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References
Jones (1985); Steriade et al. (1990b, 1997a); Steriade (2001b, 2003a).
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Steriade et al. (1987a).
Bazhenov et al. (1999).
Paré et al. (1991); Curró Dossi et al. (1992b).
Timofeev and Steriade (1996). The relations between thalamic RE and TC cells have also been investigated in slices from the perigeniculate nucleus, the visual sector of RE nucleus (Bal et al., 1995a, b). In those in vitro studies, the spike-burst of RE neurons lasted for about 30 ms, while the IPSP generated in TC neurons by burst discharges in reticular neurons was about 130 ms in duration if it was followed by a rebound LTS, and about 150 ms in duration if it was not. The spike-burst in TC cells was about 10 ms in duration. These differences between spike-bursts crowning low-threshold spikes (LTSs) in RE and TC cells, displaying much longer duration in RE cells, corroborate data from in vivo recordings during natural sleep (Domich et al., 1986; Steriade et al., 1986).
Mulle et al. (1985); Paré et al. (1987).
Steriade et al. (1984a); Velayos et al. (1989).
Wilcox et al. (1988).
Liu et al. (1995).
Steriade et al. (1985).
Steriade (1999b).
This hypothesis derived from a study on the activity of RE neurons during the natural waking-sleep cycle (Steriade et al., 1986). The circuit illustrated in Fig. 4.4 was proposed in Steriade (1991) and was redrawn by E.G. Jones.
Fast-conducting pyramidal neurons of Macaca mulatta stopped firing upon arousal for periods ranging from 4 to 33 s in different units (Steriade et al., 1974a).
Jones (1975b).
Somogyi et al. (1983, 1985); Somogyi (1989); DeFelipe and Jones (1992); DeFelipe (1993); Kawaguchi and Kubota (1997).
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Reviewed in Seymour et al. (1994) and Berlucchi et al. (1995).
Steriade et al. (2001a).
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These electrophysiological data, from experiments on the slow sleep oscillation (Steriade et al., 1993b) and paroxysmal discharges (Steriade and Contreras, 1995; Timofeev et al., 1998), are supported by recent studies showing that the numbers of glutamate receptor subunits GluR4 are 3.7 times higher at corticothalamic synapses in RE neurons, compared to TC neurons, and the mean peak amplitude of corticothalamic excitatory postsynaptic currents (EPSCs) is about 2.5 higher in RE, than in TC, neurons (Golshani et al., 2001).
Steriade et al. (1986).
Amaral and Witter (1989); Lopes da Silva et al. (1990); Freund and Buzsáki (1996).
Andersen et al. (1964, 1969); Ben-Ari et al. (1981a).
Somogyi et al. (1983, 1985). The importance of chandelier (axoaxonic) cells in controlling the excitability of hippocampal pyramidal neurons is demonstrated by the loss of axons of chandelier neurons in rat’s hippocampal transplants that display paroxysmal discharges (Freund and Buzsáki, 1988). There is also a decrease in chandelier neurons in entorhinal cortex and subiculum of epileptic patients (DeFelipe, 1999).
Alonso and Klink (1993). Layer II neurons receive cholinergic innervation from the septum (Alonso and Köhler, 1984) and a muscarinic agonist, carbachol, produces membrane depolarization of stellate cells associated with oscillations in the theta frequency range.
Paré et al. (2002).
Kreindler and Steriade (1964).
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(2005). Neuronal Circuits in the Thalamus, Neocortex, and Hippocampus, Targets of Diffuse Modulatory Systems. In: Brain Control of Wakefulness and Sleep. Springer, Boston, MA. https://doi.org/10.1007/0-387-26270-9_4
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DOI: https://doi.org/10.1007/0-387-26270-9_4
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