Cholinergic neurons of the basal forebrain mediate biochemical and electrophysiological mechanisms underlying sleep homeostasis.

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Bibliographic Details
Title:	Cholinergic neurons of the basal forebrain mediate biochemical and electrophysiological mechanisms underlying sleep homeostasis.
Authors:	Kalinchuk, Anna V., Porkka-Heiskanen, Tarja, McCarley, Robert W., Basheer, Radhika
Source:	European Journal of Neuroscience. Jan2015, Vol. 41 Issue 2, p182-195. 14p.
Subjects:	Cholinergic mechanisms, Neurons, Prosencephalon, Biochemistry, Electrophysiology, Homeostasis, Nitric-oxide synthases
Abstract:	The tight coordination of biochemical and electrophysiological mechanisms underlies the homeostatic sleep pressure ( HSP) produced by sleep deprivation ( SD). We have reported that during SD the levels of inducible nitric oxide synthase (i NOS), extracellular nitric oxide ( NO), adenosine [ AD]ex, lactate [ Lac]ex and pyruvate [ Pyr]ex increase in the basal forebrain ( BF). However, it is not clear whether all of them contribute to HSP leading to increased electroencephalogram ( EEG) delta activity during non-rapid eye movement ( NREM) recovery sleep ( RS) following SD. Previously, we showed that NREM delta increase evident during RS depends on the presence of BF cholinergic ( Ch BF) neurons. Here, we investigated the role of Ch BF cells in coordination of biochemical and EEG changes seen during SD and RS in the rat. Increases in low-theta power (5-7 Hz), but not high-theta (7-9 Hz), during SD correlated with the increase in NREM delta power during RS, and with the changes in nitrate/nitrite [ NOx]ex and [ AD]ex. Lesions of Ch BF cells using Ig G 192-saporin prevented increases in [ NOx]ex, [ AD]ex and low-theta activity, during SD, but did not prevent increases in [ Lac]ex and [ Pyr]ex. Infusion of NO donor DETA NONOate into the saporin-treated BF failed to increase NREM RS and delta power, suggesting Ch BF cells are important for mediating NO homeostatic effects. Finally, SD-induced i NOS was mostly expressed in Ch BF cells, and the intensity of iNOS induction correlated with the increase in low-theta activity. Together, our data indicate ChBF cells are important in regulating the biochemical and EEG mechanisms that contribute to HSP. [ABSTRACT FROM AUTHOR]
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Database:	Psychology and Behavioral Sciences Collection

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Abstract:	The tight coordination of biochemical and electrophysiological mechanisms underlies the homeostatic sleep pressure ( HSP) produced by sleep deprivation ( SD). We have reported that during SD the levels of inducible nitric oxide synthase (i NOS), extracellular nitric oxide ( NO), adenosine [ AD]ex, lactate [ Lac]ex and pyruvate [ Pyr]ex increase in the basal forebrain ( BF). However, it is not clear whether all of them contribute to HSP leading to increased electroencephalogram ( EEG) delta activity during non-rapid eye movement ( NREM) recovery sleep ( RS) following SD. Previously, we showed that NREM delta increase evident during RS depends on the presence of BF cholinergic ( Ch BF) neurons. Here, we investigated the role of Ch BF cells in coordination of biochemical and EEG changes seen during SD and RS in the rat. Increases in low-theta power (5-7 Hz), but not high-theta (7-9 Hz), during SD correlated with the increase in NREM delta power during RS, and with the changes in nitrate/nitrite [ NOx]ex and [ AD]ex. Lesions of Ch BF cells using Ig G 192-saporin prevented increases in [ NOx]ex, [ AD]ex and low-theta activity, during SD, but did not prevent increases in [ Lac]ex and [ Pyr]ex. Infusion of NO donor DETA NONOate into the saporin-treated BF failed to increase NREM RS and delta power, suggesting Ch BF cells are important for mediating NO homeostatic effects. Finally, SD-induced i NOS was mostly expressed in Ch BF cells, and the intensity of iNOS induction correlated with the increase in low-theta activity. Together, our data indicate ChBF cells are important in regulating the biochemical and EEG mechanisms that contribute to HSP. [ABSTRACT FROM AUTHOR]
ISSN:	0953816X
DOI:	10.1111/ejn.12766