China
Africa
Explore chapters and articles related to this topic
The neurobiology of sleep
Published in Philip N. Murphy, The Routledge International Handbook of Psychobiology, 2018
Roman Rutka, Sonia Pellissier, Pascal Hot
As described above, wakefulness is made possible by the activity of specific brain structures. This activity must therefore be inhibited to allow sleep onset, and a number of mechanisms may be involved. In the anterior part of the hypothalamus, several groups of neurons are selectively active during sleep. Some of these groups are clustered in the median preoptic nucleus (MnPO), which is thought to have an important role in triggering sleep onset. Moreover, an estimated 40% of the MnPO’s neurons use the well-known inhibitory neurotransmitter gamma aminobutyric acid (GABA) (Gong et al., 2004; Gvilia, Angara, McGinty, & Szymusiak, 2005). These neurons are connected to several wake-promoting regions, including the locus coeruleus and the dorsal raphe nucleus; the results of animal studies have confirmed that the MnPO’s neurons can inhibit these structures (Suntsova et al., 2007). These data support the hypothesis whereby the MnPO is responsible for sleep onset (Suntsova, Szymusiak, Alam, Guzman-Marin, & McGinty, 2002). Even though it has been proposed that the MnPO’s only hypnic function is to trigger sleep onset, Benedetto and colleagues found that pharmacological inhibition of this structure not only prevents NREM sleep but also inhibits REM sleep and promotes awakening in sleeping cats (Benedetto, Chase, & Torterolo, 2012). Therefore, it is currently thought that the MnPO promotes both sleep onset and sleep maintenance.
Neuropsychiatric Aspects of Vestibular Disorders
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Julius Bourke, Georgia Jackson, Gerald Libby
Functional connectivity between the vestibular nuclei and hippocampus is also of importance. Animal models have suggested that this connectivity is a potential link between vestibular lesions and the cognitive deficits seen in patients affected by them,63,64 with long-term non-spatial memory deficits arising in rats after bilateral (but not unilateral) vestibulectomy.65 A small case control series has provided support for this in humans, with hippocampal down-regulation in patients with bilateral vestibular lesions as compared to healthy controls, suggesting that functional hippocampal deficits occur as a consequence of a chronic lack of vestibular input.66 It has been proposed that anxiety disorders arising in the context of vestibular disorders occur as an indirect consequence of these cognitive deficits.43 However, research in this area is contradictory67 and, given that the dorsal raphe nucleus innervates limbic structures, including amygdala, in addition to vestibular nuclei,48,68 it is possible that affective aberrations directly influence vestibular networks, while the contribution of the vestibular system to autonomic control69,70 may explain how vestibular dysfunction gives rise to anxiety.71 This interaction between networks, affective tone modulating vestibular function versus vestibular function affecting autonomic tone, has the potential to explain why vestibular complaints are common in psychiatric disorders and why psychopathology is common in vestibulopathy.
Can Physical Activity Prevent or Treat Clinical Depression? 1
Published in Henning Budde, Mirko Wegner, The Exercise Effect on Mental Health, 2018
Nanette Mutrie, Katie Richards, Stephen Lawrie, Gillian Mead
Neurotransmitters are biochemical substances that send signals from one nerve cell to another. Monoamines are a group of neurotransmitters thought to play a critical role in the regulation of emotions and in the treatment of depression (Dunn & Dishman 1991). Long-term voluntary exercise in rats leads to an increased expression of monoamines in the locus coeruleus (LC) and dorsal raphe nucleus (DRN), and these increases are accompanied by a reduction in depressive behaviors (Dishman et al. 1997; Kim, Lim, Baek, Ryu, & Seo 2015). In humans, brain monoamine activity is indirectly estimated from blood and urine, and evidence is mixed as to whether exercise leads to an increase in monoamine metabolites or not (Dunn & Dishman 1991).
Voluntary wheel running promotes resilience to the behavioral effects of unpredictable chronic mild stress in male and female mice
Published in Stress, 2023
Elias Elias, Ariel Y. Zhang, Abigail G. White, Matthew J. Pyle, Melissa T. Manners
One mechanism by which exercise improves brain function is by modulating serotonin. Serotonin levels are affected by both voluntary and forced exercise paradigms, with reports indicating either increased or decreased activity and behavioral effects (Clark et al., 2015; Lin & Kuo, 2013). Forced exercise can be acutely stressful, but may have long-term protective effects which can differentially affect the 5-HT system in specific brain regions. Neurons that project from the dorsal raphe nucleus to the medial pre-frontal cortex (mPFC) are involved in regulating behaviors associated with depression (Warden et al., 2012), however, lesions of the mPFC had no effect on diminishing the protective potential of VWR (Greenwood et al., 2013). More investigation is necessary to determine the role of the serotonergic circuit in the mPFC in conferring the protective effects of exercise, and if this circuit is differentially affected in females versus males (Fallon et al., 2020; Tanner et al., 2019).
Pindolol potentiates the antidepressant effect of venlafaxine by inhibiting 5-HT1A receptor in DRN neurons of mice
Published in International Journal of Neuroscience, 2021
Serotonin (5-HT) has major roles in the regulation of mood, appetite, sleep and memory in CNS [1]. Decreases in the level of 5-HT, which is synthesized by the serotonergic neurons of the raphe nuclei, results in some psychiatric conditions like major depression (MD). Especially, the dorsal raphe nucleus (DRN) among the raphe nuclei sends serotonergic projections to limbic system and regulate mood. Clarification of synthesis, oscillation and reuptake processes of 5-HT in the DRN has importance to find better and more effective cures of mood disorders. MD is one of the most common psychiatric disorders [2]. It ranks second in the life-long burden of disease in developed countries and is expected to rank first by 2030 [3]. MD is mainly caused by decreased level of 5-HT in neurosynaptic junction between serotonergic raphe nuclei neurons and postsynaptic neurons in brain [4]. Increases in the number of presynaptic somatodendritic 5-HT1A autoreceptors in the raphe nuclei as well as decreases in the number of postsynaptic 5-HT1A receptors augment the risk of MD [5].
Updated review on the link between cortical spreading depression and headache disorders
Published in Expert Review of Neurotherapeutics, 2021
Doga Vuralli, Hulya Karatas, Muge Yemisci, Hayrunnisa Bolay
There is a complex and poorly understood relationship between sleep hygiene changes and migraine. Migraineurs report deprived sleep as a precipitating factor of an attack. Sleep disturbances also have an important role in the development and persistence of chronic migraine [85]. Serotonin (5-HT), which affects many human behaviors including sleep, mood, appetite, sexual function, and pain, may have a key role in triggering migraine. From sleep perspective, serotonin promotes wakefulness and inhibits rapid eye movement (REM) sleep and clinical studies showed that migraine patients have low serotonin levels interictally and increased levels during an attack [86]. Migraineurs having attacks associated with unhygienic sleep experience increased awakenings in the night preceding headache [87]. It is not known how increased 5-HT levels are involved in the trigeminovascular nociceptive pathway. However, rats with low 5-HT levels have increased numbers of CSD waves [86]. The dorsal raphe nucleus in the pons and midbrain produces 5-HT. The dorsal raphe nucleus has a crucial role in sleep and the cessation of the serotonergic neuron firing initiates REM [88]. Migraine patients may also have subcortical serotoninergic system dysfunction resulting in unhygienic sleep [89].