Effect of rapid eye movement sleep deprivation on rat brain monoamine oxidases
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REM sleep loss increases brain excitability: Role of noradrenalin and its mechanism of action
2011, Sleep Medicine ReviewsCitation Excerpt :Although we do not have direct evidence of elevated NA in the brain after REMSD, for example, by estimating brain NA level before, during and after REMSD, we will observe as we go along that all associated findings and circumstantial evidence support this contention. Monoamine oxidase-A (MAO-A), which degrades NA, decreases in the brain upon REMSD and thus, would contribute towards the elevation of NA levels in the brain upon REMSD.116 Further, initially, the neurons would release the NA already stored in the neuronal presynaptic terminal; however, for sustained release of NA, the synthesis of NA in the neurons must proportionately increase upon REMSD.
Hypobaric hypoxia modulates brain biogenic amines and disturbs sleep architecture
2011, Neurochemistry InternationalCitation Excerpt :However, there is hardly any information available on neurotransmitter mechanisms regulating sleep in HH. Neurotransmitters of the brain stem region are key regulators of sleep-wakefulness cycle (Thakkar and Mallick, 1993). It is reported that REM sleep deprivation stimulates neuronal and inhibits glial Na-K ATPase and these changes are mediated by NE via α1 adrenoceptors (Baskey et al., 2009).
Noradrenaline involvement in basic and higher integrated REM sleep processes
2008, Progress in NeurobiologyNoradrenaline acting on α1-adrenoceptor mediates REM sleep deprivation-induced increased membrane potential in rat brain synaptosomes
2008, Neurochemistry InternationalIncreased apoptosis in rat brain after rapid eye movement sleep loss
2006, NeuroscienceCitation Excerpt :Although the detailed mechanism of neuronal apoptosis after REMSD needs further study, increased NE could be a possible candidate for inducing such effects (Fu et al., 2004). The level of NE increases in the brain after REMSD because i) noradrenergic neurons in LC are continuously active (Mallick et al., 1990) unlike during normal REM sleep when they cease activity (Hobson et al., 1975; Aston-Jones and Bloom, 1981); ii) NE levels increase (Porkka-Heiskanen et al., 1995; Shouse et al., 2000); iii) NE synthetic machinery viz. tyrosine hydroxylase (TH) (Majumdar and Mallick, 2003) and its mRNA are activated (Basheer et al., 1998); iv) NE degrading enzyme, monamine oxidase-A, is inhibited (Thakkar and Mallick, 1993); v) such increased NE is responsible for REMSD induced increased Na+,K+-ATPase activity (Gulyani and Mallick, 1995; Mallick et al., 2000; Majumdar et al., 2003) as well as neuronal size and shape (Majumdar and Mallick, 2005); and vi) if the LC neurons were not allowed to be inhibited by electrical stimulation (Singh and Mallick, 1996) or by applying GABA blocker, picrotoxin, there was reduced REM sleep and increased Na+,K+-ATPase activity (Kaur et al., 2004) simulating REMSD. On the other hand, increased NE has been reported to facilitate apoptosis in rat (Communal et al., 1998) and ferret (Qin et al., 2001) cardiomyocytes, and cause cellular hypertrophy by increasing the levels of c-myc coded mRNA, which is reported to be responsible for cell proliferation (Starksen et al., 1986) and apoptosis (Pelengaris and Khan, 2003).