FUNDAMENTOS DE LA SALA:

In chaptersIII-Vwe looked at a range of different attentional behaviours and the degree to which their performance was affected by lesions in the cTRN

sector associated with the sensory modality they were carried out in. In chapterIIIwe observed that combined TRNvis and TRNaud lesions did not affect the ability to divide attention between the visual and auditory modalities, as there was neither an increase nor a reduction in the behavioural costs associated with the simultaneous monitoring of two informational channels, compared to the monitoring of only one. Nonetheless, the animals’ ability to discriminate between the test stimuli (within each modality) was poorer following the lesions, an effect however unrelated to the division of attention. Having in mind the idea that cTRN may act as a “noise filter” in

thalamocortical cells (see6.2.), the finding that TRNvis/aud lesions resulted in poorer discriminatory ability could be explained by elevated background noise activities in thalamocortical cells due to the absence of TRNvis/aud

intervention. In other words, the lack of TRNvis/aud hyperpolarisation on visual and auditory thalamocortical cells may have prevented the clearance of unwanted, interfering, noise, which could have hampered the detailed

analysis of the transmitted signal, making the identification of the stimulation more ambiguous. The greater ambiguity of signal identification could have then resulted in more erroneous identifications of the stimuli and the

generation of more incorrect responses. However, it has to be noted that high levels of baseline noise activity are not always bad for the analysis of

stimulation. More specifically, relatively high levels of noise, when relatively stable across time, can provide more “room” for the better delineation of certain stimulus properties, especially those related to contrasts or movement within sensory space (Sherman and Guillery, 2001). However, cTRN inhibition

may be specifically targeting irregular noise that is likely to interfere with the perception of the signal of interest and not baseline noise in general.

In a very similar scenario to the above, the greater ambiguity in stimulus identification could have resulted from the expansion of receptive fields of thalamocortical cells, the result of the cessation of TRNvis/aud inhibition upon them (Lee, Friedberg and Ebner, 1994a). The expansion of thalamocortical cell receptive fields, however, could be simply an alternative way of defining increased noise transmission in these cells as it could represent a reduction in the specificity of the sensory signal that activates them.

6.3.2. Chapters IV and V: cTRN lesioning and visual covert orienting.

In the last two chapters we investigated the role of TRNvis in the animals’ ability to move covert orienting within visual space. We looked at two different expressions of covert orienting triggered by either exogenous means (Posner task, chapterV) or endogenous ones (ASP task, chapters IVandV).

We found that TRNvis lesions (bilateral and unilateral alike) did not prevent the covert movement of attention, as the behavioural benefits (and costs) stemming from covert orienting (regardless of its endogenous or exogenous nature) were preserved following surgery. This suggested that despite the topography of its signal, TRNvis may not be responsible for the generation and movement of the attentional spotlight as once suggested (see Crick, 1984), at least to the degree that this was assessed by the two

of Weeseet al.(1999), who reported impaired contralateral covert orienting in the Posner task following TRNvis lesions. The lack of covert orienting deficits in chapterIVwas initially attributed to three possible reasons (or any

combination of these):a)the fact that, in contrast to the Posner task used by Weeseet al., covert orienting in the ASP task was generated by endogenous means and could therefore depend on a different neuronal substrate that required little or no involvement by TRNvis,b)the comparatively longer duration of the stimuli used in the ASP task that may have not compromised detection and thus prevented possible post-lesion stimulus acquisition deficits from being expressed, andc)the different nature of the lesions in the two studies. However, after observing that similar lesions to the ones in chapterIV

did not result in covert orienting deficits in the Posner task too (chapterV), we dismissed the first two assumptions and we concluded that the different behavioural results reported here and in Weeseet al. were more likely to be due to differences in the lesions. Due to the verifiable selectivity of the lesions in our investigations, we believe that our results reflect more reliably the role of TRNvis in covert orienting.

6.4.Stimulus detection and cTRN involvement

Due to the hypothesised implication of thalamocortical burst activity (and consequently of cTRN involvement) in processes of stimulus detection

(Guido, Lu, Vaughan, Godwin and Sherman, 1995; Guido and Weyand, 1995) we had postulated that the lesioning of cTRN would result in stimulus

detection detriments. The lack of such effects following the lesions in the divided attention and ASP tasks was attributed to the relatively long duration

of the stimuli used in these tasks, which may have resulted in a floor-effect regarding the difficulty of these stimuli at being detected. In the Posner task, where targets were considerably shorter in duration (thus a greater challenge to detect), we observed that TRNvis lesions somewhat slowed response latencies to contralateral target stimuli. Even though this effect was not

statistically significant, it approached significance and therefore some caution must be exercised in accepting this negative result. If it is replicated, such an effect would imply that TRNvis’s involvement in stimulus detection processes may be specifically required for stimuli of short duration (i.e. detection

challenging stimuli). This would have to be looked in more detail, by

investigating the involvement of TRNvis in the detection of stimuli of variable duration and saliency under identical attentional/behavioural conditions (unlike here, where the stimuli of variable duration were presented in different

contexts (tasks)).

In addition to being optimal for the detection of brief and sub-threshold stimuli, burst firing has also been suggested to represent the ideal “stimulus

acquisition” means for novel or unexpected stimuli, regardless of their duration and saliency (Sherman and Guillery, 2001). Indeed some evidence suggests that novel or surprising stimuli generate burst firing in

thalamocortical cells (see Weyand, Boudreaux and Guido, 2001). Due to the lack of paired-pulse depression (see Swadlow and Gusev, 2001; Sherman, 2001) burst firing in thalamocortical cells could maximally activate post- synaptic cortical cells, acting as a wake-up call also for the presence of unforeseeable and potentially behaviourally-relevant stimulation. Such an

optimisation of detection of unpredictable stimuli could be behaviourally invaluable especially to prey species but also, in general, to any species with natural enemies. Possessing the ability to detect such stimuli, especially when brief or near threshold, can enhance significantly one’s chances of surviving a predator attack. One may consider the ASP task as an example of a situation where unpredictable stimulation takes place (i.e. when a target appears at a temporally improbable location). In the ASP task, however, the degree of “surprise” caused by a spatiotemporaly improbable target was minimal, as it represented the only alternative to a probable target and moreover it could only appear at a fixed location. If novelty/unpredictability is indeed one of the factors that determines the generation of burst firing in thalamocortical cells, and thus the degree of involvement by cTRN, then it is possible that the repetitive training/testing regime of the behavioural tests we used, took away this element from the test stimuli and thus minimised the requirement for both the generation of burst firing in dorsal thalamus and consequently for cTRN involvement, thus explaining the lack of detection detriments following its lesioning.