Olfaction and food intake are interrelated and regulated. In the process of feeding, the metabolic signals in the body and the feeding signals produced by food stimulation are first sensed by the arcuate nucleus of hypothalamus and the nucleus tractus solitarius of brain stem, and then these neurons project to the paraventricular nucleus of hypothalamus. The paraventricular nucleus transmits the signals to other brain regions related to feeding and regulates feeding behavior. In this process, olfactory signals can be transmitted to hypothalamus through olfactory bulb and olfactory cortex to regulate feeding behavior. At the same time, gastrointestinal hormones (ghrelin, insulin, leptin, etc.) and some neurotransmitters (acetylcholine, norepinephrine, serotonin, endocannabinoid, etc.) produced in the process of feeding act on the olfactory system to regulate olfactory function, which in turn affects the feeding itself. This review summaries the research progress of the interaction between olfaction and food intake and its internal mechanism from the aspects of neuronal and hormonal regulation.
Arcuate Nucleus of Hypothalamus/metabolism* ; Feeding Behavior/physiology* ; Hypothalamus ; Paraventricular Hypothalamic Nucleus ; Smell

Acetylcholine ; metabolism ; Animals ; Arcuate Nucleus of Hypothalamus ; metabolism ; Dopamine ; metabolism ; Epinephrine ; metabolism ; Female ; Neurotransmitter Agents ; metabolism ; Norepinephrine ; metabolism ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission

Animals ; Arcuate Nucleus of Hypothalamus ; drug effects ; metabolism ; Body Temperature Regulation ; Cyclic AMP ; metabolism ; Dinoprostone ; metabolism ; Eugenol ; pharmacology ; Fever ; metabolism ; Preoptic Area ; drug effects ; metabolism ; Rabbits

This study was aimed to investigate the changes of orexin-A (OXA) and neuropeptide Y (NPY) expression in the hypothalamus of the fasted and high-fat diet fed rats. For the experiments, the male Sprague-Dawley (SD) rats were used as the model of high-fat diet-induced obesity. The mean loss of body weight (MLBW) did not show the linear pattern during the fasting; from 24 h to 84 h of fastings, the MLBW was not significantly changed. The numbers of OXA-immunoreactive (IR) neurons were decreased at 84 h of fasting compared with those in other five fasting subgroups. The NPY immunoreactivities in the arcuate nucleus (ARC) and the suprachiasmatic nucleus (SCN) observed at 84 h of fasting were higher than that observed at 24 h of fasting. The number of OXA-IR neurons of the LHA (lateral hypothalamic area) in the high-fat (HF) diet fed group was more increased than that of the same area in the normal-fat (NF) diet fed group. The NPY immunoreactivities of the ARC and the SCN were higher in HF group than those observed in the same areas of NF group. Based on these results, it is noteworthy that the decrease of the body weight during the fast was not proportionate to the time-course, implicating a possible adaptation of the body for survival against starvation. The HF diet might activate the OXA and the NPY in the LHA to enhance food intake.
Adaptation, Physiological/physiology ; Animals ; Arcuate Nucleus/metabolism ; Dietary Fats ; Eating ; Fasting/*physiology ; Hypothalamic Area, Lateral/metabolism ; Hypothalamus/*metabolism ; Immunohistochemistry/veterinary ; Intracellular Signaling Peptides and Proteins/*metabolism ; Male ; Neuropeptide Y/*metabolism ; Neuropeptides/*metabolism ; Obesity ; Rats ; Rats, Sprague-Dawley/physiology ; Suprachiasmatic Nucleus/metabolism

OBJECTIVETo explore the expressions and functions of the kisspeptin/kiss1r system and GnRH in the hypothalamic arcuate nucleus (HAN) and the influence of the kisspeptin/kiss1r system on the hypothalamic-pituitary-testis (HPT) axis in the rat models of diet-induced obesity.

METHODSNinety newborn SD male rats were randomly assigned to receive normal diet (n = 30) and high-fat diet (n = 60) for the establishment of obesity models. The model rats were again equally divided into a control group and an experimental group, the latter injected with kisspeptin via the lateral ventricle. Then the body mass index (BMI) and endocrine hormone levels of the rats were recorded, the protein expressions of LepR, kisspeptin, kiss1r, and GnRH in the HAN determined by immunohistochemistry and Western blot, and the levels of GnRH mRNA in the HAN measured by qRT-PCR.

RESULTSSignificantly increased BMI and hormone levels indicated the successful establishment of diet-induced obesity models. Compared with the normal rats, the protein expressions of LepR, kisspeptin, and GnRH in the HAN were markedly decreased in the controls, and that of GnRH and the levels of LH and T significantly increased, but the expressions of LepR and kiss1r showed no remarkable changes in the experimental rats.

CONCLUSIONLateral ventricular injection of kisspeptin can upregulate obesity-induced low expression of GnRH, correct the dysfunction of the HPT axis, and thus improve reproductive function in rats.

Animals ; Arcuate Nucleus of Hypothalamus ; metabolism ; Diet, High-Fat ; Disease Models, Animal ; Female ; Gonadotropin-Releasing Hormone ; metabolism ; Hypothalamo-Hypophyseal System ; Kisspeptins ; metabolism ; Male ; Obesity ; metabolism ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled ; metabolism ; Receptors, Kisspeptin-1 ; Receptors, Leptin ; metabolism

The study was conducted to investigate the effect of melatonin (MEL) on the expression of β-endorphin (β-EP) in the hypothalamic arcuate nucleus (ARH) of morphine-dependent mice. For a period of 8 consecutive days, male Kunming strain mice were injected subcutaneously (s.c.) with normal saline or increasing doses (10-80 mg/kg) of morphine, and intraperitoneally (i.p.) with MEL (10, 20 or 40 mg/kg) or vehicle (5% ethanol saline) simultaneously. Withdrawal response was induced by naloxone (3 mg/kg, s.c.) at 2 h after final morphine injection on the 8th day. The potency of withdrawal response was evaluated according to the jumping times and the body weight loss. After that, the expressions of β-EP and proopiomelanocortin (POMC) mRNA in ARH were examined by immunohistochemistry and RT-PCR, respectively. The results showed that MEL (i.p., 20 mg/kg) decreased the naloxone-precipitated withdrawal responses in morphine-dependent mice significantly (P<0.05). Meanwhile, MEL increased the intensity of β-EP-like immunoreactivity and enhanced the expression of POMC mRNA in ARH (P<0.05). These results suggest that MEL increases the expression of β-EP in ARH of morphine-dependent mice, which may partly contribute to the action of MEL to inhibit the development of morphine dependence.
Animals ; Arcuate Nucleus of Hypothalamus ; drug effects ; metabolism ; Male ; Melatonin ; pharmacology ; Mice ; Morphine ; pharmacology ; Morphine Dependence ; metabolism ; Naloxone ; pharmacology ; Pro-Opiomelanocortin ; metabolism ; RNA, Messenger ; metabolism ; Substance Withdrawal Syndrome ; metabolism ; beta-Endorphin ; metabolism

Kisspeptins are a group of peptide fragments encoded by the KISS1 gene in humans. They bind to kisspeptin receptors with equal efficacy. Kisspeptins and their receptors are expressed by neurons in the arcuate and anteroventral periventricular nuclei of the hypothalamus. Oestrogen mediates negative feedback of gonadotrophin-releasing hormone secretion via the arcuate nucleus. Conversely, it exerts positive feedback via the anteroventral periventricular nucleus. The sexual dimorphism of these nuclei accounts for the differential behaviour of the hypothalamic-pituitary-gonadal axis between genders. Kisspeptins are essential for reproductive function. Puberty is regulated by the maturation of kisspeptin neurons and by interactions between kisspeptins and leptin. Hence, kisspeptins have potential diagnostic and therapeutic applications. Kisspeptin agonists may be used to localise lesions in cases of hypothalamic-pituitary-gonadal axis dysfunction and evaluate the gonadotrophic potential of subfertile individuals. Kisspeptin antagonists may be useful as contraceptives in women, through the prevention of premature luteinisation during in vitro fertilisation, and in the treatment of sex steroid-dependent diseases and metastatic cancers.
Animals ; Arcuate Nucleus of Hypothalamus ; metabolism ; Estrogens ; metabolism ; Feedback, Physiological ; Female ; Fertilization in Vitro ; Gonadotropin-Releasing Hormone ; metabolism ; Homeostasis ; Humans ; Kisspeptins ; physiology ; Male ; Mice ; Neoplasms ; metabolism ; Neurons ; metabolism ; Protein Binding ; Rats ; Reproduction ; Sex Factors ; Signal Transduction

The present study was undertaken to investigate the effect of melatonin on the content of β-endorphin (β-EP) in the hypothalamic arcuate nucleus (Arc) and periaqueductal grey (PAG) of midbrain in morphine withdrawal mice. Male Kunming mice were injected subcutaneously (s.c.) with an increasing dose of morphine continuously for 8 d to establish morphine dependence model. Withdrawal response was induced by naloxone (3 mg/kg body weight, s.c.). The potency of withdrawal response was evaluated according to the jumping times and body weight loss. Ninty minutes prior to the precipitation of naloxone, 80 mg/kg body weight of melatonin (MEL) was injected intraperitoneally (i.p.) to observe its antagonistic effect on the withdrawal response in morphine-dependent mice. After behavioral observation, radioimmunoassay was used to determine the content of β-EP in the PAG of midbrain, and immunohistochemical assay was used to observe the intensity of β-EP-like immunoreactivity in the Arc in mice. It was shown that MEL inhibited the naloxone-precipitated withdrawal responses in mice significantly (P<0.05). In the meantime, MEL increased the content of β-EP in the PAG of midbrain significantly (P<0.05) and attenuated the intensity of β-EP-like immunoreactivity in the Arc in mice (P<0.05). The results suggest that MEL increases the content of β-EP in the PAG of midbrain, decrease the content of β-EP in the Arc in morphine withdrawal mice.
Animals ; Arcuate Nucleus of Hypothalamus ; drug effects ; metabolism ; Male ; Melatonin ; pharmacology ; Mesencephalon ; drug effects ; metabolism ; Mice ; Morphine Dependence ; Naloxone ; Periaqueductal Gray ; drug effects ; metabolism ; Substance Withdrawal Syndrome ; beta-Endorphin ; metabolism

Ghrelin, an endogenous ligand for the growth hormone secretagogue (GHS) receptor, stimulates feeding and increases body weight. The primary action site of ghrelin has been reported to be the neuropeptide Y (NPY)/agouti-related peptide (AgRP) neurons in the hypothalamic arcuate nucleus (ARC). In addition to the hypothalamus, the caudal brainstem also appears to be an important mediator for the orexigenic activity of ghrelin. However, it is not clear whether ghrelin applied directly to the caudal brainstem activates forebrain structures. The aim of this study was to determine whether recruitment of forebrain structures was required for hyperphagic responses stimulated by ghrelin delivery within the caudal brainstem. In our experiment, all rats were surgically implanted with indwelling cannulas in the dorsal vagal complex (DVC), and ghrelin (20 pmol in 0.5 μL) was delivered to the DVC. After the injection, the orexigenic response to ghrelin was recorded by Feeding and Activity Analyser, and NPY/AgRP mRNA expressions in rat hypothalamus were detected by real-time PCR. In addition, the NPY immunoreactive neurons in the ARC were assayed by immunohistochemistry. The results showed that ghrelin significantly increased cumulative food intake at 1, 2 and 3 h after ghrelin injection, maximal response occurring at 2 h after injection. NPY/AgRP mRNA levels in ARC treated with ghrelin increased significantly compared with those in control group (injected with saline). The highest levels of NPY and AgRP mRNA were detected at 2 h after injection. The total number and mean optical density of NPY-positive neurons increased in ghrelin treated rats compared with those in control group. Consistently, ghrelin's effect was most pronounced at 2 h after injection. Taken together, we conclude that the activation of NPY/AgRP neurons in the ARC is involved in the mediation of the hyperphagic response to brainstem ghrelin administration in neurologically intact rats.
Agouti-Related Protein ; genetics ; metabolism ; Animals ; Arcuate Nucleus of Hypothalamus ; metabolism ; physiology ; Brain Stem ; metabolism ; physiology ; Feeding Behavior ; drug effects ; Ghrelin ; pharmacology ; Hyperphagia ; physiopathology ; Hypothalamus ; metabolism ; physiology ; Male ; Neurons ; metabolism ; physiology ; Neuropeptide Y ; genetics ; metabolism ; Peptide Fragments ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe the mechanism of SHU-Dihuang on the function of learning and memory.

METHODOn the dementia model mouse caused by AlCl3 and the rats model damaged thalamic arcuate nucleus with MSG, we observed the function of learning and memory by step down task and Morris water maze task, mensurated the content of glutamic acid and gamma-aminobutyric acid by TLC, and observed the expression of NMDAR1 and GABAR in hippocampi by immunohistochemical means.

RESULTShu Di Huang could decrease the times of mistakes and prolong the incubation period in step down task, and shorten the incubation period of seeking the platform in Morris water maze task. Shu Di Huang could adjust the content of Glu and GABA in brain, and increase the expression of hippocampal NMDAR1 and GABAR as well.

CONCLUSIONShu Di Huang can improve the function of learning and memory of dementia animal model, and its mechanism may be related to the adjustment of the content of Glu and GABA in brain, and increase of the expression of hippocampal NMDAR1 and GABAR.

Animals ; Arcuate Nucleus of Hypothalamus ; drug effects ; Dementia ; chemically induced ; physiopathology ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Female ; Hippocampus ; metabolism ; Male ; Maze Learning ; drug effects ; Memory ; drug effects ; Mice ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA ; metabolism ; Receptors, N-Methyl-D-Aspartate ; metabolism ; Rehmannia ; chemistry