Hypothalamic sites affecting masticatory neurons in rats

doi:10.1016/0361-9230(91)90001-Z

Brain Research Bulletin

Volume 26, Issue 3, March 1991, Pages 321-325

https://doi.org/10.1016/0361-9230(91)90001-Z Get rights and content

Abstract

The effects of hypothalamic electrical stimulation and dl-sulpiride injections on the unit activity of masticatory trigeminal neurons were assessed in rats. Unilateral electrodes or bilateral cannulas were implanted in the perifomical hypothalamus. The animals which exhibited eating to electrical stimulation or to sulpiride injections were selected. Then, under urethane anesthesia, electrical stimuli or sulpiride injections were applied at sites which elicited eating while a passive jaw movement-related neuron was recorded. Electrical stimulation or sulpiride injections affected the basal firing rate of 15 out of 32 (53%), and 13 out of 17 (76%) jaw movement-related neurons, respectively. The basal firing rate of 3 out of 18 (16.6%) was affected by electrical stimulation of noneliciting feeding nearby places. Facilitation was observed in 7 out of those 13 jaw movement-related trigeminal neurons after intrahypothalamic sulpiride injections. When dopamine was injected in the hypothalamus 3 minutes before sulpiride, this drug could only affect the basal firing rate of 1 out of 12 (8%) jaw movement-related neurons. The electrical stimulation and sulpiride injections into the hypothalamus had the same inhibitory or excitatory effect on a given trigeminal neuron as the passive jaw movement did. A similar phenomenon was observed with the sulphide-induced facilitation. These results suggest that hypothalamic D₂ satiety receptors modulate brain stem feeding reflexes.

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Cited by (19)

Posterior lateral hypothalamic axon terminals are in contact with trigeminal premotor neurons in the parvicellular reticular formation of the rat medulla oblongata
2008, Brain Research
Citation Excerpt :
The hypothalamus has been known to be a responsible site for inducing attack or defense responses including opening and closing movement of jaws (Brody et al., 1969; Brown et al., 1969; Chi and Flynn, 1971). Within the hypothalamus, the LHA has been considered to play a crucial role on the control of jaw movements (Achari and Thexton, 1972; Landgren and Olsson, 1980; Murzi et al., 1991; Inoue et al., 2001), and the LHA projection to the RFp, where premotor neurons of the Vm exist, has been suggested to represent an anatomical substrate for the LHA modulation of masticatory motoneurons (Holstege, 1991). In support of this suggestion, here we demonstrated the existence of the PLH-RFp-Vm pathway at the light and electron microscopic levels.
This study was performed to understand the anatomical substrates of hypothalamic modulation of jaw movements. After cholera toxin B subunit (CTb) injection into the parvicellular reticular formation (RFp) of the rat medulla oblongata, where many trigeminal premotor neurons have been known to exist, numerous CTb-labeled neurons were found in the posterior lateral hypothalamus (PLH) bilaterally with a clear-cut ipsilateral dominance. After ipsilateral injections of biotinylated dextran amine (BDA) into the PLH and CTb into the motor trigeminal nucleus (Vm), the prominent distribution of BDA-labeled axon terminals around CTb-labeled neurons was found in the RFp region just ventral to the nucleus of the solitary tract and medial to the spinal trigeminal nucleus ipsilateral to the injection sites. Within the neuropil of the RFp, BDA-labeled axon terminals made an asymmetrical synaptic contact predominantly with dendrites and additionally with somata of the RFp neurons, some of which were labeled with CTb. It was further revealed that these BDA-labeled axon terminals were immunoreactive for vesicular glutamate transporter 2. The present data suggest that the PLH plays an important role in the control of jaw movements by exerting its glutamatergic excitatory action upon RFp neurons presynaptic to trigeminal motoneurons.
Novel role of Y1 receptors in the coordinated regulation of bone and energy homeostasis
2007, Journal of Biological Chemistry
Citation Excerpt :
Although there is a lack of involvement of hypothalamic Y1 receptors in the regulation of energy homeostasis, these receptors play a significant role in the regulation of feeding and other feeding-related behavior. The exact reasons for food grinding in mice are not clear (31), although it has been shown that electrical and chemical stimulation of the hypothalamus influences the activity of masticatory trigmental neurons in the brain stem important for jaw movement (32). It is therefore possible that ablation of Y1 receptors in the hypothalamus leads to altered responses to these neurons in the brainstem, leading to increased grinding of food.
The importance of neuropeptide Y (NPY) and Y2 receptors in the regulation of bone and energy homeostasis has recently been demonstrated. However, the contributions of the other Y receptors are less clear. Here we show that Y1 receptors are expressed on osteoblastic cells. Moreover, bone and adipose tissue mass are elevated in Y1^-/- mice with a generalized increase in bone formation on cortical and cancellous surfaces. Importantly, the inhibitory effects of NPY on bone marrow stromal cells in vitro are absent in cells derived from Y1^-/- mice, indicating a direct action of NPY on bone cells via this Y receptor. Interestingly, in contrast to Y2 receptor or germ line Y1 receptor deletion, conditional deletion of hypothalamic Y1 receptors in adult mice did not alter bone homeostasis, food intake, or adiposity. Furthermore, deletion of both Y1 and Y2 receptors did not produce additive effects in bone or adiposity. Thus Y1 receptor pathways act powerfully to inhibit bone production and adiposity by nonhypothalamic pathways, with potentially direct effects on bone tissue through a single pathway with Y2 receptors.
Clozapine's effects on body weight and resting metabolic rate: A case series
2004, Schizophrenia Research
The purpose of this pilot study is to determine if an association exists between clozapine-associated weight gain and resting metabolic rate (RMR). In doing so, we used a “pretest–posttest” single group design in which we measured resting metabolic rate and total body weight prior to implementing clozapine therapy and then again approximately 1 month after initiating clozapine therapy. The results of three patients treated with clozapine revealed an inverse relationship between resting metabolic rate and total body weight. Resting metabolic rates were notably reduced by 10.3–16.0% whereas total body weights had increased between 2.9 and 9 kg. To our knowledge, this is the first documentation of an antipsychotic medication being associated with the reduction in resting metabolic rate.
Naltrexone does not prevent the weight gain and hyperphagia induced by the antipsychotic drug sulpiride in rats
2000, Appetite
Few pharmacological tools are currently available to counteract the excessive body weight gain often observed during prolonged administration of antipsychotic drugs. Most antipsychotic drugs block dopamine receptors, and both the brain dopaminergic and opioid systems appear to be involved in initiation and maintenance of feeding behavior, respectively. We evaluated whether the opioid antagonist naltrexone (NAL, 0.5–16 mg/kg/ip for 21 days) (a) affects body weight and food intake in gonadally-intact and drug-free female rats, (b) prevents obesity, hyperphagia, hyperprolactinemia and vaginal cycle disruption induced by long-term administration of the antipsychotic drug sulpiride (SUL, 20 mg/kg/ip for 21 days), or (c) reverses the acute hyperphagia induced by SUL (15 μg bilaterally), when directly applied in the perifornical lateral hypothalamus (PFLH). In drug-free rats, only NAL doses above 4 mg/kg, significantly decreased weight gain and food intake. Even though NAL (1 and 8 mg/kg) significantly attenuated SUL-induced hyperphagia and hyperprolactinemia, it did not reverse at any dose the weight gain and permanent diestrous induced by SUL. In addition, local NAL did not prevent the hyperphagia and polidypsia observed after acute intrahypothalamic SUL. Unexpectedly, the cumulative and 24 h food intake in SUL-treated rats was significantly increased by NAL. Collectively, these results do not support a role for endogenous opiates in the neural and endocrine mechanisms involved in weight gain during prolonged antipsychotic drug administration in rats.
Antipsychotic drugs and reproductive hormones relationship to body weight regulation
1999, Pharmacology Biochemistry and Behavior
Excessive body weight gain is an undesirable side effect of prolonged administration of antipsychotic drugs (AP), which affects health and interferes with treatment compliance. It has been suggested that hyperprolactinemia-induced endocrine and metabolic abnormalities, particularly in the gonadal steroids, might be involved in the development of this type of weight gain. To test this hypothesis, reproductive hormones, cortisol, dehydro-epiandrosterone-sulfate (DHEA-S), thyroid hormones, and body weight gain were assessed in 18 patients (9 men, 9 women) with mental disorders receiving AP who had been medication-free for at least 3 months before the study, and in 27 placebo-treated subjects (10 men, 17 women). In women, hormones were evaluated during several phases of the menstrual cycle. A significant weight gain was observed in men but not in women. Under AP administration, women displayed significantly lower serum levels of estradiol and progesterone, whereas in men the levels of free testosterone and DHEA-S were significantly lower than in controls. Hyperprolactinemia was observed in both sexes. The levels of follicle-stimulating hormone in women and luteinizing hormone in men were significantly elevated by treatment, thus suggesting that the functioning of the hypothalamus–pituitary–gonads was preserved. In men, such an endocrine profile resembles that observed in subjects with primary obesity. Women under AP administration were found to be relatively hyperandrogenic because of decreased serum estradiol levels, whereas women with primary obesity are known to display actual increased levels of androgens. These endocrine abnormalities may contribute to the excessive weight gain observed after AP treatment, and these could be the target of novel pharmacological treatments.
Glucose tolerance and serum insulin levels in an animal model of obesity induced by sub-acute or chronic administration of antipsychotic drugs
1999, Progress in Neuro-Psychopharmacology and Biological Psychiatry
- 1.
  1. To assess the role of insulin in the development of the obesity induced by antipsychotic drugs, a glucose tolerance test was conducted in female rats after 10 or 30 days of sulpiride administration.
- 2.
  2. At day 10, the area under the glucose curve did not differ between sulpiride and vehicle-treated rats, however, the area under the insulin curve was significantly decreased by sulpiride. At day, 30 the insulin response was similar in both groups, but the area under the glucose curve was significantly lower in the sulpiride-treated rats.
- 3.
  3. The results suggest that insulin resistance and hyperinsulinemia are not involved in the development and maintenance of the obesity induced by sulpiride. Contrarily, these findings may be related to an increased insulin sensitivity.
- 4.
  4. The absence of hyperinsulinemia and insulin resistance indicates important differences between primary obesity in humans and rodents and this model of drug-induced excessive weight gain.

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Hypothalamic sites affecting masticatory neurons in rats

Abstract

Pharmacol. Biochem. Behav.

Brain Res.

Anim. Behav.

J. Neurosci. Methods

Physiol. Behav.

Physiol. Behav.

Pharmacol. Biochem. Behav.

Physiol. Behav.

Life Sci.

Brain Res.

Hypothalamic input to brain stem neurons responsive to oropharyngeal stimulation

Exp. Brain Res.