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S T Mason

Publications and source records attributed to S T Mason.

72 records · Page 4Linked to original sources
PubMed1978

Reward, attention and the dorsal noradrenergic bundle.

The resistance to extinction seen after lesion to the dorsal noradrenergic bundle has been suggested to arise from a deficit in internal inhibition or a 'perseverative' type of deficit. This hypothesis is tested by examining the ability of 6-hydroxydopamine-treated animals to inhibit a previously developed preference for saccharine solution as a result of poisoning with lithium chloride. Unimpaired taste aversion is found, arguing against a deficit in the ability to inhibit a prepotent response. An alternative explanation of the dorsal bundle extinction effect (DBEE), that of alterations in attention, is tested by acquisition and reversal of a successive light-dark discrimination. Both acquisition and reversal are severely impaired, suggesting that the treated animals have difficulty in attending to a specific stimulus in the environment when this is required in order to structure behaviour appropriately, and thus being consistent with a role for the dorsal bundle in the control of attentional processes.

Adrenergic Fibers↗
PubMed1978

Parameters of the dorsal bundle extinction effect: previous extinction experience.

Lesion to the dorsal noradrenergic bundle using the selective neurotoxin 6-hydroxydopamine which depleted telencephalic noradrenaline to less than 5% of control values was found to cause prolonged responding in extinction of a continuously reinforced (CRF) operant lever pressing response (a further replication of the dorsal bundle extinction effect). The parameters involved in causing this effect). The parameters involved in causing this effect were investigated, particularly the role of previous extinction experience. Although resistance to extinction was seen the first time animals were placed in extinction, it disappeared when they were retrained on CRF and extinguished a second time. Experience of extinction as part of the acquisition process, brought about by training on a successive visual discrimination, also prevented the development of over-responding in subsequent extinction. These results are discussed in the context of related demonstrations of the absence of the dorsal bundle extinction effect after partially reinforced acquistion training.

Animals↗
PubMed1978

Noradrenaline and partial reinforcement in rats.

Lesions of the dorsal nonadrenergic bundle produced by 6-hydroxydopamine, which depleted telencephalic noradrenaline by over 95%, were found to produce resistance to extinction in animals trained on a continuously reinforced schedule for food reward but not to alter the extinction rate after partial reinforcement training. These results confirm the dorsal bundle extinction effect reported previously but suggest that it is confined to continuously reinforced situations. The pattern of results is consistent with a role for the dorsal bundle in attentional processes but appears to contradict the predictions required if the dorsal bundle were to have a role in frustrative nonreward.

Animals↗
PubMed1978

The effects of dorsal bundle injections of 6-hydroxydopamine on avoidance responding in rats.

1 The effect of injection of 6-hydroxydopamine (6-OHDA) into the fibres of the dorsal noradrenergic bundle on acquisition, retention and extinction of active avoidance in rats were examined. 2 6-OHDA injections severely depleted noradrenaline in all forebrain areas assayed, with the interesting exception of the septum. No significant effect on dopamine concentrations in various forebrain regions was found. 3 Acquisition and retention of active avoidance was not altered by the lesion. Marked resistance to extinction was seen when the unconditioned stimulus (shock) was removed. 4 A comparison with work by other authors in which both forebrain noradrenaline and dopamine were depleted suggest that the alteration in extinction seen in both studies is a noradrenergic effect, whereas the deficits in acquisition and retention found previously are dopaminergic in origin.

Animals↗
PubMed1977

Behavioural basis of the dorsal bundle extinction effect.

Lesion to the fibres of the dorsal noradrenergic bundle arising from the locus coeruleus using the selective neurotoxin 6-hydroxydopamine has been shown to produce a resistance to extinction on a number of behavioural tests without affecting the acquisition learning process itself. The experiments reported here are aimed at elucidating the behavioural mechanisms involved in this resistance to extinction. Theories invoking general hyperactivity, internal inhibition and perseveration are tested in the following experiments and all are shown to be contrary to the observed facts. On the basis of other data it is tentatively concluded that the dorsal noradrenergic bundle may play a role in the filtering out of irrelevant stimuli or in the memory of non-reward.

Animals↗
PubMed1977

Effects of selective forebrain noradrenaline loss on behavioral inhibition in the rat.

Virtually total depletion of cortical and hippocampal noradrenaline by stereotaxic injection of 6-hydroxydopamine into the fibers of the dorsal noradrenergic bundle produced no impairment in acquisition learning of a runway response for food reward. Extinction of this response, once learned, was markedly slower in the treated group than in controls, the treated animals perseverating in rapid running to the goal box even with no food present there. Similarly, no impairment was found on acquisition of a continuously reinforced lever-pressing response for food. Extinction of this response, however, was again slower in the treated group. Subsequent acquisition of a successive light-dark discrimination task was also slower in the treated group, with these animals perseverating in responding to the negative stimulus. Although selective forebrain noradrenaline loss does not impair the acquisition of appetitive responses, the suppression of responses in the absence of reward is impeded. A parallel is drawn with those effects found classically after surgical lesion to the hippocampus.

Animals↗