Publications by authors named "Wayner M"

The newly identified neuropeptide S (NPS) is a ligand for a previously orphan G protein-coupled GPR 154 receptor, now named the NPS receptor (NPSR). Previous studies have shown that NPS induces hyperlocomotion, increases arousal and suppresses anxiety-like behaviors via NPSR. Although NPS also inhibits food intake, nothing is known about the neuronal mechanisms underlying this action.

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Ghrelin, a gut and brain peptide, is a potent stimulant for growth hormone (GH) secretion and feeding. Recent studies further show a critical role of ghrelin in the regulation of sleep-wakefulness. Laterodorsal tegmental nucleus (LDT), that regulates waking and rapid eye movement (REM) sleep, expresses GH secretagogue receptors (GHS-Rs).

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Orexin (ORX), also called hypocretin, and ghrelin are newly identified peptides in the brain and/or peripheral organs, and they are involved in the regulation of sleep-wakefulness as well as feeding. In our previous studies we have found that ORX and ghrelin each depolarizes more than half of the cholinergic neurons recorded in the pedunculopontine tegmental nucleus (PPT) via a dual ionic mechanism including a decrease of K(+) conductance and an increase of nonselective cationic conductance. Thus, the present study was carried out to investigate whether ORX-A and ghrelin both depolarize the same PPT neuron.

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Orexin-A (ORX-A) and orexin-B (ORX-B) play critical roles in the regulation of sleep-wakefulness, energy homeostasis, neuroendocrine system and autonomic functions. Although ORXs are also implicated in the reward process, their electrophysiological effects on neurons in the shell of nucleus accumbems (NAcSh) have not been described thoroughly. Therefore we examined the electrophysiological effects of ORXs on rat NAcSh neurons.

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Ghrelin is a potent stimulant for growth hormone (GH) secretion and feeding. Recent studies further show a critical role of ghrelin in the regulation of sleep-wakefulness. Pedunculopontine tegmental nucleus (PPT), which regulates waking and rapid eye movement (REM) sleep, expresses GH secretagogue receptors (GHS-Rs).

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Orexin-A (ORX-A) and orexin-B (ORX-B) play critical roles in the regulation of sleep-wakefulness and feeding. ORX neurons project to the pedunculopontine tegmental nucleus (PPT), which regulates waking and rapid eye movement (REM) sleep. Thus, we examined electrophysiological effects of ORXs on rat PPT neurons with a soma size of more than 30 microm.

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Ghrelin is an endogenous ligand for the growth hormone (GH) secretagogue (GHS) receptor (GHS-R) and a potent stimulant for GH secretion even in infantile rats before puberty. Although the ventromedial nucleus of the hypothalamus (VMH) might be a site of action for ghrelin to induce GH release, the electrophysiological effect of ghrelin on VMH neurons in infantile rats remains to be elucidated. Thus, the purpose of the present study was to investigate the effect of ghrelin on VMH neurons using hypothalamic slices of infantile rats.

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Leptin, an adipocytokine encoded by an obesity gene and expressed in adipose tissue, affects feeding behavior, thermogenesis, and neuroendocrine status via leptin receptors distributed in the brain, especially in the hypothalamus. Leptin may also modulate the synaptic plasticity and behavioral performance related to learning and memory since: leptin receptors are found in the hippocampus, and both leptin and its receptor share structural and functional similarities with the interleukin-6 family of cytokines that modulate long-term potentiation (LTP) in the hippocampus. We therefore examined the effect of leptin on (1) behavioral performance in emotional and spatial learning tasks, (2) LTP at Schaffer collateral-CA1 synapses, (3) presynaptic and postsynaptic activities in hippocampal CA1 neurons, (4) the intracellular Ca(2+) concentration ([Ca(2+)](i)) in CA1 neurons, and (5) the activity of Ca(2+)/calmodulin protein kinase II (CaMK II) in the hippocampal CA1 tissue that exhibits LTP.

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Sleep frequently fragmented or disrupted for prolonged periods can result in mood changes and impaired mental ability and performance. Sleep deprivation is defined as depriving a person or organism of sleep for various periods of fixed durations. Sleep disruption (SD) occurs when a person is awakened at any time when they would normally be sleeping; sometimes on a schedule but usually unexpectedly.

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Orexin-A (ORX-A) and orexin-B (ORX-B), also called hypocretin-1 and hypocretin-2, respectively, act upon orexin 1 (OX1R) and orexin 2 (OX2R) receptors, and are involved in the regulation of sleep-wakefulness and energy homeostasis. Orexin neurons in the lateral hypothalamic perifornical region project heavily to the paraventricular nucleus of the thalamus (PVT), which is deeply involved in the control of motivated behaviors. In the present study, electrophysiological and cytosolic Ca2+ concentration ([Ca2+]i) imaging studies on the effects of ORX-A and ORX-B on neurons in the PVT were carried out in rat brain slice preparations.

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Orexin-A (Hypocretin-1) has been localized in the posterior and lateral hypothalamic perifornical region. Orexin containing axon terminals have been found in hypothalamic nuclei and many other parts of the brain; for example, the hippocampus. Two types of orexin receptors have been discovered.

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In previous studies we identified a lateral hypothalamic area (LHA) sensitive to ethanol, < 5.0 mM, when the perifornical region of the area is perfused with different concentrations of ethanol. Some of these perifornical neurons contain angiotensin (Ang) and project directly to the dentate gyrus where angiotensin is released and inhibits LTP in medial perforant path-dentate granule cell synapses.

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Glucose-sensitive neurons in the lateral hypothalamic area produce orexin-A (hypocretin-1) and orexin-B (hypocretin-2) and send their axons to the hippocampus, which predominantly expresses orexin receptor 1 showing a higher sensitivity to orexin-A. The purpose of the present study was to assess the effects of orexin-A on the performance of Wistar rats during the Morris water maze test and then to determine the effects of orexin-A on both the long-term potentiation and long-term depression in Schaffer collateral/commissural-CA1 synapses in hippocampal slices. The results of the Morris water maze test show that 1.

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A review of previous results and the new data in this report show clearly that the Falk model of adjunctive behavior is an adequate analogue of human alcoholism and can be applied to induce excessive ethanol consumption. New data on the consumption of sweet flavored ethanol solutions and, especially, sweet alone solutions during brief periods of ethanol withdrawal provide some significant insights concerning the possible physiological basis for cravings in humans. Because voluntary consumption of ethanol is the normal process by which alcoholism develops, a general set of environmental and other experimental conditions that produce behavioral excess; adjunctive behavior, electrical stimulation of the brain, and salt arousal of drinking are discussed in some detail.

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Angiotensins have been shown to play a significant role in a variety of physiological functions including learning and memory processes. Relatively recent evidence supports the increasing importance of angiotensin IV (Ang IV), in many of these functions previously associated only with Ang II, including learning and memory. An interesting hypothesis generated by these results has been that Ang II is a precursor for the production of a more active peptide fragment, Ang IV.

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Within the brain-renin angiotensin system, it is generally assumed that angiotensin peptide fragments shorter than angiotensins II and III, including angiotensin IV (AngIV), are inactive. This belief has been challenged by the recent discovery that AngIV, and AngIV-like analogs, bind with high affinity and specificity to a putative angiotensin binding site termed AT4. In the brain these sites include the hippocampus, cerebellum, and cerebral cortex, and influence associative and spatial learning tasks.

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The lateral hypothalamic area (LHA) and the ventromedial hypothalamic nucleus (VMH) have historically been implicated in ingestive behavior, energy balance and body mass regulation. The LHA is more closely associated with the initiation of eating; whereas the VMH mediates the cessation of eating. The parvocellular part of the paraventricular nucleus (pPVN) is also included in the suppressing mechanism.

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Air righting results in an animal turning over when it is dropped from a height in an inverted position. In the rat, air righting is a complex set of movements that depends only on an intact labyrinth and the normal vestibular input. Visual modulation of air righting does not develop until adulthood; and the ability to estimate the time to impact requires bilateral visual cues and indicates that air righting is a complex set of perceptually controlled movements and learning.

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Decreased GABA function in the hypothalamus increases mean arterial pressure (MAP) and heart rate (HR). Since ethanol acts on GABA-A receptors, blocking GABA-A receptors can prevent a decrease of MAP and HR by ethanol in the lateral hypothalamus (LH). Ethanol at 5-30 mM, with or without 25 ng/microl bicuculline, was infused into the LH, and the activity of the site was validated with 100 nmoles of serotonin.

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Results of our previous research in rats demonstrate the following: (a) Angiotensin II (Ang II) inhibits long term potentiation (LTP) in dentate granule cell-perforant path synapses and that this inhibition can be blocked by losartan, an Ang II AT1 receptor antagonist; (b) both ethanol and diazepam inhibit LTP induction and this inhibition can be blocked by losartan; (c) impairment of air righting by ethanol and diazepam (DZ) and eight-arm radial maze performance by ethanol can be blocked by pretreatment with losartan: (d) inhibition of dentate granule cell LTP by Ang II can also be prevented by pretreatment with nicotine. Therefore, it seemed reasonable to hypothesize that ethanol and diazepam impairment of air righting and maze performance might also be blocked by pretreatment with nicotine. The purpose of the present study was to determine the effects of nicotine 0.

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We have previously demonstrated that intra-hippocampal injection of corticotrophin-releasing factor improved memory retention of an inhibitory avoidance learning in rats; while the electrophysiological effects corticotrophin-releasing factor produces on hippocampal neurons are largely uncharacterized. In the present study, we found that corticotrophin-releasing factor injected into the dentate gyrus of hippocampus produced a dose-dependent and long-lasting enhancement in synaptic efficacy of these neurons, as measured by an increase in the amplitude and slope of population excitatory postsynaptic potentials, as well as the amplitude of population spike. The onset of corticotrophin-releasing factor-induced potentiation was slow.

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The wild white-footed mouse, Peromyscus leucopus, is commonly used for photoperiod studies utilizing physiological, behavioral, and other biological measures indicative of hypothalamic functions. Indoleamines, like melatonin and serotonin, are implicated in regulating these hypothalamic functions. Although neurochemical analyses of hypothalamic serotonin and its receptors have been reported for this species, the relevant neuroanatomy of the serotonin system within mouse hypothalamus has not been studied.

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We had previously discovered that both diazepam (DZ) and ethanol inhibited long-term potentiation (LTP) in medial perforant path-dentate granule cell synapses and the inhibition was mediated by angiotensin II (Ang II) because it could be blocked by pretreatment with losartan, an Ang II AT1 receptor antagonist. In addition, we had shown that ethanol intoxicating effects on air righting can be significantly reduced by losartan. Therefore, the purpose of the present study was to determine the effects of DZ, 1 and 2 mg/kg i.

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Purpose: To report a case of Ewing sarcoma metastatic to the iris.

Methods: A 19-year-old woman with metastatic Ewing sarcoma of the femur developed a diffuse, fluffy iris mass with a pseudohypopyon in the left eye. A fine-needle aspiration biopsy confirmed iris metastasis, and external beam radiotherapy was given to the affected eye.

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Results of previous research demonstrate that angiotensin II (Ang II) inhibits long-term potentiation (LTP) in medial perforant path-dentate gyrus granule cells and that the inhibition is mediated by the AT1 receptor because it can be blocked by losartan, a specific AT1 receptor antagonist. Ang II impairment of retention and ethanol inhibition of LTP can both be blocked by pretreatment with losartan. Because losartan pretreatment also prevents ethanol intoxication measured in terms of the aerial righting reflex, the purpose of the present study was to assess the effects of 2.

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