Cellular and chemical neuroscience of mammalian sleep

Abstract

Extraordinary strides have been made toward understanding the complexities and regulatory mechanisms of sleep over the past two decades, thanks to the help of rapidly evolving technologies. At its most basic level, mammalian sleep is a restorative process of the brain and body. Beyond its primary restorative purpose, sleep is essential for a number of vital functions. Our primary research interest is to understand the cellular and molecular mechanisms underlying the regulation of sleep and its cognitive functions. Here I will reflect on our own research contributions to fifty years of extraordinary advances in the neurobiology of slow-wave sleep (SWS) and rapid eye movement (REM) sleep regulation. I conclude this review by suggesting some potential future directions to further our understanding of the neurobiology of sleep.

The effect of thiamin tetrahydrofurfuryl disulfide on behavior of juvenile DBA/2J mice

“…Thiamin-related cholinergic enhancement may also be involved in 563 regulation of circadian rhythm for reviews see (Datta, 2010;564 Rosenwasser, 2009;Turner et al, 2010), which could explain 565 differences observed here during the light/dark transition. Subclinical 566 dietary thiamin deficiency altered circadian rhythm in 6 week-old 567 C57BL/6J mice (Bennett and Schwartz, 1999).…”

Mechanisms underlying sleep–wake disturbances in alcoholism: Focus on the cholinergic pedunculopontine tegmentum

“…Sleep in mammals is not a homogenous behavioral state, but rather is a continuum of mixed states that differ in their physiology, chemistry, and phenomenological experiences [12, 13]. Because some human sleep stages are named differently from those in animals, and since the present description on the possible neurobiological mechanisms of AUD is based on animal research, the following text describes the similarities and differences between human sleep stages and those of animals.…”

“…This cyclic NREM-REM sleeps epochs in rodents and cats continue throughout the day and night, except when the animal is engaged in activities that require wakefulness. In humans, NREM sleep is further subdivided into four stages (I, II, III and IV), each corresponding to an increasing depth of sleep [12, 13]. NREM Stage one (NREM-I) sleep is characterized by relatively low-amplitude (<50 µV) theta frequency activity (4–7 cycles per second (Hz) and vertex sharp waves in the EEG.…”

“…SWS-II is considered deep sleep and is identified by the presence of high-amplitude, low frequency waves in the cortical EEG (delta sleep). Human NREM stages I and II sleep are comparable to mouse, rat, and cat SWS-I, whereas stages III and IV NREM sleep in humans are comparable to the animal SWS-II [12, 13]. …”

“…Ethanol also increases the activity of GABA receptors by facilitating the release of GABA and by elevating levels of neuroactive steroids that act to positively modulate GABA A receptor systems [128, 129]. Also, both GABA and glutamate receptors are involved in the regulation of S-W states [12, 13, 81, 130–138], specifically: a) Increased release of GABA from the preoptic-hypothalamic areas (POA) activates GABA receptors (mainly GABA A -type) on the neurons in the W-promoting areas of the brain that ultimately induce SWS (for details of this mechanism, see [12]); b) Activation of GABA B receptors on pedunculopontine tegmental (PPT) cholinergic cells suppresses neuronal activity, which in turn suppresses both REM sleep and W [135, 138]; c) Inhibition of NMDA-type glutamate receptors on PPT cholinergic cells suppresses W and inhibition of kainate-type receptors suppresses REM sleep [130–133]. Therefore, it is logical to suggest that the primary causal mechanisms of acute alcohol consumption-induced increased SWS could be the inhibition of W-promoting neurons via activation of GABA A receptors, whereas decreased REM sleep could be caused by the activation of GABA B receptors and/or inhibition of kainate-type of glutamate receptors on PPT cholinergic cells.…”