Ventromedial hypothalamic and paraventricular nucleus lesions damage a common system to produce hyperphagia

Cox, James E.; Sims, Joanne S.

doi:10.1016/0166-4328(88)90132-5

Cited by 14 publications

(6 citation statements)

References 28 publications

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“…This argument is supported by an observation reported by Cox and Sims: simultaneously damaging one side of the VMH and the contralateral PVN produced significant hyperphagia and weight gains not significantly different from that in rats with bilateral lesions of the VMH or the PVN. The results suggest that VMH lesion induced obesity may be the result of damaging efferent projections of the PVN neurons that run through the VMH (Cox and Sims 1988).…”

Section: Pvn May Excite and Inhibit Dmnv Neuronsmentioning

confidence: 89%

Glutamate Mediates an Excitatory Influence of the Paraventricular Hypothalamic Nucleus on the Dorsal Motor Nucleus of the Vagus

Zhang

Fogel

2002

Journal of Neurophysiology

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Data have shown that the paraventricular nucleus of the hypothalamus (PVN) and the dorsal motor nucleus of the vagus (DMNV) play important roles in the regulation of gastrointestinal function and eating behavior. Anatomical studies have demonstrated direct projections from the PVN to the DMNV and physiological studies showed that the DMNV mediates many of the effects of PVN stimulation and electrical current stimulation of the PVN excites a subset of DMNV neurons. The aim of this study was to characterize the role of glutamate receptors in the excitatory influence of the PVN on gut-related DMNV neurons. Using single-cell recording techniques, we determined the effects of kynurenic acid, 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX), and DL-2-amino-5-phosphonopentanoic acid (DL-AP5) on the increase in firing rate due to electrical current stimulation of the PVN. In initial experiments, we studied 24 DMNV neurons excited by electrical current stimulation of the PVN. Kynurenic acid, a broad-spectrum glutamate receptor antagonist, prevented the PVN effect in 22 neurons and significantly attenuated the effect in the other cells. Nine of these neurons demonstrated an inhibition in firing rate with PVN stimulation after pretreatment with kynurenic acid. In a separate group of 12 neurons, we determined the effects of CNQX (1.2 nmol) injected into the DMNV. This AMPA receptor antagonist completely blocked the excitatory response to PVN stimulation of six DMNV neurons and significantly attenuated the response of the other six DMNV neurons. The addition of 1.2 nmol DL-AP5, a N-methyl-D-aspartate (NMDA) receptor antagonist, further attenuated the response to PVN stimulation in four of the five DMNV neurons that were still excited after CNQX treatment. The fifth neuron demonstrated PVN- induced inhibition of firing rate after treatment with CNQX and DL-AP5. In a separate group of 11 DMNV neurons excited by electrical stimulation of the PVN, DL-AP5 partially attenuated the excitatory responses of only four DMNV neurons and did not block the excitation of any cells. The mean latency (14 neurons tested) from the PVN to the DMNV was 37.71 +/- 2.40 (SE) ms. Monosynaptic action potentials and excitatory postsynaptic potentials were demonstrated in three DMNV neurons by intracellular recording. Our results indicate that glutamate released from PVN neurons projecting to the DMNV excite the gut-related vagal motor neurons by acting predominantly on the AMPA receptor. The NMDA receptor plays only a minor role in the excitatory effect.

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Section: Pvn May Excite and Inhibit Dmnv Neuronsmentioning

confidence: 89%

Glutamate Mediates an Excitatory Influence of the Paraventricular Hypothalamic Nucleus on the Dorsal Motor Nucleus of the Vagus

Zhang

Fogel

2002

Journal of Neurophysiology

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“…Interestingly, insulin secretion by the β cell of the endocrine pancreas is under an inhibitory tonus by the sympathetic nervous system. More precisely, bilateral VMH lesions induced activation of the parasympathetic outflow and hyperinsulinemia 29 . Reduced VMH c-Fos expression in response to DON could explain the early hyperinsulinemia and consecutive hypoglycemia.…”

Section: Discussionmentioning

confidence: 95%

The food contaminant deoxynivalenol provokes metabolic impairments resulting in non-alcoholic fatty liver (NAFL) in mice

Barbouche

Gaigé

Airault

et al. 2020

Sci Rep

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The ribotoxin deoxynivalenol (DON) is a trichothecene found on cereals responsible for mycotoxicosis in both humans and farm animals. DON toxicity is characterized by reduced food intake, diminished nutritional efficiency and immunologic effects. The present study was designed to further characterize the alterations in energy metabolism induced by DON intoxication. We demonstrated that acute DON intoxication triggered liver steatosis associated with an altered expression of genes related to lipids oxidation, lipogenesis and lipolysis. This steatosis was concomitant to anorexia, hypoglycemia and a paradoxical transient insulin release. DON treatment resulted also in stimulation of central autonomic network regulating sympathetic outflow and adrenaline and glucocorticoids secretion. Furthermore, an increased expression of genes linked to inflammation and reticulum endoplasmic stress was observed in the liver of DON-treated mice. Finally, we propose that lipids mobilization from adipose tissues (AT) induced by DON intoxication drives hepatic steatosis since (1) genes encoding lipolytic enzymes were up-regulated in AT and (2) plasma concentration of triglycerides (TGs) and nonesterified fatty acids were increased during DON intoxication. Altogether, these data demonstrate that DON induced hormonal and metabolic dysregulations associated with a spectrum of hepatic abnormalities, evocative of a non-alcoholic fatty liver disease.

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“…Electrolytic lesions of the PVN produce hyperphagia and obesity (7,28,31). Studies examining c-fos expression have indicated activation of PVN neurons after admin- istration of duodenal Intralipid (20) as well as after administration of substances thought to decrease food intake by direct action on the PVN, such as ␣-melanocyte stimulating hormone, cocaine-amphetamine-regulated transcript, and serotonin (18,21,32).…”

Section: Discussionmentioning

confidence: 99%

“…3, 15, 27, and 34). For example, bilateral lesions of the PVN can produce hyperphagia (7,28,31) and local infusions of neuroactive substances such as melanotan II (MT II) into the PVN can suppress food intake (11). Moreover, the PVN receives a variety of signals from the periphery by both vagally mediated and vagally independent routes.…”

mentioning

confidence: 99%

Jejunal administration of linoleic acid increases activity of neurons in the paraventricular nucleus of the hypothalamus

Randich¹,

Chandler²,

Mebane³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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administration of linoleic acid increases activity of neurons in the paraventricular nucleus of the hypothalamus. Am J Physiol Regul Integr Comp Physiol 286: R166-R173, 2004; 10.1152/ajpregu.00431.2003.-The present experiment examined whether neurons located in the paraventricular nucleus of the hypothalamus (PVN) respond to intestinal infusions of long-chain fatty acids. Single-unit recordings were made of neurons located in and adjacent to the PVN during jejunal administration of linoleic acid. Jejunal administration of linoleic acid increased single-unit activity of neurons located in the PVN but did not affect activity of neurons located in adjacent tissue outside the PVN. The largest increases in neuronal activity were observed in the anterior PVN (0.9-1.3 mm posterior to bregma) compared with the posterior PVN (1.8-2.1 mm posterior to bregma). Jejunal administration of saline failed to affect activity of neurons located either inside or outside the PVN. When the same neurons were subsequently tested for their response to intravenous administration of 2 g/kg of CCK-8, excitatory responses were more frequently observed than inhibitory responses, but both types of responses were observed regardless of whether neurons were located inside or outside the PVN. In addition, there was no strong correlation between the magnitude of the neuronal response evoked by jejunal administration of linoleic acid compared with intravenous CCK-8. These data suggest that neurons located in the anterior PVN may play a role in the mediation of suppression of food intake produced by intestinal administration of lipids.INFUSIONS OF LIPIDS INTO the small intestine can suppress food intake. Under some conditions, the suppression is large enough to result in negative energy balance (4,8,9,35), suggesting a potential clinical role for weight management in humans. For example, we found that jejunal infusions of the long-chain fatty acids (linoleic acid or oleic acid) reduced total caloric intake by ϳ15%. When infusions were administered on 21 consecutive days, body weight was reduced by 10% and carcass fat by 48% compared with controls (8). This effect depends, in part, on activation of vagal afferents, especially those in the celiac branches. Infusions of lipids into the small intestine increase celiac vagal afferent activity (23,25). In addition, we observed that selective celiac vagotomy attenuated linoleic acid-induced suppression of food intake by ϳ50% (Ref. 9; but see Ref. 33). However, because total subdiaphragmatic vagotomy was no more effective in this regard than was celiac vagotomy (6), there must be a nonvagal component that also contributes to suppression of food intake.Our laboratories were especially interested in the potential role of the paraventricular nucleus of the hypothalamus (PVN) in mediating suppression of intake produced by intraintestinal lipids because of its central role in energy balance (cf. Refs. 3, 15, 27, and 34). For example, bilateral lesions of the PVN can produce hyperphagia (7, 28, 31) and local in...

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Ventromedial hypothalamic and paraventricular nucleus lesions damage a common system to produce hyperphagia

Cited by 14 publications

References 28 publications

Glutamate Mediates an Excitatory Influence of the Paraventricular Hypothalamic Nucleus on the Dorsal Motor Nucleus of the Vagus

Glutamate Mediates an Excitatory Influence of the Paraventricular Hypothalamic Nucleus on the Dorsal Motor Nucleus of the Vagus

The food contaminant deoxynivalenol provokes metabolic impairments resulting in non-alcoholic fatty liver (NAFL) in mice

Jejunal administration of linoleic acid increases activity of neurons in the paraventricular nucleus of the hypothalamus

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