Mesencephalic trigeminal nucleus (MTN) neurons innervate the stretch receptors of the jaw elevator muscles and periodontal ligament mechanoreceptors, Bruxism activates the MTN. We analyzed how MTN cells are structured, their anatomy and physiology, and the effects of their activation.To induce and maintain sleep, gamma-aminobutyric acid (GABA), an inhibitor neurotransmitter, is released from the ventro-lateral preoptic area of the hypothalamus and acts on the ascending reticular activating system (ARAS) nuclei. The GABA neurotrasmitter induces the entry of chlorine into cells, hyperpolarizing and inhibiting these. MTN cells, on the contrary, are depolarized by GABA, as their receptors are activated upon GABA binding. They "let out" chlorine and activate ARAS cells. MTN cells release glutamate, an excitatory neurotransmitter onto their target cells, in this case onto ARAS cells. During wakefulness, ARAS activation causes cerebral cortex activation; instead, during sleep (sleep bruxism), ARAS activation avoids an excessive reduction in ARAS neurotransmitters, including noradrenaline, dopamine, serotonin, acetylcholine and glutamate. These neurotransmitters, in addition to activating the cerebral cortex, modulate vital functions such as cardiac and respiratory functions. Polysomnography shows that sleep bruxism is always accompanied by cardiac and respiratory activation and, most importantly, by brain function activation. Bruxism is not a parafunction, and it functions to activate ARAS nuclei.

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Objective The purpose of this study is to examine the pathophysiology underlying sleep apnea (SA). Background We consider several critical features of SA including the roles played by the ascending reticular activating system (ARAS) that controls vegetative functions and electroencephalographic findings associated with both SA and normal sleep. We evaluate this knowledge together with our current understanding of the anatomy, histology, and physiology of the mesencephalic trigeminal nucleus (MTN) and mechanisms that contribute directly to normal and disordered sleep. MTN neurons express γ-aminobutyric acid (GABA) receptors which activate them (make chlorine come out of the cells) and that can be activated by GABA released from the hypothalamic preoptic area. Method We reviewed the published literature focused on sleep apnea (SA) reported in Google Scholar, Scopus, and PubMed databases. Results The MTN neurons respond to the hypothalamic GABA release by releasing glutamate that activates neurons in the ARAS. Based on these findings, we conclude that a dysfunctional MTN may be incapable of activating neurons in the ARAS, notably those in the parabrachial nucleus, and that this will ultimately lead to SA. Despite its name, obstructive sleep apnea (OSA) is not caused by an airway obstruction that prevents breathing. Conclusions While obstruction may contribute to the overall pathology, the primary factor involved in this scenario is the lack of neurotransmitters.

Aim: In this review paper we propose a method to make an early diagnosis of the Alzheimer's Disease (AD), the most common form of neurodegenerative dementia. Background: Glymphatic System (GS) is the main means of eliminating waste substances in the central nervous system (CNS); if it does not work properly, waste substances accumulate in CNS until to cause AD. Basal Forebrain is the most important component of a much broader system of cholinergic cells distributed throughout the Central Nervous System (CNS). This structure regulates attention, learning and memory and its destruction is considered responsible for the cognitive AD alterations. The characteristics of AD patients, that interest us most, are the lack of Acetylcholine, and the Orexin excess; we think that the hypothalamus produces more Orexin to stimulate cholinergic cells, indispensable for a correct CNS functioning. We want to identify these patients by detecting the Orexin excess. Early Diagnosis Model. Of course we could take a cerebrospinal fluid sample and dose Orexin but this method is risky and painful for the patient's health, therefore unsuitable for large numbers of patients. We propose a fairly simple method for the early diagnosis of AD: if we temporarily eliminate the Orexin excess, with Dual Orexin Receptor Antagonist (DORA), i.e. Suvorexant, we can intercept the Orexin increase and demonstrate the decrease in Acetylcholine with a Functional Magnetic Resonance or a Polysomnography, many years before the AD symptoms occur.