The input/output circuitry of the thalamic relay nuclei shares common principles across the various sensory modalities (Jones, 1985). The somatosensory system is served by the ventroposteromedial (VPM) and ventroposterolateral (VPL) nuclei (often referred to together as the ventrobasal (VB) complex), the visual system by the dorsal and ventral lateral geniculate nuclei (LGN), and the auditory system by the medial geniculate nucleus (MGN). These nuclei receive inputs which are specific for their particular sensory modality and project to their specific areas of cerebral cortex (Jones, 1985). In addition, the cortical areas project back to the thalamic areas from which they receive their input. These cortical terminals are located more distally on the dendrites of the thalamic relay neurones than the terminals of the sensory afferents (Montero 1989; Ohara & Lieberman, 1985; Peschanski et al., 1984; Robson 1983, 1993). The thalamic nuclei are closely associated with the nucleus reticularis thalami (nrt), a thin sheet of GABAergic neurones which project into the thalamic nuclei. The nrt neurones receive inputs from collaterals of thalamic relay neurone projections to the cerebral cortex and from collaterals of cortico-fugal axons originating in the sensory cortices. In addition, apart from the rodent ventrobasal complex and ventrolateral nucleus, there are one or more types of Golgi II GABAergic interneurones within the body of the mammalian thalamic nuclei (Ohara & Lieberman, 1993; Ralston, 1983; Shosaku et al., 1989; Somogyi 1989). The terminals and dendritic processes of these neurones are intimately connected with the dendrites of relay neurones and with the terminals of sensory afferents in so-called triadic arrangements, which are enswathed by glial processes.
The advent of immunostaining for glutamate has revealed L-glutamate-like immunoreactivity in optic nerve terminals and lemniscal terminals, and in terminals of cortico-fugal axons in the thalamus (Broman 1994; De Biasi et al., 1994; Kechagias & Broman, 1995; Kharazia et al., 1995; Montero & Wenthold, 1989; Montero, 1994; Rustioni et al., 1988). In contrast, it appears that immunostaining for L-homocysteate is in glia rather than in neuronal elements in various parts of the brain, including the lateral geniculate nucleus of the thalamus (Grandes et al., 1991a,b). Immunostaining for N-acetyl-aspartyl-glutamate (NAAG) has also been shown in the thalamus, including in retinal afferents to the lateral geniculate nucleus (Moffett et al., 1991; Molinar-Rode & Pasik, 1992; Tieman et al., 1991). However, it is noteworthy that this dipeptide is also found in populations of presumed cholinergic and GABAergic neurones, including the GABAergic neurones of the nrt (Henderson & Salt, 1988). This would tend to argue against a role for NAAG as the primary transmitter of sensory and cortical afferents to the thalamus.
Release of the excitatory amino acids L-glutamate and L-aspartate, together with L-homocysteate and the inhibitory amino acid GABA has been demonstrated from thalamic tissue in vitro using various types of stimuli (Do et al., 1986; Nicholls, 1989). However, the release of excitatory amino acids from thalamic nuclei by stimulation of sensory afferents in vivo has not been conclusively demonstrated (Sandberg & Lindström, 1983), although L-glutamate can be released from the avian optic tectum upon electrical stimulation of the optic nerve (Canzek et al., 1981). In contrast, the release of NAAG has been demonstrated both in vitro and in vivo (Tsai et al., 1988; 1990).
Please note: this document is part of the HTML version of a paper
originally published in print in Progress in Neurobiology.
Contents 
Previous Section 
Next Section
Reference List
Return to Tom Salt's Home Page