Mechanism of noradrenaline-induced stimulation of Na–K ATPase activity in the rat brain: implications on REM sleep deprivation-induced increase in brain excitability

Mallick, Birendra Nath; Singh, Sudhuman; Singh, A. K.

doi:10.1007/s11010-009-0260-9

Cited by 16 publications

(6 citation statements)

References 133 publications

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“…In addition, it was shown that the increased expression of α1-NaKA was developmental and preceded the increased expression of NaV1.6 and ankyrin-G (Kaphzan et al, 2011). It has been shown that increased expression and activity of α1-NaKA lowers the resting membrane potential and induces a less excitable state (Brodie et al, 1987; Gadsby, 1984; Mallick et al, 2010; Silva et al, 2006). Moreover, it was shown that disrupting presynaptic input, which also decreases neuronal excitability results in AIS changes similar to what was observed in AS model mice (Kuba et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Genetic Reduction of the α1 Subunit of Na/K-ATPase Corrects Multiple Hippocampal Phenotypes in Angelman Syndrome

et al. 2013

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Summary Angelman syndrome (AS) is associated with symptoms that include autism, intellectual disability, motor abnormalities, and epilepsy. We recently showed that AS model mice have increased expression of the alpha1 subunit of Na/K-ATPase (α1-NaKA) in the hippocampus, which was correlated with increased expression of axon initial segment (AIS) proteins. Our developmental analysis revealed that the increase in α1-NaKA expression preceded those of the AIS proteins. Therefore, we hypothesized that α1-NaKA overexpression drives AIS abnormalities, and that by reducing its expression these and other phenotypes could be corrected in AS model mice. Herein we report the genetic normalization of α1-NaKA levels in AS model mice corrects multiple hippocampal phenotypes, including alterations in the AIS, aberrant intrinsic membrane properties, impaired synaptic plasticity, and memory deficits. These findings strongly suggest that increased expression of α1-NaKA plays an important role in a broad range of abnormalities in the hippocampus of AS model mice.

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Section: Introductionmentioning

confidence: 99%

Genetic Reduction of the α1 Subunit of Na/K-ATPase Corrects Multiple Hippocampal Phenotypes in Angelman Syndrome

et al. 2013

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“…NA is one of the key neurotransmitters involved in REMS regulation [14]; its level in the brain reduces during REMS [15] and increases during REMSD [3,16]. The NA-ergic neurons are predominantly concentrated in the LC of rats [17] and these neurons are primarily responsible for supplying most of the NA throughout the brain, including the dorsal raphe (DR), the main site for serotonergic neurons in the brain [18,19].…”

Section: Introductionmentioning

confidence: 99%

“…The DR neurons continue firing during REMS without atonia [21]. Further, since our previous studies have shown that REMSD-induced cytomorphometric changes in neurons were induced by NA [12] and that NA level increases in the brain after REMSD [16,22,23], we hypothesized that DR neurons also are likely to get affected by REMSD induced elevated levels of NA. Alzheimer's disease associated reduction in both REMS as well as serotonin level [24,25] supports our hypothesis.…”

Section: Introductionmentioning

confidence: 99%

Cytomorphometric changes in the dorsal raphe neurons after rapid eye movement sleep deprivation are mediated by noradrenalin in rats

2010

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ObjectivesThis study was carried out to investigate the effect of rapid eye movement sleep (REMS) deprivation (REMSD) on the cytomorphology of the dorsal raphe (DR) neurons and to evaluate the possible role of REMSD-induced increased noradrenalin (NA) in mediating such effects.MethodsRats were REMS deprived by the flowerpot method; free moving normal home cage rats, large platform and post REMS-deprived recovered rats were used as controls. Further, to evaluate if the effects were induced by NA, separate sets of experimental rats were treated (i.p.) with α1-adrenoceptor antagonist, prazosin (PRZ). Histomorphometric analysis of DR neurons in stained brain sections were performed in experimental and control rats; neurons in inferior colliculus (IC) served as anatomical control.ResultsThe mean size of DR neurons was larger in REMSD group compared to controls, whereas, neurons in the recovered group of rats did not significantly differ than those in the control animals. Further, mean cell size in the post-REMSD PRZ-treated animals was comparable to those in the control groups. IC neurons were not affected by REMSD.ConclusionsREMS loss has been reported to impair several physiological, behavioral and cellular processes. The mean size of the DR neurons was larger in the REMS deprived group of rats than those in the control groups; however, in the REMS deprived and prazosin treated rats the size was comparable to the normal rats. These results showed that REMSD induced increase in DR neuronal size was mediated by NA acting on α1-adrenoceptor. The findings suggest that the sizes of DR neurons are sensitive to REMSD, which if not compensated could lead to neurodegeneration and associated disorders including memory loss and Alzheimer's disease.

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“…Sleep can be categorized as non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep [55]. These states of sleep are identified and classified based on variouselectrophysiological signals electroencephalogram (EEG) recorded from the brain and neck as well as the eye muscles [39]. NREM sleep is known as slow wave sleep (SWS) due to its synchronous slow-oscillation of membrane potentials in neurons of neocortex area [49].…”

Section: Categories Of Sleepmentioning

confidence: 99%

“…NREM sleep is known as slow wave sleep (SWS) due to its synchronous slow-oscillation of membrane potentials in neurons of neocortex area [49]. REM sleep, being an important component of sleep, is also known as active sleep, desynchronized sleep, or paradoxical sleep and is characterised by a desynchronised pattern, high frequency low amplitude waves in electroencephalogram, rapid eye movements and atonia in antigravity muscles [39].…”

Section: Categories Of Sleepmentioning

confidence: 99%

The Potential Role of Nicotine in the Treatment of Learning and Memory Impairment after REM Sleep Deprivation

Long

Rashid

2015

JMRH

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Sleep deprivation has become a contributing factor to the world's health concerns such as cardiovascular disease, mental illness and inattentiveness in occupationand decision making. It can also disturb synaptic plasticity that can lead to learning and memory impairment. Therefore, boosting cholinergic activity using acetylcholine imitator that can be found in the tobacco plant, known as nicotine, is essential in reversing the negative influences of sleep loss in the brain. Thus, studies on the effects of nicotine treatment on molecular mechanisms and structural changes of hippocampal brain cells are vital in order to gain more understanding and to overcome the detrimental consequencesof learning and memory impairment related to sleep divest.

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Mechanism of noradrenaline-induced stimulation of Na–K ATPase activity in the rat brain: implications on REM sleep deprivation-induced increase in brain excitability

Cited by 16 publications

References 133 publications

Genetic Reduction of the α1 Subunit of Na/K-ATPase Corrects Multiple Hippocampal Phenotypes in Angelman Syndrome

Genetic Reduction of the α1 Subunit of Na/K-ATPase Corrects Multiple Hippocampal Phenotypes in Angelman Syndrome

Cytomorphometric changes in the dorsal raphe neurons after rapid eye movement sleep deprivation are mediated by noradrenalin in rats

The Potential Role of Nicotine in the Treatment of Learning and Memory Impairment after REM Sleep Deprivation

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