Biomedical subjects

S S Al-Zahrani

Publications and source records attributed to S S Al-Zahrani.

4 recordsLinked to original sources

PubMed1999

Effect of central 5-hydroxytryptamine depletion on tolerance of delay of reinforcement: evidence from performance in a discrete-trials "time-left" procedure.

This experiment examined the effect of destruction of the ascending 5-hydroxytryptaminergic (5HTergic) pathways on performance on a new discrete-trials version of the "time-left" procedure. Rats received either injections of 5,7-dihydroxytryptamine into the dorsal and median raphe nuclei or sham lesions. They were trained in a discrete trials schedule in which reinforcers were provided for responding on either of two levers, A and B. At a random time point, t s after the start of each trial, the two levers were inserted into the operant chamber: a response on A resulted in the delivery of one food pellet after dA s, whereas a response on B resulted in the delivery of two pellets after 84-t s. The value of dA was varied between 1 and 12 s in different phases of the experiment. Both groups showed an increasing tendency to respond on lever B as a function of time within the trial. Logistic functions were fitted to the data from each group, and a value of the "indifference point" (T50: the time within the trial at which proportional choice of B attained a value of 50%) was derived for each rat. For each value of dA, the values of T50 were significantly greater in the lesioned rats than in the control rats, reflecting a rightward shift of the logistic function in the lesioned group. The levels of 5HT and 5-hydroxyindoleacetic acid were reduced in the brains of the lesioned rats, but the levels of noradrenaline and dopamine were not significantly altered. The results provide further evidence for the involvement of the ascending 5HTergic pathways in the control of operant behaviour by delayed positive reinforcers.

5,7-Dihydroxytryptamine↗

PubMed1998

Effect of destruction of noradrenergic neurones with DSP4 on performance on a free-operant timing schedule.

This experiment examined the effect of destroying central noradrenergic neurones, using the selective neurotoxin DSP4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine], on performance in a free-operant timing schedule. Rats received either systemic treatment with DSP4 or vehicle-alone injections. They were trained to press levers for a sucrose reinforcer. Training sessions consisted of 40, 50-s trials in which reinforcers were available on a variable-interval 25-s schedule; in the first 25 s of each trial, reinforcers were only available for responses on lever A, whereas in the last 25 s reinforcers were available only for responses on lever B. Data were collected from probe trials (four per session), in which no reinforcers were delivered, during the last ten of 60 training sessions. Both groups showed decreasing response rates on lever A, and increasing response rates on lever B, as a function of time from the onset of the trial. Quantitative indices of timing behaviour were derived from a two-parameter logistic function fitted to the relative response rates on lever B (response rate on lever B, expressed as a percentage of overall response rate); this function accounted for > 90% of the data variance in each group. The DSP4-treated group showed a significantly lower value of the indifference point (i.e. the time corresponding to 50% responding on lever B) than the control group. The slope of the function and the rate of switching between response alternatives did not differ significantly between the two groups. The concentrations of noradrenaline were markedly reduced in the neocortex and hippocampus of the DSP4-treated group, but the concentrations of dopamine, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid were not significantly altered. It is suggested that results may be consistent with a role of the dorsal ascending noradrenergic pathway in behavioural "arousal".

Animals↗

PubMed1998

5-hydroxytryptamine and impulse control: prospects for a behavioural analysis.

Impulsiveness is a significant clinical problem associated with a variety of psychiatric and neuropsychiatric disorders. Clinical and experimental studies have provided evidence that individuals displaying impulsive behaviour tend to show signs of deficient functioning of the ascending 5-hydroxytryptaminergic (5-HTergic) pathways of the brain. A persistent problem in investigations of the biological basis of impulsive behaviour has been the lack of a satisfactory definition of 'impulsiveness', as distinct from other behavioural features, such as aggression, which are often apparent in 'impulsive' individuals. Research in the experimental analysis of behaviour suggests that two important characteristics of 'impulsiveness' are (i) deficient tolerance of delay of gratification and (ii) inability to inhibit or delay voluntary behaviour; both of these characteristics are amenable to study in laboratory animals. We describe some delayed reinforcement and delayed response paradigms which purport to capture these behavioural characteristics, and review recent evidence that manipulation of 5-HTergic function alters behaviour in these paradigms. It is argued that the two characteristics of 'impulsiveness' are themselves the product of disturbance of more fundamental behavioural processes; the nature of these processes is considered.

Animals↗

PubMed1996

Effect of destruction of the 5-hydroxytryptaminergic pathways on the acquisition of temporal discrimination and memory for duration in a delayed conditional discrimination task.

This experiment examined the effect of destruction of the ascending 5-hydroxytryptaminergic (5HTergic) pathways on the acquisition of a temporal discrimination and on memory for duration, using a delayed conditional discrimination task. In phase I, rats that had received injections of 5,7-dihydroxytryptamine into the dorsal and median raphe nuclei, and sham-lesioned control rats, were trained in a series of discrete trials to press lever A following a 2-s presentation of a light stimulus, and lever B following an 8-s presentation of the same stimulus. Following stimulus offset, a response on a panel placed midway between the two levers was required in order to initiate lever presentation; a single response on either lever resulted in withdrawal of both levers and, in the case of a "correct" response, reinforcer delivery. Both groups gradually acquired accurate discrimination, achieving > 90% correct choices within 20-30 sessions; the lesioned group acquired accurate performance significantly faster than the control group. In phase II, delays were interposed between stimulus offset and lever presentation in 50% of the trials (2, 4, 8, 16 and 32 s; 10% of trials in each case). Accuracy declined as a function of post-stimulus delay in both groups, and there was no significant difference between the performances of the two groups. Both groups showed an increasing tendency to respond on lever A following longer post-stimulus delays ("choose-short" effect); this effect was somewhat enhanced in the lesioned group. The levels of 5HT and 5-hydroxyindoleacetic acid were reduced in the brains of the lesioned rats, but the levels of noradrenaline and dopamine were not altered.

Animals↗