Waking state

Webster, HH and Jones, BE (1988) Neurotoxic lesions of the dorsalateral pontomesencephalic tegmentum-cholinergic cell area in the rat. II Effects upon sleep-waking states. Brain Res. 458 285-302. 

Cape EG and Jones, BE (1998) Differential modulation of high-frequency gamma-electroencephalogram activity and sleep-wake state by noradrenaline and serotonin microinjections into the region of cholinergic basalis neurons. J. Neurosci. 18 2653-2666. 

Sleepiness Wakefulness state in rats Increases waking [8]... 

Nitz, D. Siegel, J. M. (1997b). GABA release in the locus coeruleus as a function of sleep/wake state. Neuroscience 78, 795-801. 

Figure 2.4 Flip-flop switch model of wake and slow wave sleep active systems. Mutually inhibitory connections exist between GABAergic/Galaninergic slow wave sleep active neurons in the ventrolateral preoptic area (VLPO) of the anterior hypothalamus and aminergic neurons in the hypothalamus (histamine (HA) neurons in the tuberomammillary nucleus (TMN)) and brainstem (serotonin (5-HT) neurons in the dorsal raphe (DR) and noradrenaline (NA) neurons in the locus coeruleus (LC)). Orexinergic neurons in the perifornical hypothalamus (PFH) stabilize the waking state via excitation of the waking side of the flip-flop switch (aminergic neurons).

Cirelli, C., Pompeiano, M. Tononi, G. (1996). Neuronal gene expression in the waking state a role for the locus coeruleus. Science 274, 1211-15. 

Jones, B. E., Harper, S. T. Halaris, A. E. (1977). Effects of locus coeruleus lesions upon cerebral monoamine content, sleep-wakefulness states and the response to amphetamine in the cat. Brain Res. 124, 473-96. 

Holmes, C. J. Jones, B. E. (1994). Importance of cholinergic, GABAergic, serotonergic and other neurons in the medial medullary reticular formation for sleep-wake states studied by cytotoxic lesions in the cat. Neuroscience 62, 1179-200. 

Jones, B. (1993). The organization of central cholinergic systems and their functional importance in sleep-waking states. In Cholinergic Function and Dysfunction. Progress in Brain Research, ed. A. Cuello. Amsterdam Elsevier. 

Figure 7.2 Diurnal variation of extracellular dopamine in the non-human primate putamen. Dopamine concentrations (dm) as determined by high-pressure liquid chromatography of microdialysates obtained from the putamen of two rhesus monkeys across their 12 12 h lights-on (waking 7 00 am 7 00 pm) and lights off (sleep 7 00 pm-7 00 am) periods. Ten minute samples (2 pl/min sampling rate) were derived from nine individual 8 h sessions in each animal in which the sleep-wake state was monitored simultaneously by standard electrophysiological parameters.

Figure 7.4 Summary of some of the wide array of afferent and efferent connections of midbrain dopaminergic neurons (SN/A9, RRF/A8, and VTA/A10 in center of figure). This emphasizes their potential involvement in coordination of seemingly disparate behaviors inclusive of the sleep-wake state of the organism. Abbreviations BP, blood pressure BST, bed nucleus of the stria terminalis CEA, central nucleus of the amygdala MEA, midbrain extrapyramidal area NTS, nucleus of the solitary tract O2, oxygen tension PPN, pedunculopontine tegmental nucleus RRF, retrorubral field SN, substantia nigra VTA, ventral tegmental area.

Sleep-wake state alterations in PD can be broadly classified into disturbances of (1) thalamocortical arousal state and (2) excessive nocturnal movement (Rye and Bliwise 2004 Rye and Iranzo 2005). The former includes the loss of sleep spindles and SWS, daytime sleepiness, and intrusion of REM sleep into daytime naps (i.e. sleep onset REM periods, or SOREMs), and the latter encompass periodic leg movements of sleep (PLMs) and REM sleep behavior disorder (RBD). The pathophysiological basis of sleepiness and SOREMs appears to be dopaminergic cell loss in PD, though excessive nocturnal movements are not as clearly related to dopaminergic deficits. 

Rye D. B Jankovic J. (2002). Emerging views of dopamine in modulating sleep/wake state from an unlikely source PD. Neurology 58(3), 341-6. 

Intoxication Development of a substance-specific syndrome after recent ingestion and presence in the body of a substance, and it is associated with maladaptive behavior during the waking state caused by the effect of the substance on the CNS. 

Jacobs, B. L., and Jones, B. E. (1978) The role of central monoamine and acetylcholine systems in sleep-wakefulness states Mediation or modulation In Cholinergic-Monoaminergic Interactions in the Brain, edited by L. Butcher, pp. 271-290. Academic Press, New York. 

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