The lateral hypothalamic area revisited: Ingestive behavior

Bernardis, Lee L.; Bellinger, Larry L.

doi:10.1016/0149-7634(95)00015-1

Cited by 369 publications

(202 citation statements)

References 771 publications

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“…In the cockroach-hunting model, this region was also activated; however, its activity was not specific to hunting as the effects of feeding (the control treatment in this model) were similarly strong [28]. Indeed, the lateral hypothalamus is crucially involved in feeding [38]; hence, one can assume that the effects of cockroach killing 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 were masked by the effects of food intake. Interestingly, the lateral hypothalamus was also overactivated in the glucocorticoid dysfunction model of abnormal aggression, the subjects of which deliver bites to highly vulnerable targets of their opponents (head, throat and belly) on the background of diminished social signaling of attacks by threats, which make their behavior similar to that seen during predation [22].…”

Section: Comparisons With Earlier Findingsmentioning

confidence: 82%

Neural mechanisms of predatory aggression in rats—Implications for abnormal intraspecific aggression

Tulogdi

Biró

Barsvári

et al. 2015

Behavioural Brain Research

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Our recent studies showed that brain areas that are activated in a model of escalated aggression overlap with those that promote predatory aggression in cats. This finding raised the interesting possibility that the brain mechanisms that control certain types of abnormal aggression include those involved in predation. However, the mechanisms of predatory aggression are poorly known in rats, a species that is in many respects different from cats. To get more insights into such mechanisms, here we studied the brain activation patterns associated with spontaneous muricide in rats. Subjects not exposed to mice, and those which did not show muricide were used as controls. We found that muricide increased the activation of the central and basolateral amygdala, and lateral hypothalamus as compared to both controls; in addition, a ventral shift in periaqueductal gray activation was observed.Interestingly, these are the brain regions from where predatory aggression can be elicited, or enhanced by electrical stimulation in cats. The analysis of more than 10 other brain regions showed that brain areas that inhibited (or were neutral to) cat predatory aggression were not affected by muricide. Brain activation patterns partly overlapped with those seen earlier in the cockroach hunting model of rat predatory aggression, and were highly similar with those observed in the glucocorticoid dysfunction model of escalated aggression. These findings show that the brain mechanisms underlying predation are evolutionarily conservative, and indirectly support our earlier assumption regarding the involvement of predation-related brain mechanisms in certain forms of escalated social aggression in rats.

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Section: Comparisons With Earlier Findingsmentioning

confidence: 82%

Neural mechanisms of predatory aggression in rats—Implications for abnormal intraspecific aggression

Tulogdi

Biró

Barsvári

et al. 2015

Behavioural Brain Research

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“…AMYG lesions impair US tasks (Gaffan, 1994), CS tasks (Kantak et al, 2001;Cardinal et al, 2002), and FSS tasks (Murray et al, 1996;Malkova et al, 1997). LH lesions impair US tasks Bernardis and Bellinger, 1996;Touzani and Sclafani, 2002). Orbitofrontal cortex (MORB and ORB) lesions impair US tasks (Baylis and Gaffan, 1991), SVD tasks (Easton and Gaffan, 2000) and FSS tasks (Baxter et al, 2000;Cardinal et al, 2002).…”

Section: Neurobiological Basis Of the Modelmentioning

confidence: 99%

Dopaminergic and non-dopaminergic value systems in conditioning and outcome-specific revaluation

2008

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“…Recently, the ventromedial hypothalamic nucleus has been identified as a key target for leptin, which acts on the hypothalamus to inhibit feeding, stimulate energy expenditure and cause weight loss (Satoh et al 1997); the dorsomedial hypothalamic nucleus (DMH), which has extensive connections with other medial hypothalamic nuclei and the lateral hypothalamus, and is thought to serve an integrative role in processing information from neuronal populations in these sites ; the vaguely-defined lateral hypothalamic area (LHA) which has a lower density of cell bodies than the obvious nuclei but includes neurones expressing MCH and the orexins. It also contains numerous fibre systems projecting to and from the medial hypothalamus, brainstem structures that are concerned with various visceral functions and with relaying taste and gastric distension (nucleus of the solitary tract and parabrachial nucleus), and the locus coeruleus, concerned with arousal and the sleep-wake cycle (Bernardis & Bellinger, 1996). The LHA was the classical 'feeding' centre; interestingly, as well as encompassing neurones and terminals containing orexigenic peptides, it also contains glucose-sensitive neurones that are stimulated by hypoglycaemia (mainly indirectly, by pathways ascending from the brainstem), and it is crucial in mediating the marked hyperphagia which is normally induced by hypoglycaemia (Bernardis & Bellinger, 1996).…”

Section: Basic Anatomy Of the Hypothalamusmentioning

confidence: 99%

“…It also contains numerous fibre systems projecting to and from the medial hypothalamus, brainstem structures that are concerned with various visceral functions and with relaying taste and gastric distension (nucleus of the solitary tract and parabrachial nucleus), and the locus coeruleus, concerned with arousal and the sleep-wake cycle (Bernardis & Bellinger, 1996). The LHA was the classical 'feeding' centre; interestingly, as well as encompassing neurones and terminals containing orexigenic peptides, it also contains glucose-sensitive neurones that are stimulated by hypoglycaemia (mainly indirectly, by pathways ascending from the brainstem), and it is crucial in mediating the marked hyperphagia which is normally induced by hypoglycaemia (Bernardis & Bellinger, 1996). The perifornical part of the LHA, surrounding the longitudinal fibre bundle of the fornix, contains a high density of NPY receptors, notably the 'Y5' type thought to be the NPY 'feeding' receptor, and like the adjacent PVN, is highly sensitive to the hyperphagic effect of locally-injected NPY.…”

Section: Basic Anatomy Of the Hypothalamusmentioning

confidence: 99%

The hypothalamus and the regulation of energy homeostasis: lifting the lid on a black box

2000

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The hypothalamus is the focus of many peripheral signals and neural pathways that control energy homeostasis and body weight. Emphasis has moved away from anatomical concepts of ‘feeding’ and ‘satiety’ centres to the specific neurotransmitters that modulate feeding behaviour and energy expenditure. We have chosen three examples to illustrate the physiological roles of hypothalamic neurotransmitters and their potential as targets for the development of new drugs to treat obesity and other nutritional disorders. Neuropeptide Y (NPY) is expressed by neurones of the hypothalamic arcuate nucleus (ARC) that project to important appetite-regulating nuclei, including the paraventricular nucleus (PVN). NPY injected into the PVN is the most potent central appetite stimulant known, and also inhibits thermogenesis; repeated administration rapidly induces obesity. The ARC NPY neurones are stimulated by starvation, probably mediated by falls in circulating leptin and insulin (which both inhibit these neurones), and contribute to the increased hunger in this and other conditions of energy deficit. They therefore act homeostatically to correct negative energy balance. ARC NPY neurones also mediate hyperphagia and obesity in the ob/ob and db/db mice and fa/fa rat, in which leptin inhibition is lost through mutations affecting leptin or its receptor. Antagonists of the Y5 receptor (currently thought to be the NPY ‘feeding’ receptor) have anti-obesity effects. Melanocortin-4 receptors (MC4-R) are expressed in various hypothalamic regions, including the ventromedial nucleus and ARC. Activation of MC4-R by agonists such as α-melanocyte-stimulating hormone (a cleavage product of pro-opiomelanocortin which is expressed in ARC neurones) inhibits feeding and causes weight loss. Conversely, MC4-R antagonists such as ‘agouti’ protein and agouti gene-related peptide (AGRP) stimulate feeding and cause obesity. Ectopic expression of agouti in the hypothalamus leads to obesity in the AVY mouse, while AGRP is co-expressed by NPY neurones in the ARC. Synthetic MC4-R agonists may ultimately find use as anti-obesity drugs in human subjects Orexins-A and -B, derived from prepro-orexin, are expressed in specific neurones of the lateral hypothalamic area (LHA). Orexin-A injected centrally stimulates eating and prepro-orexin mRNA is up regulated by fasting and hypoglycaemia. The LHA is important in receiving sensory signals from the gut and liver, and in sensing glucose, and orexin neurones may be involved in stimulating feeding in response to falls in plasma glucose.

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The lateral hypothalamic area revisited: Ingestive behavior

Cited by 369 publications

References 771 publications

Neural mechanisms of predatory aggression in rats—Implications for abnormal intraspecific aggression

Neural mechanisms of predatory aggression in rats—Implications for abnormal intraspecific aggression

Dopaminergic and non-dopaminergic value systems in conditioning and outcome-specific revaluation

The hypothalamus and the regulation of energy homeostasis: lifting the lid on a black box

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