GORDILLO VEGA, ELMER VICTOR

The activation of TRNvis observed in chapterIIfollowing the performance of a visual discrimination task may reflect the involvement of this sector in the active modulation of the signal carried by visual thalamocortical relay cells, which constitute its only output projection targets (Hale and Sefton, 1982; Coleman and Mitrofanis, 1996). Given that TRNvis’ projections are exclusively GABAergic (Houser, Vaughn, Barber and Roberts, 1980; DeBiasi, Frassoni and Spreafico, 1986), and thus exert inhibitory post-synaptic effects upon thalamocortical cells, their modulatory function could be carried out in two possible ways. The first possible modulatory function is thought to be one of minimisation of background noise activity in thalamocortical cells, aiming at enhancing their communication of behaviourally relevant visual signals to cortex. This could be achieved by hyperpolarising thalamocortical cells, not enough however to prevent action potentials from being generated, but

sufficiently to minimise spontaneous activity within them, thus allowing signals from behaviourally-relevant stimuli to emerge as more salient. Because of the presumed interference of the low luminance levels (under which the visual discrimination task was carried out) with the perception of the visual aspect of interest (colour of digging bowl) a minimisation of noise levels in

visual identification/discrimination. It has to be said, however, that due to the presence of GABABand extrasynaptic GABAAreceptors in thalamocortical cells (e.g. von Krosigk, 1992; Ulrich and Huguenard, 1996a; 1996b; also see Cox, Huguenard and Prince, 1997; Jia,et al., 2005), and the resultant long- lasting hyperpolarizing effects of their activation, it is possible that TRNvis’ GABAergic output could have also de-inactivated IT in these cells thus causing a transition of firing mode from tonic (the predominant firing mode during awake states) to burst. Even though burst firing may appear

inappropriate for the analysis of stimulation, due to its non-linear signal transmission properties (Sherman and Guillery, 2001), its better signal-to noise ratio of transmission may have made it preferable over the usually “noisy” tonic activity in the communication of visual signals under the

unfavourable visual conditions that the visual discrimination was performed. This issue was also raised in chapterIV,where it has been postulated that the duration or saliency of a stimulus (in other words, the sensitivity of that

stimulus’ detection to background noise) may be the determining factor for the generation of burst activity in thalamocortical cells and thus the involvement of TRNvis. Whether TRNvis’ activation, seen in visually attentive animals, and its resultant inhibition of visual thalamic cells induced burst firing or not in the latter could only be answered through single-cell electrophysiological recordings over the performance of the task.

The second modulatory function that TRNvis’ selective activation in chapterII

could have reflected is one of lateral inhibition. Lateral inhibition mechanisms can be very effective in “weakening” activity in sensory areas adjacent to the

one(s) of interest, thus minimising the degree by which these could interfere with the latter’s processing. In other words, lateral inhibition can eliminate potential attentional competition from other sensory areas, thus enhancing the processing of the signal of interest. Given that in our visual discrimination task attentional competition did not come from within the visual modality but,

instead, mainly from somatosensation (i.e. the other sensory modality that the animals had been trained to make discriminations), a lateral inhibition

mechanism may have been aiming at the weakening of activities in the somatosensory thalamus. It has been suggested (Crick, 1984; also see Montero, 1997) that in situations where there is competition for attentional resources between different sensory modalities, the long dendritic arbours of TRN cells (see Scheibel and Scheibel, 1966) may be put into use, contributing to a lateral inhibition mechanismbetween cTRN sectors. In such a

mechanism, cells of the cTRN sector corresponding to the attended modality would inhibit cells in the cTRN sector(s) corresponding to the non-attended modality/-ies in order to preserve the attentional focus. In our task, for

example, cells in TRNvis may have activated in order not only to lower noise levels in visual thalamocortical cells but also in order to inhibit TRNsom cells (i.e. the cTRN cells corresponding to the “competing” modality) and thus prevent them from performing a similar action on somatosensory

thalamocortical cells. The spatial proximity of the cTRN sectors corresponding to the three main sensory modalities in which attentional competition is more likely to take place (i.e. vision: TRNvis, audition: TRNaud and

somatosensation: TRNsom) is such that a model of triadic, inter-sector, lateral inhibition would be favoured (see Figure 1.3, ingeneral introduction).

However, although this seems plausible, it has to be noted that there is no empirical evidence in support of such a mechanism. Furthermore, this scenario does not explain how the activation of cells in one sector results in the inhibition of cells in other sectors without also resulting in the inhibition of cells within the same sector. In addition, as mentioned above, the inter-sector cTRN lateral inhibition hypothesis is based on the assumption that the

majority of cTRN cells possess long enough dendrites to cross sectors’ borders, an anatomical feature the actuality of which is currently questioned (see Pinault, Smith and Deschênes, 1997).

The contribution of cTRN (as reflected by its modality-specific activation) in attentional behaviours is thought to be dictated by its multiple inputs coming from cortex (Jones, 1975; see1.2.4.), basal forebrain (e.g. Jourdain, Semba and Fibiger, 1989; Asanuma, 1989, Semba, 2000, also see1.2.8.2.), brain stem (e.g. Jourdainet al.,1989; Asanuma, 1992; Spreaficoet al., 1993, see

1.2.8.2.) and the dorsal thalamus itself (Jones, 1975, see1.2.4.). Of these projections, the one with the most influence on cTRN function is believed to be the heavy glutamatergic corticothalamic feedback projection from layer VI of sensory cortices, which collateralises within the nucleus en route to dorsal thalamus (Liu and Jones, 1999). These corticothalamic projections are thought to carry top-down instructions, which directly, but also indirectly through cTRN, modulate activity in selected areas of the dorsal thalamus according to the immediate attentional/behavioural demands (see Montero, 2000). Discontinuation of these projections diminishes attention-related activation within cTRN (Montero, 2000), but it is unknown whether it also

results in attentional deficits. The role of the basal forebrain and the various brainstem projections in the recruitment of cTRN during attention-demanding situations could be of equal importance. Despite the lack of sensory

topography in their signal, some of these projections do posses a crude segregation of their signals to the different modality sectors of the cTRN (e.g. see Spreaficoet al., 1993; Semba, 2000). This could allow these projections to target selectively only specific sensory cTRN sectors, thus contributing to a sensory-selective manner to any attentional processes taking place there.

The fact that no cellular Fos activation was observed in TRNsom after tactile attentive behaviours in chapterIIwas seen as a potential indication that the involvement of cTRN in attentional behaviours may differ between different forms of attention (the other alternative explanation being the overall low Fos activation in somatosensory thalamic pathways). This is because the visual and tactile attentional tasks were not analogous within their respective modalities and could have, therefore, required different degrees of

involvement from their respective cTRN sectors in order to be carried out. Indeed, as was seen in chaptersIII-V, cTRN is not involved in all attentional processes as its destruction did not affect several aspects of some attentional behaviours.

6.3. Chapters III-V: cTRN lesions and attentional behaviours