were trained on a spatial reversal task in a two-lever operant chamber where food reward was contingent on lever pressing. Training continued from day 15 to day 21 after surgery. Cortical focal ischemia resulted in learning/performance deficits that were reduced by GM1 ganglioside treatment. The cognitive deficits were characterized by a significantly higher number of nonperseverative errors and number of responses to criterion. There was a significant difference between left and right lever performance in the saline-treated ischemic group, which was absent in shams and GM1-treated ischemic rats. On all measures GM1-treated rats were not different from sham controls.

Animals↗
PubMed1984

Patterns of ethanol consumption as a function of the schedule of ethanol access.

The present experiment demonstrated that patterns of ethanol consumption can be controlled by altering the schedule of ethanol availability. Thirty-two male albino rats, maintained at 80% of their ad libitum weight, were first exposed to 10 base-line sessions in which access to either 8 or 32% ethanol was unrestricted. Each subject was then exposed to one of four restricted access schedules for 30 sessions. During each 23-hr session, the ethanol access period was held constant at 20 min while the time between ethanol access periods was either 70, 160, 340 or 700 min. After restricted access, all subjects were returned to unrestricted access for 10 sessions. Water was continually available throughout the experiment. When ethanol access periods occurred every 70 or 160 min, animals at both concentrations consumed more ethanol (grams per kilogram) than during the initial period of unrestricted access. When the time between ethanol access periods was 340 or 700 min, animals consumed an equal amount or half as much, respectively, as during unrestricted access. Analysis of responding revealed that the mean amount of ethanol consumed per bout was greater during restricted than during unrestricted access. The longer the time between access periods the greater the amount consumed per bout. Upon return to unrestricted access, total daily consumption increased, but the amount consumed per bout decreased to base-line levels.

Alcohol Drinking↗