Functional correlations between lateral hypothalamic glucose-sensitive neurons and hepatic portal glucose-sensitive units in rat

Shimizu, Nobuaki; Osuga, Yutaka; Novin, Donald; Grijalva, Carlos V.; Cooper, Peter

doi:10.1016/0006-8993(83)91332-x

Cited by 158 publications

(57 citation statements)

References 28 publications

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“…GSNs are particularly abundant in the LHA, where they account for 30 -40% of all neurons (3,5). These cells are stimulated directly by low glucose in vitro (3,6) but are also regulated indirectly in vivo, being inhibited by rising glucose levels in the hindbrain and viscera and by gastric distension (1,7). These indirect signals are presumed to be relayed to the LHA from the nucleus of the solitary tract (NTS) in the medulla, which contains glucose-sensing neurons and also receives vagal afferents from visceral glucose sensors and gastric stretch receptors (7).…”

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confidence: 99%

“…These cells are stimulated directly by low glucose in vitro (3,6) but are also regulated indirectly in vivo, being inhibited by rising glucose levels in the hindbrain and viscera and by gastric distension (1,7). These indirect signals are presumed to be relayed to the LHA from the nucleus of the solitary tract (NTS) in the medulla, which contains glucose-sensing neurons and also receives vagal afferents from visceral glucose sensors and gastric stretch receptors (7). In view of these properties, lateral hypothalamic GSNs are assumed to participate in triggering and controlling glucoprivic feeding (1)(2)(3).…”

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confidence: 99%

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Orexin A Preferentially Excites Glucose-Sensitive Neurons in the Lateral Hypothalamus of the Rat In Vitro

Liu

Morris²,

Spiller³

et al. 2001

Diabetes

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Falls in blood glucose induce hunger and initiate feeding. The lateral hypothalamic area (LHA) contains glucose-sensitive neurons (GSNs) and orexin neurons, both of which are stimulated by falling blood glucose and are implicated in hypoglycemia-induced feeding. We combined intracellular electrophysiological recording with fluorescein labeling of GSNs to determine their neuroanatomic and functional relationships with orexin neurons. Orexin A (1 mol/l) caused a 500% increase (P < 0.01) in spontaneous firing rate and rapid and lasting depolarization that was tetrodotoxin-resistant and thus a direct postsynaptic effect. Orexin A altered the intrinsic neuronal properties of GSNs, consistent with increased excitability. Confocal microscopy showed that GSNs were intimately related to orexin neurons: orexin-immunoreactive axons were frequently entwined around GSN dendrites, establishing close and putatively synaptic contacts. Orexin-cell axons also passed in close proximity to glucose-responsive neurons, which are inhibited by low glucose, but orexin A caused smaller depolarization than on GSNs and only a 200% increase in spontaneous firing rate (P < 0.05 vs. GSN). We conclude that GSNs are specific target neurons for orexin A and suggest that they may mediate, at least in part, the acute appetite-stimulating effect of orexin A. Orexin neurons may regulate GSNs so as to control the onset and termination of hypoglycemiainduced feeding. Diabetes 50:2431-2437, 2001 R educed availability of glucose, the brain's main metabolic fuel, causes intense hunger (1). The lateral hypothalamic area (LHA) is crucial to the hyperphagia induced by hypoglycemia and glucoprivation, as this feeding response is abolished by LHA lesions (1). The LHA neuronal systems that drive glucoprivic feeding are unknown, but promising candidates include the glucose-sensing neurons and orexin (hypocretin) neurons that are prominent in this region.Glucose-sensing neurons, which alter their firing behavior in response to changes in ambient glucose concentration, are found in the hypothalamus and in several other central nervous system regions (2). Glucose-sensitive neurons (GSNs) are inhibited by rising glucose concentrations but excited when glucose falls, whereas glucose-responsive neurons (GRNs) are stimulated as glucose rises and are inhibited by hypoglycemia (3,4). GSNs are particularly abundant in the LHA, where they account for 30 -40% of all neurons (3,5). These cells are stimulated directly by low glucose in vitro (3,6) but are also regulated indirectly in vivo, being inhibited by rising glucose levels in the hindbrain and viscera and by gastric distension (1,7). These indirect signals are presumed to be relayed to the LHA from the nucleus of the solitary tract (NTS) in the medulla, which contains glucose-sensing neurons and also receives vagal afferents from visceral glucose sensors and gastric stretch receptors (7). In view of these properties, lateral hypothalamic GSNs are assumed to participate in triggering and controlling glucoprivic feeding...

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confidence: 99%

mentioning

confidence: 99%

Orexin A Preferentially Excites Glucose-Sensitive Neurons in the Lateral Hypothalamus of the Rat In Vitro

Liu

Morris²,

Spiller³

et al. 2001

Diabetes

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“…They suggested that duodenal receptor signals are conveyed to the rat brain by way of NA inhibitory neurons in the hypothalamus to terminate feeding. It has been suggested that the NA pathway transmits signals related to blood glucose level from the portal system to GS neurons in the LHA [49] through GS neurons in the NTS [1]. Selective lesions of the ventral NA bundle produce hyperphagia and obesity, and NA injection into the LHA suppresses food intake.…”

Section: Chemical Sensingmentioning

confidence: 99%

“…1 A, B). Visual [33, see 37, 58], olfactory [55], and gustatory [14,32] signals, plus internal visceral information, such as that from hepatic and intestinal glucose sensors [19,49] and stomach mechanoreceptor afferents [35], converges in the limbic system [34], especially the VMH and the LHA, to integrate sensory and effector information. The LHA, VMH, and other parts of the limbic system then mediate feeding processes.…”

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confidence: 99%

“…Ascending NTS fibers project to the parabrachial nucleus (PBN), where excitatory inputs transmit taste signals [32], and both excitatory and inhibitory inputs have been suggested for the transmission of signals from general visceral afferents. The inhibitory pathway from the NTS through the PBN to the LHA could be responsible for decreasing the activity of GS neurons in the LHA when decrease in NTS activity causes disinhibition at the level of the PBN [49]. The PBN has been shown to have a high concentration of noradrenaline (NA) and is one of the origins of the ventral NA pathway.…”

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Feeding control through bioassay of body chemistry.

Osuga¹

1985

Jpn.J.Physiol

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Organisms function, in part, through processes of continuous assay of chemical conditions in the body. The body's ability to do this is evident from the many examples of bioassay that have been used since the earliest studies of biology. Some monitoring systems in the body respond rather specifically to individual factors, while others are dedicated to control of specialized mechanisms that are essential to survival. Evidence obtained from lesions produced in various sites within the hypothalamus led to early conclusions that feeding behavior was controlled or could at least be modified within that general region. There was, of course, controversy as to whether this was due to specific control centers or to fibers of passage through the hypothalamus. MORGANE [24] found that lesions of the lateral hypothalamic area (LHA) at the level of the ventromedial hypothalamic nucleus (VMH) did, in fact, greatly affect feeding behavior, while rostral or caudal lesions did not. This gave credence to the idea of control from a center, but still the controversy continued. Later GROSSMAN and GROSSMAN [6], with their kainic acid technique, managed to lesion neurons while leaving fibers of passage intact. This further supported the control center idea. More direct evidence in support of control centers has accumulated from micro injections, either directly or intracerebroventricularly, from electrophysiology and from electrophoretic drug applications. At present, widely distributed networks are known, and these certainly involve some rather extensive pathways. However, the networks join centers that lie not just in the nervous system, but in other organs as well, especially the viceral organs. With techniques now available it has been shown, without doubt, both directly and by deductive methods, that feeding can be, and probably is, controlled from several discrete centers. Some of this proof will be presented in this review which discusses progress in the study of neuronal and behavioral responses to body fluid factors and their consequent control of the feeding process. NEURONAL NETWORKS INVOLVED IN FEEDINGImportant information relevant to the regulation of feeding goes to the hypo-

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Central Regulation of Peripheral Glucose Metabolism

Hileman

Bjørbæk

2004

Insulin Resistance

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Functional correlations between lateral hypothalamic glucose-sensitive neurons and hepatic portal glucose-sensitive units in rat

Cited by 158 publications

References 28 publications

Orexin A Preferentially Excites Glucose-Sensitive Neurons in the Lateral Hypothalamus of the Rat In Vitro

Orexin A Preferentially Excites Glucose-Sensitive Neurons in the Lateral Hypothalamus of the Rat In Vitro

Feeding control through bioassay of body chemistry.

Central Regulation of Peripheral Glucose Metabolism

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