In the brain, the histaminergic (HAergic) neurons only gathered in the TMN. VLPO neurons send axons to many regions that are implicated in the regulation of wakefulness, including the locus coeruleus (LC), median raphe nuclei, and the tuberomammillary nucleus (TMN) ( Saper et al., 2010 Chung et al., 2017). More than 85% of the neurons in the VLPO region are GABAergic neurons, which co-express the inhibitory neurotransmitters GABA and galanin ( Sherin et al., 1996, 1998). Lesions of the VLPO reduced sleep time and caused insomnia in cats and rats ( Nauta, 1946 McGinty and Sterman, 1968 Lu et al., 2000). Chemoactivating and photoactivating galanin-expressing neurons promoted total sleep time (TST), while photoinhibiting galanin-expressing neurons decreased NREM sleep ( Kroeger et al., 2018). Extracellularly electrophysiological recording results show that VLPO neurons have more activation during sleep, and the firing rate significantly increased during paradoxical sleep ( Koyama and Hayaishi, 1994). It is believed that GABAergic neurons in the ventral lateral hypothalamus (VLPO) and central preoptic region are the basis for the occurrence and maintenance of sleep ( Sherin et al., 1996 Saper et al., 2010).
The inhibitory relationship between sleep and wakefulness systems work as a trigger for the rapid conversion of sleep and wakefulness in the form of a positive feedback-loop ( Wang et al., 2013). The sleep-wake cycle is controlled by homeostasis and circadian rhythm, which regulates the amount, and the time of sleep, respectively ( Borbely, 1982). In conclusion, VLPO GABAergic neurons and TMN histaminergic neurons may interact with each other in regulating the sleep-wake cycle. Those results reveal that TMN neuron activating may manipulate VLPO neurons via HRH 1, and induce wakefulness. These phenomena were reversed by blocking HRH 1 with Trip microinjected into VLPO. On the contrary, exciting TMN neurons by L-Glu during the day, the wakefulness time was significantly increased. Those results reveal that VLPO neurons activated, which may inhibit TMN neurons inducing sleep via GABA A receptors. Microinjecting L-Glu into VLPO during the night significantly increased the NREM sleep time, and this phenomenon was weakened after selectively blocking GABA A receptors with Bic microinjected into TMN. Here, bicuculline (Bic), a GABA A-receptor antagonist, L-glutamate ( L-Glu), an excitatory neurotransmitter, and triprolidine (Trip), a HA 1 receptor (HRH 1) inhibitor, were bilaterally microinjected into TMN or VLPO after surgically implanting the electroencephalogram (EEG) and electromyography (EMG) electrode recording system.
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Previous studies have shown that the two regions are innervated between each other, but how to regulate the sleep-wake cycle are not yet clear. Most of the VLPO neurons are sleep-promoting neurons, which co-express γ-aminobutyric acid (GABA) and galanin, while TMN neurons express histamine (HA), a key wake-promoting neurotransmitter. The ventrolateral preoptic nucleus (VLPO) in the anterior hypothalamus and the tuberomammillary nucleus (TMN) in the posterior hypothalamus are critical regions which involve the regulation of sleep-wakefulness flip-flop in the central nervous system.
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