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References
Steriade and Demetrescu (1960).
Hubel (1960).
Steriade et al. (1971).
Steriade et al. (1985).
McCarley et al. (1983).
Glenn and Steriade (1982).
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Hirsch et al. (1983).
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Carli et al. (1967).
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Jones et al. (1976); Hallanger et al. (1988); Semba et al. (1988).
Earlier extracellular data reported excitatory responses of cortical neurons to stimulation of peripallidal and basal forebrain areas (Edstrom and Phillis, 1980). Contradictory results have been obtained by investigating the action of muscarinic and nicotinic blockers, administered systemically, upon the brainstem-induced potentiation of electrically evoked field responses in the visual cortex (Bremer and Stoupel, 1959; Singer, 1979) since the action could have been exerted either at the thalamic LG level or at the cortical level (see note [20]).
Jones and Cuello (1989).
Khateb et al. (1997).
Fort et al. (1995). Contrary to the depolarizing effect on cholinergic neurons, norepinephrine hyperpolarizes and inhibits noncholinergic neurons in the basal forebrain (Fort et al., 1998).
Steriade and Glenn (1982).
Endo et al. (1977).
Adams et al. (1988). Those experiments also attempted to dissociate the thalamic from the cortical level of action after administration of cholinergic blockers (see note [14]).
Steriade et al. (1969).
Kulics et al. (1977); Kulics (1982).
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Maffei et al. (1965a, b,c).
The cholinergic nature of the effects induced by stimulating the upper brainstem reticular core was shown by Francesconi et al. (1988; see also intracellular data in Section 8.1.4).
Stimulation of locus coeruleus increases the spontaneous firing as well as the responses of thalamic LG neurons to optic tract stimulation (Kayama et al., 1982), a response mediated by alpha-1 adrenergic receptors (Rogawski and Aghajanian, 1982).
Pape and Eysel (1988). Opposite, facilitatory effects were obtained in vitro by McCormick and Prince (1988).
Rivner and Sutin (1981).
Filion et al. (1971); Steriade et al. (1971); MacLeod et al (1984).
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Hu et al. (1989b).
Steriade and Deschêenes (1988).
The increased membrane conductance during the early nicotinic depolarization ranges from 10% up to 50% in animals treated with reserpine to avoid costimulation of axons arising from locus coeruleus. The increased conductance is sometimes observed even in the absence of overt membrane depolarization and is reflected by the decreased amplitude of the voltage deflection to a hyperpolarizing current pulse and by reduction of the rebound LTS (Curró Dossi et al., 1991). These results obtained by stimulating synaptic brainstem-thalamic pathways in vivo are similar to the effects elicited by applying ACh in vitro (McCormick and Prince, 1987a, b).
Hu et al. (1989c).
Under reserpine treatment, the duration of the late (muscarinic), long-lasting depolarization is prolonged to 40–60 s (see [42]. The late and very prolonged excitation in LG relay cells depicted in Fig. 8.4. may well be due to the action of peptides that are found in brainstem cholinergic neurons (Vincent et al, 1983, 1986).
Marks and Roffwarg (1987).
Hirsch et al. (1983).
Steriade et al (1990a).
Williams et al. (1994).
Timofeev et al. (1996).
Paré and Steriade (1990); Paré et al. (1990b). The anterior nuclear group of cat thalamus was chosen to investigate the long-term activation process induced by brainstem cholinergic stimulation because it is devoid of inputs from the thalamic reticular complex (Steriade et al, 1984a; Velayos et al., 1989) and, thus, the prolonged potentiation (up to 4 min) is not attributable to disinhibition through the cholinergic inhibition of GABAergic thalamic reticular cells.
The monkey model of severe amnesia consists of mammillary nuclei and midline/medial thalamic lesions (Aggleton and Mishkin, 1983a,b; Bentivoglio et al., 1997).
See Squire and Alvarez (1995).
This statement is based, among many other data, on the following evidence showing that thalamic (1) LG neurons exhibit far greater reduction in response to stimuli including the field surround than do retinal ganglion cells or optic tract axons (Hubel and Wiesel, 1961) and larger coefficient of variation than retinal cells, with little variability added at the cortical level (Hartveit and Heggelund, 1994); and (2) ventroposterior (VP) thalamic neurons have receptive fields that are different from those of neurons in brainstem relay stations and dynamic responses demonstrating that they are not simple relays for somatosensory signals (Alloway et al., 1994; Nicolelis and Chapin, 1994).
Hicks et al. (1986); Salt (1989). Selective lesions of thalamic reticular GABAergic neurons increase the receptive field size of VP neurons by ∼ 3-fold (Lee et al., 1994).
Jones (1985); Steriade et al. (1997a).
Liu et al. (1995).
Steriade et al. (1985). We showed that, after thalamic transections separating the thalamic reticular nucleus from the remaining thalamus or after excitotoxic lesions of reticular neurons, there was an increased number of GABAA-receptor-mediated IPSPs in TG neurons, as if local-circuit inhibitory neurons were released from the inhibition arising in reticular neurons. See also Fig. 4.4 in Chapter 4, depicting the circuitry of reticular, local-circuit, and TC neurons.
Jones and Powell (1969); Ralston (1971); Ohara and Lieberman (1993).
Paré et al. (1991).
Hirsch and Burnod (1987); Crunelli et al. (1988).
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The failure to observe a nicotinic response in reticular neurons maintained in vitro (McCormick and Prince, 1986a) could well be attributed to the mode of ACh application leading to a rapid desensitization of the response. Nicotinic receptors have been mapped within the reticular thalamic nucleus of monkeys (Jones, 1985) and rats (Clarke et al., 1985). The suggestion that the early excitation in reticular neurons is produced by nicotinic receptors (Hu et al., 1989a) was subsequently confirmed in work done in thalamic slices (Lee and McCormick, 1995).
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Notable exceptions are Evarts and his colleagues (Evarts and Tanji, 1976; Tanji and Evarts, 1976) who have recorded identified pyramidal tract neurons in the primary motor cortex.
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See details for the visual thalamocortical system in Steriade et al. (1990e).
Steriade and Deschênes (1974).
Swadlow and Weyand (1987).
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(2005). Brainstem and State dependency of Thalamocortical Systems. In: Brain Control of Wakefulness and Sleep. Springer, Boston, MA. https://doi.org/10.1007/0-387-26270-9_8
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