Birendra Nath Mallick

Learn More
Rapid eye movement (REM) sleep loss impairs several physiological, behavioral and cellular processes; however, the mechanism of action was unknown. To understand the effects of REM sleep deprivation on neuronal damage and apoptosis, studies were conducted using multiple apoptosis markers in control and experimental rat brain neurons located in areas either(More)
In this study we have constructed a mathematical model of a recently proposed functional model known to be responsible for inducing waking, NREMS and REMS. Simulation studies using this model reproduced sleep-wake patterns as reported in normal animals. The model helps to explain neural mechanism(s) that underlie the transitions between wake, NREMS and REMS(More)
The noradrenergic "REM-off" neurons in the locus coeruleus cease firing, whereas some cholinergic and non-cholinergic "REM-on" neurons increase firing during rapid eye movement sleep. A reciprocal interaction between these neurons was proposed. However, acetylcholine did not inhibit neurons in the locus coeruleus. Nevertheless, since GABA levels increase(More)
Pedunculopontine tegmentum (PPT) has GABA-ergic neurons and receives GABA-ergic projections from substantia nigra pars reticulata (SNrpr). Based on the recent studies from our and other laboratories, it was hypothesized that GABA in PPT promotes rapid eye movement (REM) sleep. In order to further study the role of GABA in PPT in REM sleep regulation, we(More)
Rapid eye movement (REM) sleep deprivation elevates noradrenaline level, which upon acting on alpha1-adrenoceptors increases Na-K-ATPase activity; however, the detailed intracellular mechanism of action was unknown. Since membrane integrity is crucial for maintaining Na-K-ATPase activity as well as ionic exchange and noradrenaline affects membrane(More)
Rapid eye movement sleep deprivation is reported to increase Na+,K+-ATPase activity. This increase was shown earlier to be stimulated by norepinephrine acting on alpha1-adrenoceptor. The involvement of a subtype of alpha1-adrenoceptor and the possible molecular mechanism of action of norepinephrine in increasing the enzyme activity were investigated using(More)
The preoptic area is known to regulate sleep-wakefulness and body temperature. It was suggested earlier that though sleep-wakefulness and body temperature may affect each other, the preoptic area mediated influence on those two physiological phenomena is likely to be independent of alteration in each other. Since intrapreoptic area norepinephrine could(More)
Norepinephrine, acetylcholine and GABA levels alter during rapid eye movement (REM) sleep and its deprivation. Increased synthesis of those neurotransmitters is necessary for their sustained release. Hence, in this study, the concentrations of tyrosine hydroxylase (TH), choline acetyl transferase (ChAT) and glutamic acid decarboxylase (GAD), the enzymes(More)
The norepinephrinergic neurons in the locus coeruleus (LC) cease firing during REM sleep (REMS) and increase firing during REMS deprivation. Most of the earlier studies used lesion and transection techniques which could not confirm the role of LC in REMS generation and/or its maintenance, if at all. Hence, in this study it was hypothesized that if the LC(More)
Ever since the discovery of rapid eye movement sleep (REMS), studies have been undertaken to understand its necessity, function and mechanism of action on normal physiological processes as well as in pathological conditions. In this review, first, we briefly surveyed the literature which led us to hypothesise REMS maintains brain excitability. Thereafter,(More)