Journal articles: 'Ventrolateral preoptic nucleus (VLPO)'

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Arrigoni, Elda, and Patrick M. Fuller. "The Sleep-Promoting Ventrolateral Preoptic Nucleus: What Have We Learned over the Past 25 Years?" International Journal of Molecular Sciences 23, no. 6 (March 8, 2022): 2905. http://dx.doi.org/10.3390/ijms23062905.

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For over a century, the role of the preoptic hypothalamus and adjacent basal forebrain in sleep–wake regulation has been recognized. However, for years, the identity and location of sleep- and wake-promoting neurons in this region remained largely unresolved. Twenty-five years ago, Saper and colleagues uncovered a small collection of sleep-active neurons in the ventrolateral preoptic nucleus (VLPO) of the preoptic hypothalamus, and since this seminal discovery the VLPO has been intensively investigated by labs around the world, including our own. Herein, we first review the history of the preoptic area, with an emphasis on the VLPO in sleep–wake control. We then attempt to synthesize our current understanding of the circuit, cellular and synaptic bases by which the VLPO both regulates and is itself regulated, in order to exert a powerful control over behavioral state, as well as examining data suggesting an involvement of the VLPO in other physiological processes.

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Li, Ke Y., Yan-zhong Guan, Kresimir Krnjević, and Jiang H. Ye. "Propofol Facilitates Glutamatergic Transmission to Neurons of the Ventrolateral Preoptic Nucleus." Anesthesiology 111, no. 6 (December 1, 2009): 1271–78. http://dx.doi.org/10.1097/aln.0b013e3181bf1d79.

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Background There is much evidence that the sedative component of anesthesia is mediated by gamma-aminobutyric acid type A (GABA(A)) receptors on hypothalamic neurons responsible for arousal, notably in the tuberomammillary nucleus. These GABA(A) receptors are targeted by gamma-aminobutyric acid-mediated (GABAergic) neurons in the ventrolateral preoptic area (VLPO): When these neurons become active, they inhibit the arousal-producing nuclei and induce sleep. According to recent studies, propofol induces sedation by enhancing VLPO-induced synaptic inhibition, making the target cells more responsive to GABA(A). The authors explored the possibility that propofol also promotes sedation less directly by facilitating excitatory inputs to the VLPO GABAergic neurons. Methods Spontaneous excitatory postsynaptic currents were recorded from VLPO cells-principally mechanically isolated, but also in slices from rats. Results In isolated VLPO GABAergic neurons, propofol increased the frequency of glutamatergic spontaneous excitatory postsynaptic currents without affecting their mean amplitude. The action of propofol was mimicked by muscimol and prevented by gabazine, respectively a specific agonist and antagonist at GABA(A) receptors. It was also suppressed by bumetanide, a blocker of Na-K-Cl cotransporter-mediated inward Cl transport. In slices, propofol also increased the frequency of spontaneous excitatory postsynaptic currents and, at low doses, accelerated firing of VLPO cells. Conclusion Propofol induces sedation, at least in part, by increasing firing of GABAergic neurons in the VLPO, indirectly by activation of GABA(A) receptors on glutamatergic afferents: Because these axons/terminals have a relatively high internal Cl concentration, they are depolarized by GABAergic agents such as propofol, which thus enhance glutamate release.

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Novak, Colleen M., and Antonio A. Nunez. "Daily rhythms in Fos activity in the rat ventrolateral preoptic area and midline thalamic nuclei." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 5 (November 1, 1998): R1620—R1626. http://dx.doi.org/10.1152/ajpregu.1998.275.5.r1620.

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The present experiment investigated the expression of the nuclear phosphoprotein Fos over the 24-h light-dark cycle in regions of the rat brain related to sleep and vigilance, including the ventrolateral preoptic area (VLPO), the paraventricular thalamic nucleus (PVT), and the central medial thalamic nucleus (CMT). Immunocytochemistry for Fos, an immediate-early gene product used as an index of neuronal activity, was carried out on brain sections from rats perfused at zeitgeber time (ZT) 1, ZT 5, ZT 12.5, and ZT 17 (lights on ZT 0–ZT 12). The number of Fos-immunopositive (Fos+) cells in the VLPO was elevated at ZT 5 and 12.5 (i.e., during or just after the rest phase of the cycle). Fos+cell number increased at ZT 17 and ZT 1 in the PVT and CMT, 180° out of phase with the VLPO. A positive correlation was found between the numbers of Fos+ cells in the PVT and CMT, and Fos expression in each thalamic nucleus was negatively correlated with VLPO Fos+ cell number. The VLPO, PVT, and CMT may integrate circadian and homeostatic influences to regulate the sleep-wake cycle.

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Matsuo, Shin-ichiro, Il-Sung Jang, Junichi Nabekura, and Norio Akaike. "α2-Adrenoceptor-Mediated Presynaptic Modulation of GABAergic Transmission in Mechanically Dissociated Rat Ventrolateral Preoptic Neurons." Journal of Neurophysiology 89, no. 3 (March 1, 2003): 1640–48. http://dx.doi.org/10.1152/jn.00491.2002.

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The ventrolateral preoptic nucleus (VLPO) is a key nucleus involved in the homeostatic regulation of sleep-wakefulness. Little is known, however, about the cellular mechanisms underlying its role in sleep regulation and how the neurotransmitters, such as GABA and noradrenaline (NA), are involved. In the present study we investigated GABAergic transmission to acutely dissociated VLPO neurons using an enzyme-free, mechanical dissociation procedure in which functional terminals remained adherent and we investigated how this GABAergic transmission was modulated by NA. As previously reported in slices, NA hyperpolarized multipolar VLPO neurons and depolarized bipolar VLPO neurons. NA also inhibited the release of GABA onto multipolar VLPO neurons but had no effect on GABAergic transmission to bipolar neurons. The inhibition of release was mediated by presynaptic α2 adrenoceptors coupled to N-ethylmaleimide (NEM)-sensitive G-proteins which appeared to act via inhibition of adenylate cyclase and subsequent decreases in protein kinase A activity. The inhibition of GABA release did not, however, involve an inhibition of external Ca2+ influx. The results indicate that all VLPO neurons contain GABAergic inputs and that the different morphological subgroups of VLPO neurons are correlated not only to different postsynaptic responses to NA but also to different presynaptic NA responses. Furthermore our results demonstrate an additional mechanism by which NA can modulate the excitability of multipolar VLPO neurons which may have important implications for its role in regulating sleep/wakefulness.

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Ghaffarpasand, Fariborz, and Mousa Taghipour. "Ventrolateral Preoptic Nucleus of Hypothalamus: A Possible Target for Deep Brain Stimulation for Treating Sexual Dysfunction." Iranian Journal of Neurosurgery 5, no. 3 And 4 (July 1, 2020): 99–102. http://dx.doi.org/10.32598/irjns.5.3.1.

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Sexual function and orientation is a complex platform of human personality which is being modulated by several brain circuities which is less understood currently. Recently, several studies have demonstrated interesting results regarding the role of several brain locations in sexual behaviors and orientation. Sexual arousal in homosexual men is associated with activation of the left angular gyrus, left caudate nucleus, Ventrolateral Preoptic (VLPO) Nucleus of Hypothalamus and right pallidum; while it is associated with bilateral lingual gyrus, right hippocampus, and right parahippocampal gyrus in heterosexual men. We postulate that sexual-orientation behaviors are being mediated by several circuits in the brain in the center of which the VLPO is playing an indistinguishable role. We hypothesize that the different aspects of the sexual dysfunction could be associated with innate or acquired lesions of VLPO. Accordingly, the electrical stimulation of the nucleus in those with sexual dysfunction would be a treatment option. Thus the VLPO could be considered a target for Deep Brain Stimulation (DBS) in individuals with impaired sexual function.

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Alam, Md Aftab, Sunil Kumar, Dennis McGinty, Md Noor Alam, and Ronald Szymusiak. "Neuronal activity in the preoptic hypothalamus during sleep deprivation and recovery sleep." Journal of Neurophysiology 111, no. 2 (January 15, 2014): 287–99. http://dx.doi.org/10.1152/jn.00504.2013.

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The preoptic hypothalamus is implicated in sleep regulation. Neurons in the median preoptic nucleus (MnPO) and the ventrolateral preoptic area (VLPO) have been identified as potential sleep regulatory elements. However, the extent to which MnPO and VLPO neurons are activated in response to changing homeostatic sleep regulatory demands is unresolved. To address this question, we continuously recorded the extracellular activity of neurons in the rat MnPO, VLPO and dorsal lateral preoptic area (LPO) during baseline sleep and waking, during 2 h of sleep deprivation (SD) and during 2 h of recovery sleep (RS). Sleep-active neurons in the MnPO ( n = 11) and VLPO ( n = 13) were activated in response to SD, such that waking discharge rates increased by 95.8 ± 29.5% and 59.4 ± 17.3%, respectively, above waking baseline values. During RS, non-rapid eye movement (REM) sleep discharge rates of MnPO neurons initially increased to 65.6 ± 15.2% above baseline values, then declined to baseline levels in association with decreases in EEG delta power. Increase in non-REM sleep discharge rates in VLPO neurons during RS averaged 40.5 ± 7.6% above baseline. REM-active neurons ( n = 16) in the LPO also exhibited increased waking discharge during SD and an increase in non-REM discharge during RS. Infusion of A2A adenosine receptor antagonist into the VLPO attenuated SD-induced increases in neuronal discharge. Populations of LPO wake/REM-active and state-indifferent neurons and dorsal LPO sleep-active neurons were unresponsive to SD. These findings support the hypothesis that sleep-active neurons in the MnPO and VLPO, and REM-active neurons in the LPO, are components of neuronal circuits that mediate homeostatic responses to sustained wakefulness.

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Gong, Hui, Ronald Szymusiak, Janice King, Teresa Steininger, and Dennis McGinty. "Sleep-related c-Fos protein expression in the preoptic hypothalamus: effects of ambient warming." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2079—R2088. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2079.

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Preoptic area (POA) neuronal activity promotes sleep, but the localization of critical sleep-active neurons is not completely known. Thermal stimulation of the POA also facilitates sleep. This study used the c-Fos protein immunostaining method to localize POA sleep-active neurons at control (22°C) and mildly elevated (31.5°C) ambient temperatures. At 22°C, after sleep, but not after waking, we found increased numbers of c-Fos immunoreactive neurons (IRNs) in both rostral and caudal parts of the median preoptic nucleus (MnPN) and in the ventrolateral preoptic area (VLPO). In animals sleeping at 31.5°C, significantly more Fos IRNs were found in the rostral MnPN compared with animals sleeping at 22°C. In VLPO, Fos IRN counts were no longer increased over waking levels after sleep at the elevated ambient temperature. Sleep-associated Fos IRNs were also found diffusely in the POA, but counts were lower than those made after waking. This study supports a hypothesis that the MnPN, as well as the VLPO, is part of the POA sleep-facilitating system and that the rostral MnPN may facilitate sleep, particularly at elevated ambient temperatures.

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De Luca, Roberto, Stefano Nardone, Lin Zhu, and Elda Arrigoni. "066 Noradrenaline and acetylcholine inhibit sleep-promoting neurons of ventrolateral preoptic area through a local GABAergic circuit." Sleep 44, Supplement_2 (May 1, 2021): A27—A28. http://dx.doi.org/10.1093/sleep/zsab072.065.

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Abstract Introduction The ventrolateral preoptic (VLPO) nucleus is a key area involved in the initiation and maintenance of sleep. During wakefulness, sleep-promoting galanin neurons in the VLPO are directly inhibited by arousal signals including noradrenaline and acetylcholine. We have found that while these neurotransmitters directly inhibit VLPO galanin neurons, they also activate GABAergic neurons in the VLPO that do not express galanin. We propose that when activated by monoaminergic and cholinergic inputs, these local VLPO GABAergic neurons provide an additional inhibition of the VLPO galanin sleep-promoting neurons. We tested this model in brain slices in mice. Methods We studied VLPO galanin neurons in mouse brain slices using patch-clamp recordings. We recorded from fluorescently labeled VLPO galanin neurons following the injection of a cre-dependent AAV encoding for mCherry, into the VLPO of Gal-cre mice. For the optogenetic studies we expressed channelrhodopsin-2 (ChR-2) in VLPO VGAT neurons and mCherry in galanin neurons by injecting a flp-dependent and a cre-dependent AAV encoding respectively for ChR2 and mCherry into the VLPO of VGAT-flp::Gal-cre mice. We photo-stimulated local GABAergic neurons and recorded from labeled VLPO galanin neurons. Noradrenaline, carbachol and receptor antagonists were bath-applied. Results Noradrenaline and carbachol inhibited VLPO galanin neurons by alpha-2 and muscarinic receptors and these effects were maintained in the presence of tetrodotoxin (TTX) indicating, as previously proposed, a direct inhibitory effect of noradrenaline and carbachol on VLPO galanin neurons. In addition, both noradrenaline and carbachol increased the frequency of spontaneous inhibitory post-synaptic currents (sIPSCs) of VLPO galanin neurons, suggesting an additional inhibitory action on VLPO galanin neurons. Finally, optogenetic stimulation of local VLPO GABAergic neurons produced short latency, TTX-resistant, opto-evoked IPSCs in VLPO galanin neurons. Both noradrenaline and carbachol increased the amplitude of these opto-evoked IPSCs by the activation of alpha-1 and muscarinic receptors. Conclusion Our results demonstrate that noradrenaline and acetylcholine inhibit VLPO galanin neurons directly and indirectly. Both noradrenaline and acetylcholine increase GABAergic afferent inputs to VLPO galanin neurons by activating local GABAergic neurons. We propose that during wakefulness this feedforward inhibition provides additional inhibition of VLPO galanin sleep-promoting neurons. Support (if any) NS091126 and HL149630

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Kumar, Sunil, Seema Rai, Kung-Chiao Hsieh, Dennis McGinty, Md Noor Alam, and Ronald Szymusiak. "Adenosine A2A receptors regulate the activity of sleep regulatory GABAergic neurons in the preoptic hypothalamus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 1 (July 1, 2013): R31—R41. http://dx.doi.org/10.1152/ajpregu.00402.2012.

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The median preoptic nucleus (MnPN) and the ventrolateral preoptic area (VLPO) are two hypothalamic regions that have been implicated in sleep regulation, and both nuclei contain sleep-active GABAergic neurons. Adenosine is an endogenous sleep regulatory substance, which promotes sleep via A1 and A2A receptors (A2AR). Infusion of A2AR agonist into the lateral ventricle or into the subarachnoid space underlying the rostral basal forebrain (SS-rBF), has been previously shown to increase sleep. We examined the effects of an A2AR agonist, CGS-21680, administered into the lateral ventricle and the SS-rBF on sleep and c-Fos protein immunoreactivity (Fos-IR) in GABAergic neurons in the MnPN and VLPO. Intracerebroventricular administration of CGS-21680 during the second half of lights-on phase increased sleep and increased the number of MnPN and VLPO GABAergic neurons expressing Fos-IR. Similar effects were found with CGS-21680 microinjection into the SS-rBF. The induction of Fos-IR in preoptic GABAergic neurons was not secondary to drug-induced sleep, since CGS-21680 delivered to the SS-rBF significantly increased Fos-IR in MnPN and VLPO neurons in animals that were not permitted to sleep. Intracerebroventricular infusion of ZM-241385, an A2AR antagonist, during the last 2 h of a 3-h period of sleep deprivation caused suppression of subsequent recovery sleep and reduced Fos-IR in MnPN and VLPO GABAergic neurons. Our findings support a hypothesis that A2AR-mediated activation of MnPN and VLPO GABAergic neurons contributes to adenosinergic regulation of sleep.

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Gvilia, Irma, Natalia Suntsova, Sunil Kumar, Dennis McGinty, and Ronald Szymusiak. "Suppression of preoptic sleep-regulatory neuronal activity during corticotropin-releasing factor-induced sleep disturbance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 9 (November 1, 2015): R1092—R1100. http://dx.doi.org/10.1152/ajpregu.00176.2015.

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Corticotropin releasing factor (CRF) is implicated in sleep and arousal regulation. Exogenous CRF causes sleep suppression that is associated with activation of at least two important arousal systems: pontine noradrenergic and hypothalamic orexin/hypocretin neurons. It is not known whether CRF also impacts sleep-promoting neuronal systems. We hypothesized that CRF-mediated changes in wake and sleep involve decreased activity of hypothalamic sleep-regulatory neurons localized in the preoptic area. To test this hypothesis, we examined the effects of intracerebroventricular administration of CRF on sleep-wake measures and c-Fos expression in GABAergic neurons in the median preoptic nucleus (MnPN) and ventrolateral preoptic area (VLPO) in different experimental conditions. Administration of CRF (0.1 nmol) during baseline rest phase led to delayed sleep onset and decreases in total amount and mean duration of non-rapid eye movement (NREM) sleep. Administration of CRF during acute sleep deprivation (SD) resulted in suppression of recovery sleep and decreased c-Fos expression in MnPN/VLPO GABAergic neurons. Compared with vehicle controls, intracerebroventricular CRF potentiated disturbances of both NREM and REM sleep in rats exposed to a species-specific psychological stressor, the dirty cage of a male conspecific. The number of MnPN/VLPO GABAergic neurons expressing c-Fos was reduced in the CRF-treated group of dirty cage-exposed rats. These findings confirm the involvement of CRF in wake-sleep cycle regulation and suggest that increased CRF signaling in the brain 1) negatively affects homeostatic responses to sleep loss, 2) exacerbates stress-induced disturbances of sleep, and 3) suppresses the activity of sleep-regulatory neurons of the MnPN and VLPO.

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Baker, F. C., S. Shah, D. Stewart, C. Angara, H. Gong, R. Szymusiak, M. R. Opp, and D. McGinty. "Interleukin 1β enhances non-rapid eye movement sleep and increases c-Fos protein expression in the median preoptic nucleus of the hypothalamus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 4 (April 2005): R998—R1005. http://dx.doi.org/10.1152/ajpregu.00615.2004.

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Interleukin 1β (IL-1) is a key mediator of the acute phase response in an infected host and acts centrally to coordinate responses to an immune challenge, such as fever and increased non-rapid eye movement (NREM) sleep. The preoptic area (POA) is a primary sleep regulatory center in the brain: the ventrolateral POA (VLPO) and median preoptic nucleus (MnPN) each contain high numbers of c-Fos protein immunoreactive (IR) neurons after sleep but not after waking. We hypothesized that IL-1 mediates increased NREM sleep through activation of these sleep-active sites. Rats injected intracerebroventricularly with IL-1 (10 ng) at dark onset spent significantly more time in NREM sleep 4–5 h after injection. This increase in NREM sleep was associated with increased numbers of Fos-IR neurons in the MnPN, but not in the VLPO. Fos IR in the rostral MnPN was significantly increased 2 h post IL-1 injection, although the percentage of NREM sleep in the preceding 2 h was the same as controls. Fos IR was also increased in the extended VLPO 2 h postinjection. Finally, Fos IR in the MnPN did not differ significantly between IL-1 and vehicle-treated rats that had been sleep deprived for 2 h postinjection, but it was increased in VLPO core. Taken together, these results suggest that Fos IR in the MnPN after IL-1 is not independent of behavioral state and may require some threshold amount of sleep for its expression. Our results support a hypothesis that IL-1 enhances NREM sleep, in part, through activation of neurons in the MnPN of the hypothalamus.

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Gvilia, Irma, Natalia Suntsova, Bryan Angara, Dennis McGinty, and Ronald Szymusiak. "Maturation of sleep homeostasis in developing rats: a role for preoptic area neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 4 (April 2011): R885—R894. http://dx.doi.org/10.1152/ajpregu.00727.2010.

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The present study evaluated the hypothesis that developmental changes in hypothalamic sleep-regulatory neuronal circuits contribute to the maturation of sleep homeostasis in rats during the fourth postnatal week. In a longitudinal study, we quantified electrographic measures of sleep during baseline and in response to sleep deprivation (SD) on postnatal days 21/29 (P21/29) and P22/30 ( experiment 1). During 24-h baseline recordings on P21, total sleep time (TST) during the light and dark phases did not differ significantly. On P29, TST during the light phase was significantly higher than during the dark phase. Mean duration of non-rapid-eye-movement (NREM) sleep bouts was significantly longer on P29 vs. P21, indicating improved sleep consolidation. On both P22 and P30, rats exhibited increased NREM sleep amounts and NREM electroencephalogram delta power during recovery sleep (RS) compared with baseline. Increased NREM sleep bout length during RS was observed only on P30. In experiment 2, we quantified activity of GABAergic neurons in median preoptic nucleus (MnPN) and ventrolateral preoptic area (VLPO) during SD and RS in separate groups of P22 and P30 rats using c-Fos and glutamic acid decarboxylase (GAD) immunohistochemistry. In P22 rats, numbers of Fos+GAD+ neurons in VLPO did not differ among experimental conditions. In P30 rats, Fos+GAD+ counts in VLPO were elevated during RS. MnPN neuronal activity was state-dependent in P22 rats, but Fos+GAD+ cell counts were higher in P30 rats. These findings support the hypothesis that functional emergence of preoptic sleep-regulatory neurons contributes to the maturation of sleep homeostasis in the developing rat brain.

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Nelson, Laura E., Jun Lu, Tianzhi Guo, Clifford B. Saper, Nicholas P. Franks, and Mervyn Maze. "The α2-Adrenoceptor Agonist Dexmedetomidine Converges on an Endogenous Sleep-promoting Pathway to Exert Its Sedative Effects." Anesthesiology 98, no. 2 (February 1, 2003): 428–36. http://dx.doi.org/10.1097/00000542-200302000-00024.

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Background The authors investigated whether the sedative, or hypnotic, action of the general anesthetic dexmedetomidine (a selective alpha -adrenoceptor agonist) activates endogenous nonrapid eye movement (NREM) sleep-promoting pathways. Methods c-Fos expression in sleep-promoting brain nuclei was assessed in rats using immunohistochemistry and hybridization. Next, the authors perturbed these pathways using (1) discrete lesions induced by ibotenic acid, (2) local and systemic administration of gamma-aminobutyric acid receptor type A (GABA ) receptor antagonist gabazine, or (3) alpha2-adrenoceptor antagonist atipamezole in rats, and (4) genetic mutation of the alpha -adrenoceptor in mice. Results Dexmedetomidine induced a qualitatively similar pattern of c-Fos expression in rats as seen during normal NREM sleep, a decrease in the locus ceruleus (LC) and tuberomammillary nucleus (TMN) and an increase in the ventrolateral preoptic nucleus (VLPO). These changes were attenuated by atipamezole and were not seen in mice lacking functional alpha2a-adrenoceptors, which do not show a sedative response to dexmedetomidine. Bilateral VLPO lesions attenuated the sedative response to dexmedetomidine, and the dose-response curve to dexmedetomidine was shifted right by gabazine administered systemically or directly into the TMN. VLPO lesions and gabazine pretreatment altered c-Fos expression in the TMN but in not the LC after dexmedetomidine administration, indicating a hierarchical sequence of changes. Conclusions The authors propose that endogenous sleep pathways are causally involved in dexmedetomidine-induced sedation; dexmedetomidine's sedative mechanism involves inhibition of the LC, which disinhibits VLPO firing. The increased release of GABA at the terminals of the VLPO inhibits TMN firing, which is required for the sedative response.

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Peterfi, Zoltan, Dennis McGinty, Erzsebet Sarai, and Ronald Szymusiak. "Growth hormone-releasing hormone activates sleep regulatory neurons of the rat preoptic hypothalamus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 1 (January 2010): R147—R156. http://dx.doi.org/10.1152/ajpregu.00494.2009.

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We examined whether growth hormone-releasing hormone (GHRH) may promote non-rapid eye movement (NREM) sleep via activation of GABAergic neurons in the preoptic area. Male Sprague-Dawley rats were implanted with EEG, EMG electrodes and a unilateral intracerebroventricular cannula. Groups of rats received injections (3 μl icv) with gonadotropin-releasing hormone (GHRH) (0.1 nmol/100 g body wt) or equal volume of physiological saline at the onset of the dark period and were permitted spontaneous sleep for 90 min. Separate groups of rats were sleep deprived by gentle handling for 90 min, beginning at the time of GHRH or saline injection, at the onset of the dark period. Other groups of rats received intracerebroventricular octreotide (somatostatin analog OCT) injections, intracerebroventricular injection of one of two doses of competitive GHRH antagonist, or intracerebroventricular saline injection at light onset and were then permitted 90 min spontaneous sleep-waking. Rats were killed immediately after the 90-min sleep/wake monitoring period. Brain tissue was processed for immunohistochemistry for c-Fos protein and glutamic acid decarboxylase (GAD). Single c-Fos and dual Fos-GAD cell counts were determined in the median preoptic nucleus (MnPN), and in the core and the extended parts of the ventrolateral preoptic nucleus (cVLPO and exVLPO). Intracerebroventricular GHRH elicited a significant increase in NREM sleep amount. Double-labeled Fos+GAD cell counts were significantly elevated after GHRH injection in the MnPN and VLPO in both undisturbed and sleep-deprived groups. OCT and GHRH antagonist significantly decreased NREM sleep amount compared with control rats. OCT injection increased single c-Fos-labeled cell counts in the MnPN, but not in the VLPO. Double-labeled cell counts were significantly reduced after OCT and the high dose of GHRH antagonist injection in all areas examined. These findings identify GABAergic neurons in the MnPN and VLPO as potential targets of the sleep-regulatory actions of GHRH.

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Kim, Yeon-Soo, Bo Kyung Lee, Cha Soon Kim, Young-Seob Lee, Yoon Ji Lee, Kwan-Woo Kim, Dae Young Lee, and Yi-Sook Jung. "Sedum kamtschaticum Exerts Hypnotic Effects via the Adenosine A2A Receptor in Mice." Nutrients 16, no. 16 (August 8, 2024): 2611. http://dx.doi.org/10.3390/nu16162611.

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Insomnia is a common sleep disorder with significant societal and economic impacts. Current pharmacotherapies for insomnia are often accompanied by side effects, necessitating the development of new therapeutic drugs. In this study, the hypnotic effects and mechanisms of Sedum kamtschaticum 30% ethanol extract (ESK) and one of its active compounds, myricitrin, were investigated using pentobarbital-induced sleep experiments, immunohistochemistry (IHC), receptor binding assays, and enzyme-linked immunosorbent assay (ELISA). The pentobarbital-induced sleep experiments revealed that ESK and myricitrin reduced sleep latency and prolonged total sleep time in a dose-dependent manner. Based on c-Fos immunostaining, ESK, and myricitrin enhanced the GABAergic neural activity in sleep-promoting ventrolateral preoptic nucleus (VLPO) GABAergic. By measuring the level of GABA released from VLPO GABAergic neurons, ESK and myricitrin were found to increase GABA release in the hypothalamus. These effects were significantly inhibited by SCH. Moreover, ESK exhibited a concentration-dependent binding affinity for the adenosine A2A receptors (A2AR). In conclusion, ESK and myricitrin have hypnotic effects, and their underlying mechanisms may be related to the activation of A2AR.

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Novak, Colleen M., Laura Smale, and Antonio A. Nunez. "Rhythms in Fos expression in brain areas related to the sleep-wake cycle in the diurnal Arvicanthis niloticus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 5 (May 1, 2000): R1267—R1274. http://dx.doi.org/10.1152/ajpregu.2000.278.5.r1267.

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Most mammals show daily rhythms in sleep and wakefulness controlled by the primary circadian pacemaker, the suprachiasmatic nucleus (SCN). Regardless of whether a species is diurnal or nocturnal, neural activity in the SCN and expression of the immediate-early gene product Fos increases during the light phase of the cycle. This study investigated daily patterns of Fos expression in brain areas outside the SCN in the diurnal rodent Arvicanthis niloticus. We specifically focused on regions related to sleep and arousal in animals kept on a 12:12-h light-dark cycle and killed at 1 and 5 h after both lights-on and lights-off. The ventrolateral preoptic area (VLPO), which contained cells immunopositive for galanin, showed a rhythm in Fos expression with a peak at zeitgeber time (ZT) 17 (with lights-on at ZT 0). Fos expression in the paraventricular thalamic nucleus (PVT) increased during the morning (ZT 1) but not the evening activity peak of these animals. No rhythm in Fos expression was found in the centromedial thalamic nucleus (CMT), but Fos expression in the CMT and PVT was positively correlated. A rhythm in Fos expression in the ventral tuberomammillary nucleus (VTM) was 180° out of phase with the rhythm in the VLPO. Furthermore, Fos production in histamine-immunoreactive neurons of the VTM cells increased at the light-dark transitions when A. niloticus show peaks of activity. The difference in the timing of the sleep-wake cycle in diurnal and nocturnal mammals may be due to changes in the daily pattern of activity in brain regions important in sleep and wakefulness such as the VLPO and the VTM.

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Masneuf, Sophie, Lukas L. Imbach, Fabian Büchele, Giovanni Colacicco, Marco Penner, Carlos G. Moreira, Christian Ineichen, et al. "Altered sleep intensity upon DBS to hypothalamic sleep–wake centers in rats." Translational Neuroscience 12, no. 1 (January 1, 2021): 611–25. http://dx.doi.org/10.1515/tnsci-2020-0202.

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Abstract Deep brain stimulation (DBS) has been scarcely investigated in the field of sleep research. We hypothesize that DBS onto hypothalamic sleep- and wake-promoting centers will produce significant neuromodulatory effects and potentially become a therapeutic strategy for patients suffering severe, drug-refractory sleep–wake disturbances. We aimed to investigate whether continuous electrical high-frequency DBS, such as that often implemented in clinical practice, in the ventrolateral preoptic nucleus (VLPO) or the perifornical area of the posterior lateral hypothalamus (PeFLH), significantly modulates sleep–wake characteristics and behavior. We implanted healthy rats with electroencephalographic/electromyographic electrodes and recorded vigilance states in parallel to bilateral bipolar stimulation of VLPO and PeFLH at 125 Hz and 90 µA over 24 h to test the modulating effects of DBS on sleep–wake proportions, stability and spectral power in relation to the baseline. We unexpectedly found that VLPO DBS at 125 Hz deepens slow-wave sleep (SWS) as measured by increased delta power, while sleep proportions and fragmentation remain unaffected. Thus, the intensity, but not the amount of sleep or its stability, is modulated. Similarly, the proportion and stability of vigilance states remained altogether unaltered upon PeFLH DBS but, in contrast to VLPO, 125 Hz stimulation unexpectedly weakened SWS, as evidenced by reduced delta power. This study provides novel insights into non-acute functional outputs of major sleep–wake centers in the rat brain in response to electrical high-frequency stimulation, a paradigm frequently used in human DBS. In the conditions assayed, while exerting no major effects on the sleep–wake architecture, hypothalamic high-frequency stimulation arises as a provocative sleep intensity-modulating approach.

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Maruani, Julia, and Pierre A. Geoffroy. "Multi-Level Processes and Retina–Brain Pathways of Photic Regulation of Mood." Journal of Clinical Medicine 11, no. 2 (January 16, 2022): 448. http://dx.doi.org/10.3390/jcm11020448.

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Light exerts powerful biological effects on mood regulation. Whereas the source of photic information affecting mood is well established at least via intrinsically photosensitive retinal ganglion cells (ipRGCs) secreting the melanopsin photopigment, the precise circuits that mediate the impact of light on depressive behaviors are not well understood. This review proposes two distinct retina–brain pathways of light effects on mood: (i) a suprachiasmatic nucleus (SCN)-dependent pathway with light effect on mood via the synchronization of biological rhythms, and (ii) a SCN-independent pathway with light effects on mood through modulation of the homeostatic process of sleep, alertness and emotion regulation: (1) light directly inhibits brain areas promoting sleep such as the ventrolateral preoptic nucleus (VLPO), and activates numerous brain areas involved in alertness such as, monoaminergic areas, thalamic regions and hypothalamic regions including orexin areas; (2) moreover, light seems to modulate mood through orexin-, serotonin- and dopamine-dependent pathways; (3) in addition, light activates brain emotional processing areas including the amygdala, the nucleus accumbens, the perihabenular nucleus, the left hippocampus and pathways such as the retina–ventral lateral geniculate nucleus and intergeniculate leaflet–lateral habenula pathway. This work synthetizes new insights into the neural basis required for light influence mood

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Deurveilher, S., E. M. Cumyn, T. Peers, B. Rusak, and K. Semba. "Estradiol replacement enhances sleep deprivation-induced c-Fos immunoreactivity in forebrain arousal regions of ovariectomized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 4 (October 2008): R1328—R1340. http://dx.doi.org/10.1152/ajpregu.90576.2008.

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To understand how female sex hormones influence homeostatic mechanisms of sleep, we studied the effects of estradiol (E2) replacement on c-Fos immunoreactivity in sleep/wake-regulatory brain areas after sleep deprivation (SD) in ovariectomized rats. Adult rats were ovariectomized and implanted subcutaneously with capsules containing 17β-E2 (10.5 μg; to mimic diestrous E2 levels) or oil. After 2 wk, animals with E2 capsules received a single subcutaneous injection of 17β-E2 (10 μg/kg; to achieve proestrous E2 levels) or oil; control animals with oil capsules received an oil injection. Twenty-four hours later, animals were either left undisturbed or sleep deprived by “gentle handling” for 6 h during the early light phase, and killed. E2 treatment increased serum E2 levels and uterus weights dose dependently, while attenuating body weight gain. Regardless of hormonal conditions, SD increased c-Fos immunoreactivity in all four arousal-promoting areas and four limbic and neuroendocrine nuclei studied, whereas it decreased c-Fos labeling in the sleep-promoting ventrolateral preoptic nucleus (VLPO). Low and high E2 treatments enhanced the SD-induced c-Fos immunoreactivity in the laterodorsal subnucleus of the bed nucleus of stria terminalis and the tuberomammillary nucleus, and in orexin-containing hypothalamic neurons, with no effect on the basal forebrain and locus coeruleus. The high E2 treatment decreased c-Fos labeling in the VLPO under nondeprived conditions. These results indicate that E2 replacement modulates SD-induced or spontaneous c-Fos expression in sleep/wake-regulatory and limbic forebrain nuclei. These modulatory effects of E2 replacement on neuronal activity may be, in part, responsible for E2's influence on sleep/wake behavior.

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Hayaishi, Osamu. "Molecular mechanisms of sleep–wake regulation: a role of prostaglandin D 2." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1394 (February 29, 2000): 275–80. http://dx.doi.org/10.1098/rstb.2000.0564.

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Prostaglandin (PG) D 2 is a major prostanoid in the brains of rats and other mammals, including humans. When PGD synthase (PGDS), the enzyme that produces PGD 2 in the brain, was inhibited by the intracerebroventricular infusion of its selective inhibitors, i.e. tetravalent selenium compounds, the amount of sleep decreased both time and dose dependently. The amount of sleep of transgenic mice, in which the human PGDS gene had been incorporated, increased several fold under appropriate conditions. These data indicate that PGDS is a key enzyme in sleep regulation. In situ hybridization, immunoperoxidase staining and direct enzyme activity determination of tissue samples revealed that PGDS is hardly detectable in the brain parenchyma but is localized in the membrane systems surrounding the brain, namely, the arachnoid membrane and choroid plexus, from which it is secreted into the cerebrospinal fluid (CSF) to become β–trace, a major protein component of the CSF. PGD 2 exerts its somnogenic activity by binding to PGD 2 receptors exclusively localized at the ventrorostral surface of the basal forebrain. When PGD 2 was infused into the subarachnoid space below the rostral basal forebrain, striking expression of proto–oncogene Fos immunoreactivity (FosIR) was observed in the ventrolateral preoptic area (VLPO), a putative sleep centre, concurrent with sleep induction. Fos expression in the VLPO was positively correlated with the preceding amount of sleep and negatively correlated with Fos expression in the tuberomammillary nucleus (TMN), a putative wake centre. These observations suggest that PGD 2 may induce sleep via leptomeningeal PGD 2 receptors with subsequent activation of the VLPO neurons and downregulation of the wake neurons in the TMN area. Adenosine may be involved in the signal transduction associated with PGD 2 .

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Amar, Avishek. "Drugs affecting sleep and wakefulness: a review." International Journal of Basic & Clinical Pharmacology 7, no. 6 (May 22, 2018): 1057. http://dx.doi.org/10.18203/2319-2003.ijbcp20182088.

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It was in the second half of the twentieth century that Sleep Medicine was recognized as an immensely respected field of clinical research. As a result, past few decades have seen this field making some giant strides towards a better understanding of the neurochemical mechanisms that regulate the state of sleep and wakefulness. This involves a complex interplay of neuronal systems, neurotransmitters and some special nuclei located in the brain. Major wakefulness promoting nuclei being the orexinergic neurons in the lateral hypothalamic region and the tuberomammillary nucleus (TMN) while the sleep-promoting nucleus being ventrolateral preoptic nucleus (VLPO). Sleep-related complaints are one of the common complaints encountered by the physicians and the psychiatrists. As, long-standing sleep disturbances can have far-reaching implications on an individual’s physical, mental and social wellbeing, the importance of drugs affecting sleep and wakefulness could not be stressed upon anymore. Broadly, the sleep disorders are classified as insomnia, hypersomnia, and parasomnia and the presently available drugs work either by acting on the sleep-promoting GABAergic system like benzodiazepines, barbiturates etc. or by interacting with wakefulness promoting system like histaminergic system, 5- hydroxtryptaminergic system, orexinergic system etc. There are drugs which interact with other mechanisms which modulate arousal, like melatonin receptor agonists which promote sleep and adenosine receptor antagonists which promote wakefulness. This review article tries to have an overview of the available drugs for use in pathological states of sleep and wakefulness with a special emphasis on the commonly prescribed drugs and the recently approved one’s.

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Cusmano, Danielle M., Maria M. Hadjimarkou, and Jessica A. Mong. "Gonadal Steroid Modulation of Sleep and Wakefulness in Male and Female Rats Is Sexually Differentiated and Neonatally Organized by Steroid Exposure." Endocrinology 155, no. 1 (January 1, 2014): 204–14. http://dx.doi.org/10.1210/en.2013-1624.

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The paucity of clinical and preclinical studies investigating sex differences in sleep has resulted in mixed findings as to the exact nature of these differences. Although gonadal steroids are known to modulate sleep in females, less is known about males. Moreover, little evidence exists concerning the origin of these sex differences in sleep behavior. Thus, the goal of this study was to directly compare the sensitivity of sleep behavior in male and female Sprague Dawley rats to changes in the gonadal steroid milieu and to test whether the sex differences in sleep are the result of brain sexual differentiation or differences in circulating gonadal steroids. Here we report the magnitude of change in sleep behavior induced by either estradiol (E2) or testosterone (T) was greater in females compared with males, suggesting that sleep behavior in females is more sensitive to the suppressive effects of gonadal steroids. Furthermore, we demonstrated that the organizational effects of early gonadal steroid exposure result in male-like responsivity to gonadal steroids and directly alter the activity of the ventrolateral preoptic area (VLPO), an established sleep-promoting nucleus, in adult masculinized females. Moreover, the nonaromatizable androgen dihydrotestosterone did not suppress sleep in either males or females, suggesting that the T-mediated effect in females was due to the aromatization of T into E2. Together our data suggest that, like sex behavior, sex differences in sleep follow the classical organizational/activational effects of gonadal steroids.

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Han, Bo, Hilary S. McCarren, Dan O’Neill, and Max B. Kelz. "Distinctive Recruitment of Endogenous Sleep-promoting Neurons by Volatile Anesthetics and a Nonimmobilizer." Anesthesiology 121, no. 5 (November 1, 2014): 999–1009. http://dx.doi.org/10.1097/aln.0000000000000383.

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Abstract Background: Numerous studies demonstrate that anesthetic-induced unconsciousness is accompanied by activation of hypothalamic sleep-promoting neurons, which occurs through both pre- and postsynaptic mechanisms. However, the correlation between drug exposure, neuronal activation, and onset of hypnosis remains incompletely understood. Moreover, the degree to which anesthetics activate both endogenous populations of γ-aminobutyric acid (GABA)ergic sleep-promoting neurons within the ventrolateral preoptic (VLPO) and median preoptic nuclei remains unknown. Methods: Mice were exposed to oxygen, hypnotic doses of isoflurane or halothane, or 1,2-dichlorohexafluorocyclobutane (F6), a nonimmobilizer. Hypothalamic brain slices prepared from anesthetic-naive mice were also exposed to oxygen, volatile anesthetics, or F6 ex vivo, both in the presence and absence of tetrodotoxin. Double-label immunohistochemistry was performed to quantify the number of c-Fos–immunoreactive nuclei in the GABAergic subpopulation of neurons in the VLPO and the median preoptic areas to test the hypothesis that volatile anesthetics, but not nonimmobilizers, activate sleep-promoting neurons in both nuclei. Results: In vivo exposure to isoflurane and halothane doubled the fraction of active, c-Fos-expressing GABAergic neurons in the VLPO, whereas F6 failed to affect VLPO c-Fos expression. Both in the presence and absence of tetrodotoxin, isoflurane dose-dependently increased c-Fos expression in GABAergic neurons ex vivo, whereas F6 failed to alter expression. In GABAergic neurons of the median preoptic area, c-Fos expression increased with isoflurane and F6, but not with halothane exposure. Conclusions: Anesthetic unconsciousness is not accompanied by global activation of all putative sleep-promoting neurons. However, within the VLPO hypnotic doses of volatile anesthetics, but not nonimmobilizers, activate putative sleep-promoting neurons, correlating with the appearance of the hypnotic state.

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Kostin, Andrey, Md Aftab Alam, Anton Saevskiy, Dennis McGinty, and Md Noor Alam. "Activation of the Ventrolateral Preoptic Neurons Projecting to the Perifornical-Hypothalamic Area Promotes Sleep: DREADD Activation in Wild-Type Rats." Cells 11, no. 14 (July 7, 2022): 2140. http://dx.doi.org/10.3390/cells11142140.

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The ventrolateral preoptic area (VLPO) predominantly contains sleep-active neurons and is involved in sleep regulation. The perifornical-hypothalamic area (PF-HA) is a wake-regulatory region and predominantly contains wake-active neurons. VLPO GABAergic/galaninergic neurons project to the PF-HA. Previously, the specific contribution of VLPO neurons projecting to the PF-HA (VLPO > PF-HAPRJ) in sleep regulation in rats could not be investigated due to the lack of tools that could selectively target these neurons. We determined the contribution of VLPO > PF-HAPRJ neurons in sleep regulation by selectively activating them using designer receptors exclusively activated by designer drugs (DREADDs) in wild-type Fischer-344 rats. We used a combination of two viral vectors to retrogradely deliver the Cre-recombinase gene, specifically, in VLPO > PF-HA neurons, and further express hM3Dq in those neurons to selectively activate them for delineating their specific contributions to sleep–wake functions. Compared to the control, in DREADD rats, clozapine-N-oxide (CNO) significantly increased fos-expression, a marker of neuronal activation, in VLPO > PF-HAPRJ neurons (2% vs. 20%, p < 0.01) during the dark phase. CNO treatment also increased nonREM sleep (27% vs. 40%, p < 0.01) during the first 3 h of the dark phase, when rats are typically awake, and after exposure to the novel environment (55% vs. 65%; p < 0.01), which induces acute arousal during the light phase. These results support a hypothesis that VLPO > PF-HAPRJ neurons constitute a critical component of the hypothalamic sleep–wake regulatory circuitry and promote sleep by suppressing wake-active PF-HA neurons.

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Kostin, Andrey, Md Aftab Alam, Anton Saevskiy, Chenyi Yang, Peyman Golshani, and Md Noor Alam. "Calcium Dynamics of the Ventrolateral Preoptic GABAergic Neurons during Spontaneous Sleep-Waking and in Response to Homeostatic Sleep Demands." International Journal of Molecular Sciences 24, no. 9 (May 5, 2023): 8311. http://dx.doi.org/10.3390/ijms24098311.

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The ventrolateral preoptic area (VLPO) contains GABAergic sleep-active neurons. However, the extent to which these neurons are involved in expressing spontaneous sleep and homeostatic sleep regulatory demands is not fully understood. We used calcium (Ca2+) imaging to characterize the activity dynamics of VLPO neurons, especially those expressing the vesicular GABA transporter (VGAT) across spontaneous sleep-waking and in response to homeostatic sleep demands. The VLPOs of wild-type and VGAT-Cre mice were transfected with GCaMP6, and the Ca2+ fluorescence of unidentified (UNID) and VGAT cells was recorded during spontaneous sleep-waking and 3 h of sleep deprivation (SD) followed by 1 h of recovery sleep. Although both VGAT and UNID neurons exhibited heterogeneous Ca2+ fluorescence across sleep-waking, the majority of VLPO neurons displayed increased activity during nonREM/REM (VGAT, 120/303; UNID, 39/106) and REM sleep (VGAT, 32/303; UNID, 19/106). Compared to the baseline waking, VLPO sleep-active neurons (n = 91) exhibited higher activity with increasing SD that remained elevated during the recovery period. These neurons also exhibited increased Ca2+ fluorescence during nonREM sleep, marked by increased slow-wave activity and REM sleep during recovery after SD. These findings support the notion that VLPO sleep-active neurons, including GABAergic neurons, are components of neuronal circuitry that mediate spontaneous sleep and homeostatic responses to sustained wakefulness.

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Su, Yu-Jie, Pei-Lu Yi, and Fang-Chia Chang. "Transcranial Direct Current Stimulation (tDCS) Ameliorates Stress-Induced Sleep Disruption via Activating Infralimbic-Ventrolateral Preoptic Projections." Brain Sciences 14, no. 1 (January 22, 2024): 105. http://dx.doi.org/10.3390/brainsci14010105.

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Transcranial direct current stimulation (tDCS) is acknowledged for its non-invasive modulation of neuronal activity in psychiatric disorders. However, its application in insomnia research yields varied outcomes depending on different tDCS types and patient conditions. Our primary objective is to elucidate its efficiency and uncover the underlying mechanisms in insomnia treatment. We hypothesized that anodal prefrontal cortex stimulation activates glutamatergic projections from the infralimbic cortex (IL) to the ventrolateral preoptic area (VLPO) to promote sleep. After administering 0.06 mA of electrical currents for 8 min, our results indicate significant non-rapid eye movement (NREM) enhancement in naïve mice within the initial 3 h post-stimulation, persisting up to 16–24 h. In the insomnia group, tDCS enhanced NREM sleep bout numbers during acute stress response and improved NREM and REM sleep duration in subsequent acute insomnia. Sleep quality, assessed through NREM delta powers, remains unaffected. Interference of the IL-VLPO pathway, utilizing designer receptors exclusively activated by designer drugs (DREADDs) with the cre-DIO system, partially blocked tDCS’s sleep improvement in stress-induced insomnia. This study elucidated that the activation of the IL-VLPO pathway mediates tDCS’s effect on stress-induced insomnia. These findings support the understanding of tDCS effects on sleep disturbances, providing valuable insights for future research and clinical applications in sleep therapy.

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Chou, Thomas C., Alvhild A. Bjorkum, Stephanie E. Gaus, Jun Lu, Thomas E. Scammell, and Clifford B. Saper. "Afferents to the Ventrolateral Preoptic Nucleus." Journal of Neuroscience 22, no. 3 (February 1, 2002): 977–90. http://dx.doi.org/10.1523/jneurosci.22-03-00977.2002.

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Zhao, Zheng-Dong, Wen Z. Yang, Cuicui Gao, Xin Fu, Wen Zhang, Qian Zhou, Wanpeng Chen, et al. "A hypothalamic circuit that controls body temperature." Proceedings of the National Academy of Sciences 114, no. 8 (January 4, 2017): 2042–47. http://dx.doi.org/10.1073/pnas.1616255114.

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The homeostatic control of body temperature is essential for survival in mammals and is known to be regulated in part by temperature-sensitive neurons in the hypothalamus. However, the specific neural pathways and corresponding neural populations have not been fully elucidated. To identify these pathways, we used cFos staining to identify neurons that are activated by a thermal challenge and found induced expression in subsets of neurons within the ventral part of the lateral preoptic nucleus (vLPO) and the dorsal part of the dorsomedial hypothalamus (DMD). Activation of GABAergic neurons in the vLPO using optogenetics reduced body temperature, along with a decrease in physical activity. Optogenetic inhibition of these neurons resulted in fever-level hyperthermia. These GABAergic neurons project from the vLPO to the DMD and optogenetic stimulation of the nerve terminals in the DMD also reduced body temperature and activity. Electrophysiological recording revealed that the vLPO GABAergic neurons suppressed neural activity in DMD neurons, and fiber photometry of calcium transients revealed that DMD neurons were activated by cold. Accordingly, activation of DMD neurons using designer receptors exclusively activated by designer drugs (DREADDs) or optogenetics increased body temperature with a strong increase in energy expenditure and activity. Finally, optogenetic inhibition of DMD neurons triggered hypothermia, similar to stimulation of the GABAergic neurons in the vLPO. Thus, vLPO GABAergic neurons suppressed the thermogenic effect of DMD neurons. In aggregate, our data identify vLPO→DMD neural pathways that reduce core temperature in response to a thermal challenge, and we show that outputs from the DMD can induce activity-induced thermogenesis.

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Liu, Yu-Wei, Jing Li, and Jiang-Hong Ye. "Histamine regulates activities of neurons in the ventrolateral preoptic nucleus." Journal of Physiology 588, no. 21 (October 29, 2010): 4103–16. http://dx.doi.org/10.1113/jphysiol.2010.193904.

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Dubourget, Romain, Aude Sangare, Hélène Geoffroy, Thierry Gallopin, and Armelle Rancillac. "Multiparametric characterization of neuronal subpopulations in the ventrolateral preoptic nucleus." Brain Structure and Function 222, no. 3 (July 8, 2016): 1153–67. http://dx.doi.org/10.1007/s00429-016-1265-2.

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Saint-Mleux, B., L. Bayer, E. Eggermann, B. E. Jones, M. Muhlethaler, and M. Serafin. "Suprachiasmatic Modulation of Noradrenaline Release in the Ventrolateral Preoptic Nucleus." Journal of Neuroscience 27, no. 24 (June 13, 2007): 6412–16. http://dx.doi.org/10.1523/jneurosci.1432-07.2007.

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Eikermann, Matthias, Ramalingam Vetrivelan, Martina Grosse-Sundrup, Mark E. Henry, Ulrike Hoffmann, Shigefumi Yokota, Clifford B. Saper, and Nancy L. Chamberlin. "The ventrolateral preoptic nucleus is not required for isoflurane general anesthesia." Brain Research 1426 (December 2011): 30–37. http://dx.doi.org/10.1016/j.brainres.2011.10.018.

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Greco, Mary-Ann, Patrick M. Fuller, Thomas C. Jhou, S. Martin-Schild, James E. Zadina, Zhian Hu, Priyattam Shiromani, and Jun Lu. "Opioidergic projections to sleep-active neurons in the ventrolateral preoptic nucleus." Brain Research 1245 (December 2008): 96–107. http://dx.doi.org/10.1016/j.brainres.2008.09.043.

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McCarren, Hilary S., Michael R. Chalifoux, Bo Han, Jason T. Moore, Qing Cheng Meng, Nina Baron-Hionis, Madineh Sedigh-Sarvestani, Diego Contreras, Sheryl G. Beck, and Max B. Kelz. "α2-Adrenergic Stimulation of the Ventrolateral Preoptic Nucleus Destabilizes the Anesthetic State." Journal of Neuroscience 34, no. 49 (December 3, 2014): 16385–96. http://dx.doi.org/10.1523/jneurosci.1135-14.2014.

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Gaus, S. E., R. E. Strecker, B. A. Tate, R. A. Parker, and C. B. Saper. "Ventrolateral preoptic nucleus contains sleep-active, galaninergic neurons in multiple mammalian species." Neuroscience 115, no. 1 (November 2002): 285–94. http://dx.doi.org/10.1016/s0306-4522(02)00308-1.

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Walter, Augustin, Lorijn van der Spek, Eléonore Hardy, Alexis Pierre Bemelmans, Nathalie Rouach, and Armelle Rancillac. "Structural and functional connections between the median and the ventrolateral preoptic nucleus." Brain Structure and Function 224, no. 9 (September 6, 2019): 3045–57. http://dx.doi.org/10.1007/s00429-019-01935-4.

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Lu, J., P. Shiromani, and C. B. Saper. "Retinal input to the sleep-active ventrolateral preoptic nucleus in the rat." Neuroscience 93, no. 1 (June 1999): 209–14. http://dx.doi.org/10.1016/s0306-4522(99)00094-9.

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Marson, L., and A. Z. Murphy. "Identification of neural circuits involved in female genital responses in the rat: a dual virus and anterograde tracing study." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 2 (August 2006): R419—R428. http://dx.doi.org/10.1152/ajpregu.00864.2005.

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The spinal and peripheral innervation of the clitoris and vagina are fairly well understood. However, little is known regarding supraspinal control of these pelvic structures. The multisynaptic tracer pseudorabies virus (PRV) was used to map the brain neurons that innervate the clitoris and vagina. To delineate forebrain input on PRV-labeled cells, the anterograde tracer biotinylated dextran amine was injected in the medial preoptic area (MPO), ventromedial nucleus of the hypothalamus (VMN), or the midbrain periaqueductal gray (PAG) 10 days before viral injections. These brain regions have been intimately linked to various aspects of female reproductive behavior. After viral injections (4 days) in the vagina and clitoris, PRV-labeled cells were observed in the paraventricular nucleus (PVN), Barrington’s nucleus, the A5 region, and the nucleus paragigantocellularis (nPGi). At 5 days postviral administration, additional PRV-labeled cells were observed within the preoptic region, VMN, PAG, and lateral hypothalamus. Anterograde labeling from the MPO terminated among PRV-positive cells primarily within the dorsal PVN of the hypothalamus, ventrolateral VMN (VMNvl), caudal PAG, and nPGi. Anterograde labeling from the VMN terminated among PRV-positive cells in the MPO and lateral/ventrolateral PAG. Anterograde labeling from the PAG terminated among PRV-positive cells in the PVN, ventral hypothalamus, and nPGi. Transynaptically labeled cells in the lateral hypothalamus, Barrington’s nucleus, and ventromedial medulla received innervation from all three sources. These studies, together, identify several central nervous system (CNS) sites participating in the neural control of female sexual responses. They also provide the first data demonstrating a link between the MPO, VMNvl, and PAG and CNS regions innervating the clitoris and vagina, providing support that these areas play a major role in female genital responses.

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Shiromani, Priyattam J., Jun Lu, Dean Wagner, Jolleyin Thakkar, Mary Ann Greco, Radhika Basheer, and Mahesh Thakkar. "Compensatory sleep response to 12 h wakefulness in young and old rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 1 (January 1, 2000): R125—R133. http://dx.doi.org/10.1152/ajpregu.2000.278.1.r125.

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There is a pronounced decline in sleep with age. Diminished output from the circadian oscillator, the suprachiasmatic nucleus, might play a role, because there is a decrease in the amplitude of the day-night sleep rhythm in the elderly. However, sleep is also regulated by homeostatic mechanisms that build sleep drive during wakefulness, and a decline in these mechanisms could also decrease sleep. Because this question has never been addressed in old animals, the present study examined the effects of 12 h wakefulness on compensatory sleep response in young (3.5 mo) and old (21.5 mo) Sprague-Dawley and F344 rats. Old rats in both strains had a diminished compensatory increase in slow-wave sleep (SWS) after 12 h of wakefulness (0700–1900, light-on period) compared with the young rats. In contrast, compensatory REM sleep rebound was unaffected by age. To assess whether the reduced SWS rebound in old rats might result from loss of neurons implicated in sleep generation, we counted the number of c-Fos immunoreactive (c-Fos-ir) cells in the ventral lateral preoptic (VLPO) area and found no differences between young and old rats. These findings indicate that old rats, similar to elderly humans, demonstrate less sleep after prolonged wakefulness. The findings also indicate that although old rats have a decline in sleep, this cannot be attributed to loss of VLPO neurons implicated in sleep.

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Lu, Jun, Mary Ann Greco, Priyattam Shiromani, and Clifford B. Saper. "Effect of Lesions of the Ventrolateral Preoptic Nucleus on NREM and REM Sleep." Journal of Neuroscience 20, no. 10 (May 15, 2000): 3830–42. http://dx.doi.org/10.1523/jneurosci.20-10-03830.2000.

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Fernando, Antonio, and Gerald Chew. "Acute Sleep Onset Insomnia in the Elderly: Damage to the Ventrolateral Preoptic Nucleus?" Australasian Psychiatry 13, no. 3 (September 2005): 313–14. http://dx.doi.org/10.1080/j.1440-1665.2005.2208_4.x.

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LUPPI, PH, T. GALLOPIN, B. CAULI, J. ROSSIER, B. LAMBOLEZ, and P. FORT. "In vitro study of the sleep promoting neurons from the ventrolateral preoptic nucleus." Sleep and Biological Rhythms 2, s1 (May 2004): S23—S24. http://dx.doi.org/10.1111/j.1479-8425.2004.00095.x.

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Lu, Jun, Alvhild A. Bjorkum, Man Xu, Stephanie E. Gaus, Priyattam J. Shiromani, and Clifford B. Saper. "Selective Activation of the Extended Ventrolateral Preoptic Nucleus during Rapid Eye Movement Sleep." Journal of Neuroscience 22, no. 11 (June 1, 2002): 4568–76. http://dx.doi.org/10.1523/jneurosci.22-11-04568.2002.

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Castañeyra-Ruiz, Leandro, Ibrahim González-Marrero, Agustín Castañeyra-Ruiz, Juan M. González-Toledo, María Castañeyra-Ruiz, Héctor de Paz-Carmona, Agustín Castañeyra-Perdomo, and Emilia M. Carmona-Calero. "Luteinizing Hormone-Releasing Hormone Distribution in the Anterior Hypothalamus of the Female Rats." ISRN Anatomy 2013 (May 9, 2013): 1–6. http://dx.doi.org/10.5402/2013/870721.

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Luteinizing hormone-releasing hormone (LHRH) neurons and fibers are located in the anteroventral hypothalamus, specifically in the preoptic medial area and the organum vasculosum of the lamina terminalis. Most luteinizing hormone-releasing hormone neurons project to the median eminence where they are secreted in the pituitary portal system in order to control the release of gonadotropin. The aim of this study is to provide, using immunohistochemistry and female brain rats, a new description of the luteinizing hormone-releasing hormone fibers and neuron localization in the anterior hypothalamus. The greatest amount of the LHRH immunoreactive material was found in the organum vasculosum of the lamina terminalis that is located around the anterior region of the third ventricle. The intensity of the reaction of LHRH immunoreactive material decreases from cephalic to caudal localization; therefore, the greatest immunoreaction is in the organum vasculosum of the lamina terminalis, followed by the dorsomedial preoptic area, the ventromedial preoptic area, and finally the ventrolateral medial preoptic area, and in fibers surrounding the suprachiasmatic nucleus and subependymal layer on the floor of the third ventricle where the least amount immunoreactive material is found.

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Yáñez, Julián, Maider Hernández Eguiguren, and Ramón Anadón. "Neural connections of the torus semicircularis in the adult Zebrafish." Journal of Comparative Neurology 532, no. 1 (January 2024): 1–19. http://dx.doi.org/10.1002/cne.25586.

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AbstractThe torus semicircularis (TS) of teleosts is a key midbrain center of the lateral line and acoustic sensory systems. To characterize the TS in adult zebrafish, we studied their connections using the carbocyanine tracers applied to the TS and to other related nuclei and tracts. Two main TS nuclei, central and ventrolateral, were differentiable by their afferent connections. From central TS, (TSc) numerous toropetal cells were labeled bilaterally in several primary octaval nuclei (anterior, magnocellular, descending, and posterior octaval nuclei), in the secondary octaval nucleus, in the caudal octavolateralis nucleus, and in the perilemniscular region. In the midbrain, numerous toropetal cells were labeled in the contralateral TSc. In the diencephalon, toropetal cells labeled from the TSc were observed ipsilaterally in the medial prethalamic nucleus and the periventricular posterior tubercle nucleus. TSc toropetal neurons were also labeled bilaterally in the hypothalamic anterior tuberal nucleus (ATN) and ipsilaterally in the parvicellular preoptic nucleus but not in the telencephalon. Tracer application to the medial octavolateralis nucleus revealed contralateral projections to the ventrolateral TS (TSvl), whereas tracer application to the secondary octaval nucleus labeled fibers bilaterally in TSc and neurons in rostral TSc. The TSc sends ascending fibers to the ipsilateral lateral preglomerular region that, in turn, projects to the pallium. Application of DiI to the optic tectum labeled cells and fibers in the TSvl, whereas application of DiI to the ATN labeled cells and fibers in the TSc. These results reveal that the TSvl and TSc are mainly related with the mechanosensory lateral line and acoustic centers, respectively, and that they show different higher order connections.

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Venner, A., and P. M. Fuller. "0163 Investigating the Role of Vasoactive Intestinal Peptide-Containing Neurons of the Ventromedal Preoptic Area in Sleep-Wake Control." Sleep 43, Supplement_1 (April 2020): A64. http://dx.doi.org/10.1093/sleep/zsaa056.161.

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Abstract Introduction A role for vasoactive intestinal peptide (VIP) in promoting rapid eye movement (REM) sleep has been suggested, but the anatomical location of the neurons that release VIP to promote REM sleep has not been identified. Here, we investigated the role of VIP-containing cell groups in the ventromedial preoptic area (VMPOVIP) in sleep-wake regulation. The VMPO has also previously been implicated in thermoregulation and the febrile response. Methods We first investigated the native firing activity of VMPOVIP neurons, over repeated sleep-wake cycles, using in vivo fiber photometry in VIP-ires-Cre mice. We next examined the afferent and efferent profile of this cell group using conditional retrograde (pseudotyped modified rabies) and anterograde (adeno-associated viral vector-based) tracers. We finally utilized a chemogenetic strategy to selectively activate VMPOVIP neurons cells while monitoring electroencephalogram/electromyogram activity and core body temperature, in order to determine their role in sleep-wake and thermoregulatory control. Results We found that VMPOVIP cells were predominantly and strikingly REM-active, that they received many synaptic inputs from surrounding hypothalamic regions (including the ventromedial hypothalamus, dorsomedial hypothalamus and the arcuate nucleus), and that they targeted established sleep-wake nodes, such as the ventrolateral preoptic nucleus, tuberomammillary nucleus, lateral hypothalamus and ventrolateral periaqueductal gray area. To our surprise, chemogenetic activation of the VMPOVIP cell population had little effect upon all measures of sleep-wake analysed and no effect upon core body temperature. Conclusion We conclude that VMPOVIP neurons do not promote REM sleep per se. However, their REM-active profile and anatomical connectivity suggest that these neurons may play a functional role in generating certain cardinal features of REM sleep, which is an active focus of on-going research in our laboratory. Support SRSF CDA #016-JP-17 to A.V. and NS073613, NS092652 and NS103161 to P.M.

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Sun, X., S. Whitefield, B. Rusak, and K. Semba. "Electrophysiological analysis of suprachiasmatic nucleus projections to the ventrolateral preoptic area in the rat." European Journal of Neuroscience 14, no. 8 (October 2001): 1257–74. http://dx.doi.org/10.1046/j.0953-816x.2001.0001755.x.

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Liu, Yu-Wei, Wanhong Zuo, and Jiang-Hong Ye. "Propofol Stimulates Noradrenalin-Inhibited Neurons in the Ventrolateral Preoptic Nucleus by Reducing GABAergic Inhibition." Anesthesia & Analgesia 117, no. 2 (August 2013): 358–63. http://dx.doi.org/10.1213/ane.0b013e318297366e.

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Deurveilher, Samuel, Joan Burns, and Kazue Semba. "Indirect projections from the suprachiasmatic nucleus to the ventrolateral preoptic nucleus: a dual tract-tracing study in rat." European Journal of Neuroscience 16, no. 7 (October 2002): 1195–213. http://dx.doi.org/10.1046/j.1460-9568.2002.02196.x.

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Arrigoni, Elda, Jun Lu, Ramalingam Vetrivelan, and Clifford B. Saper. "Long-term synaptic plasticity is impaired in rats with lesions of the ventrolateral preoptic nucleus." European Journal of Neuroscience 30, no. 11 (December 2009): 2112–20. http://dx.doi.org/10.1111/j.1460-9568.2009.07001.x.

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Journal articles on the topic 'Ventrolateral preoptic nucleus (VLPO)'

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