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• W2018131502 endingPage "118" @default.
• W2018131502 startingPage "71" @default.
• W2018131502 abstract "The hypothalamus is a critical area for brain-stimulation reward in that it contains self-stimulation sites, lesions in or caudal to it can attenuate self-stimulation, fibres from many self-stimulation sites course to or close to it, and single neurones in the hypothalamus fire during self-stimulation of many different sites. Some hypothalamic neurones which are activated by specific natural rewards, e.g. water for a thirsty animal or the sight of a banana for a hungry animal, are also activated by brain-stimulation reward. It is suggested that brain stimulation can provide reward because it activates neurones of this general type—neurones fired by specific natural rewards. The effects of natural stimuli and of brain stimulation on some specific natural reward neurones can probably be gated in that food or brain-stimulation at one site may only provide reward if the animal is hungry, and water or brain-stimulation at another site may only provide reward if the animal is thirsty. The amygdala can modulate brain-stimulation reward. Neurones in the amygdala project to the lateral hypothalamus and are activated in self-stimulation of the lateral hypothalamus and of some other reward sites. The amygdala modulates ingestion on the asis of previous experience in that rats with lesions in the basolateral amygdala do not avoid new foods and show deficits in learning to reduce the intake of a particular food which has been associated in the past with sickness. (On this type of and on electrophysiological evidence, parts of the amygdala may be involved in the formation of stimulus-reinforcement associations in general.) The amygdala can modulate lateral hypothalamic self-stimulation in a way which may be comparable with its influence on food intake. The modulation can be demonstrated by local anaesthesia of the amygdala, which attenuates the self-stimulation. The amygdala does not appear to be essential for self-stimulation in that self-stimulation can still occur after bilateral removal of the amygdala. The prefrontal cortex is closely related to brain-stimulation reward in that in the rat and monkey self-stimulation of it can be obtained, and electrophysiological and fibre degeneration experiments show that it is closely connected with many different self-stimulation sites. In the rat anaesthesia of the sulcal prefrontal cortex attenuates self-stimulation, but the pre-frontal cortex is not essential for self-stimulation, which can occur even when much of the forebrain is ablated. It has been suggested that in the monkey the orbitofrontal cortex is involved in the disconnection of stimulus-reinforcements associations. As in the case of the amygdala, the prefrontal cortex may modulate reward, but in relation not to the formation but to the disconnection of stimulus-reinforcement associations. Through neurones in the midbrain and pons arousal is produced by hypothalamic self-stimulation. Activation of this arousal system at least partly mediates stimulus-bound locomotor activity in that the arousal and activity show a similar post-stimulation decay, are produced through directly excited neurones with the same absolute refractory period, and are not produced by rewarding stimulation of the nucleus accumbens. There is some similar evidence that activation of this arousal system partly mediates the priming effect in self-stimulation, although other factors such as incentive motivation may also contribute to the priming effect. Activation of this arousal system is not essential for reward in that the arousal system is not activated in self-stimulation of the nucleus accumbens. Although neurones in most areas of the brain are not activated as described above in self-stimulation, some activation of neurones in the hippocampus, cingulate cortex, reticular nucleus of the thalamus, and the medulla and caudal pons by brain-stimulation reward has so far been found. The function of activation of these neurones in self-stimulation is not yet known. There is considerable evidence that central catecholamines are involved in intracranial self-stimulation. Much of the evidence which has been cited to show that the release of the particular cateeholamine noradrenaline mediates brain-stimulation reward is weak in two respects. Firstly, many of the treatments which decrease self-stimulation rate (e.g. α-methyl-p-rosine, chlorpromazine, haloperidol) or increase self-stimulation rate (e.g. amphetamine) affect dopamine as well as noradrenaline. Secondly, most of the treatments affect arousal, and it has not been shown, for example, that sedation does not account for the attenuation of self-stimulation produced by agents which decrease the synthesis of noradrenaline. Thus the evidence available at present does not provide support for the view that the release of noradrenaline mediates brain-stimulation reward. Dopamine-receptor blockade attenuates self-stimulation of many different brain sites without producing major sedation. Whether this represents a true block of reward or is a result of interference with high-level motor behaviour is not yet clear. The main sections of this account of the neural basis of brain-stimulation reward are summarized in sections 1.2.1, 1.2.2, 2.6, 3.7, 4.8, and 5.7." @default.
• W2018131502 created "2016-06-24" @default.
• W2018131502 creator A5029186968 @default.
• W2018131502 date "1974-01-01" @default.
• W2018131502 modified "2023-09-26" @default.
• W2018131502 title "The neural basis of brain-stimulation reward" @default.
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