Excitatory amino acid receptor‐mediated transmission of somatosensory evoked potentials in the rat thalamus.

Abstract

SUMMARY1. To examine the role of excitatory amino acid receptors in the rat ventrobasal thalamic nucleus (v.b.t.n.) for the transmission of cortical somatosensory evoked potentials (s.e.p.s), potentials were recorded from the somatosensory cortex of barbiturate-anaesthetized and of unanaesthetized awake rats. The effects of microapplications of the selective N-methyl-D-aspartate (NMDA) antagonist (-)-2-amino-7-phosphono-heptanoate ((-)AP7) and the broad-spectrum excitatory amino acid antagonist 1-(p-chlorobenzoyl)-piperazine-2,3-dicarboxylate (pCB-PzDA) into the thalamus on the amplitudes and latencies of cortical potentials were measured.2. To define the receptor specificity of local microinjections of (-)AP7 and pCB-PzDA electroencephalogram (e.e.g.) recordings were made from the immediate vicinity of the injection cannula within the thalamus. (-)AP7 selectively antagonized epileptic discharges induced by NMDA, but not those by kainate, whereas pCB-PzDA antagonized epileptic discharges induced by both.3. In both anaesthetized and unanaesthetized rats, microapplications of pCB-PzDA into the thalamus suppressed transmission of cortical potentials as indicated by a decrease of their amplitudes and an increase of their peak latencies.Further experiments in anaesthetized rats showed that pCB-PzDA exerted its effects in a dose-dependent and site-specific way. 4. In both anaesthetized and unanaesthetized rats, microapplications of (-)AP7 into the ventrobasal thalamus did not affect cortical potentials.5. These results are consistent with the assumption that an excitatory amino acid serves as transmitter at thalamic synapses mediating transmission of cortical potentials, and that this transmitter interacts preferentially with non-NMDA receptors.

Evidence for Glutamate as Neurotransmitter in Trigemino‐ and Spinothalamic Tract Terminals in the Nucleus Submedius of Cats

“…b) we demonstrated that terminals of lamina I axons in the nucleus submedius are involved in complex synaptic aggregations with pre-and postsynaptic dendrites, similar to the organization of lemniscal afferent terminals and intrinsic neuronal components in the ventrobasal complex (Blomqvist et al, 1985;Ralston et al, 1988). Recent immunocytochemical studies (De Biasi and Rustioni, 1990;Broman and Ottersen, 1992) have shown enrichment of glutamate-like immunoreactivity (Glu-LI) in terminals of ascending somatosensory afferent fibres in the ventrobasal complex, corroborating pharmacological evidence that excitatory amino acids (EAA) mediate transmission between lemniscal terminals and thalamic neurons (Salt, 1986;Klockgether, 1987;Salt and Eaton, 1991). However, it is not known whether TSTT fibres, carrying nociceptivespecific information to the thalamus, also use glutamate as a neurotransmitter.…”

“…Although a high level of Glu-LI is probably a distinctive feature of glutamatergic terminals in the central nervous system, immunogold findings must be evaluated in conjunction with other types of data on EAA neurotransmission. With respect to the ventrobasal complex, there is abundant pharmacological evidence that supports the involvement of EAAs in the transmission from ascending somatosensory afferent fibres (Salt, 1986;Klockgether, 1987: Salt and Eaton, 1989.…”

Cervicothalamic tract terminals are enriched in glutamate-like immunoreactivity: an electron microscopic double-labeling study in the cat

“…Negative findings with this technique do not, however, rule out a transmitter role for Glu or other excitatory amino acids, as the sensitivity for detection may vary between different putative glutamatergic pathways (for reviews, see Storm-Mathisen and Ottersen, 1988;Ottersen, 199 1). Electrophysiologiopharmacologic studies in rats have recently provided increasing evidence for an involvement of excitatory amino acids in the synaptic transmission between ascending somatosensory afferents and neurons in the thalamic ventrobasal complex (Salt, 1986(Salt, ,1988Klockgether, 1987), and the response to somatosensory stimulation in the ventrobasal complex' seems to involve both NMDA and non-NMDA receptors Eaton, 1989, 1991). The present findings that Glu-LI is enriched both in peroxidase-positive CTT terminals and non-peroxidase-labeled RL terminals further support the existence of excitatory amino acid neurotransmission between these afferents and VPL neurons and strongly suggest that Glu is an endogenous agonist for the receptors.…”

“…That GABA is a neurotransmitter in VPL local circuit neurons and in reticular thalamic neurons projecting to the VPL has been well established, and there is strong evidence for excitatory amino acids, foremost glutamate (Glu), as neurotransmitters in the cortical projection to the VPL (Jones, 1985;Rustioni and Weinberg, 1989). However, electrophysiologic-pharmacologic studies have during recent years suggested that excitatory amino acids may also be involved in synaptic transmission between somatosensory afferents and thalamic neurons (Salt, 1986(Salt, , 1988Klockgether, 1987;Salt and Eaton, 1989). Immunohistochemical studies have also revealed the presence of glutamate-like immunoreactivity (Glu-LI) in lemniscal-type terminals in the VPL Spreafico et al, 1989;De Biasi and Rustioni, 1990).…”

Enrichment of glutamate immunoreactivity in lemniscal terminals in the ventropostero lateral thalamic nucleus of the rat: An immunogold and WGA‐HRP study

“…Several lines of evidence concur in suggesting that the excitatory amino acid glutamate (Glu) is an important transmitter in VP Rustioni and Weinberg, 1989): excitatory effects of Glu on VP neurons were reported in physiological studies (Hicks et al, 1986;Salt, 1986Salt, , 1987Klockgether, 1987;Salt and Eaton, 1989;Eaton and Salt, 1990) and Glu binding sites and receptors were shown in VP (Monaghan and Cotman, 1985;Cotman et al, 1987;Petralia and Wenthold, 1992;Frassoni et al, 1993). In particular, the demonstration that receptors for Glu are involved in the responses of VP neurons to stimulation of somatosensory afferents (Salt, 1986(Salt, , 1987Salt and Eaton, 1989) suggests that this excitatory amino acid functions as the transmitter mediating the responses of VP neurons to stimulation of second order sensory afferents.…”