The thalamic reticular nucleus (TRN) is an integral part of the thalamic circuitry that mediates the transfer of information to the cortex in the major sensory pathways. Here, we consider its role in visual processing. The TRN provides an inhibitory, GABA-mediated input to relay cells in the thalamus. A key feature of TRN cells is that, because of the extent of their dendritic arborization, they have the capacity to collate visual information from the ascending relay cells and feedback axons from the cortex over a wide retinotopic area, but they feed it back to the thalamus in a narrowly focused retinotopic projection. The corticofugal input to TRN cells is mediated by a higher proportion of AMPA receptors than that to thalamic relay cells and produces sharp EPSCs. We suggest that this might bias the TRN cells to precisely timed, feature-driven feedback from the visual cortex. TRN cells are particularly well driven by either phasic or moving stimuli, so the influence on relay cells provides a strong, transient, inhibitory modulation of relay-cell activity. This might aid image segmentation and highlight responses to moving contours. Although the role of the TRN has been especially linked to selective attention, we suggest that, for vision, its function is linked more closely to the operation of the thalamocortico-thalamic loop as a whole, and that retinotopically selective attentional effects draw on the interaction with the cortical mechanism that influences TRN and relay-cell circuitry equally.

It has been demonstrated in juvenile rodents that the inhibitory neurons of the nucleus reticularis thalami (NRT) communicate with each other via connexin 36-based electrical synapses. However, whether functional electrical synapses persist into adulthood is not fully known. Here we show that in the presence of the metabotropic glutamate receptor agonists, either trans-ACPD (100 μM) or DHPG (100 μM), 15% of neurons in slices of the adult cat NRT maintained in vitro exhibit stereotypical spikelets with several properties that indicate that they reflect action potentials that have been communicated through an electrical synapse. In particular, these spikelets (1) display a conserved, all-or-nothing waveform with a pronounced after-hyperpolarization (AHP), (2) exhibit an amplitude and time to peak that are unaffected by changes in membrane potential, (3) always occur rhythmically with the precise frequency increasing with depolarization, and (4) are resistant to blockers of conventional, fast, chemical synaptic transmission. Thus, these results indicate that functional electrical synapses in the NRT persist into adulthood where they are likely to serve as an effective synchronizing mechanism for the wide variety of physiological and pathological rhythmic activities displayed by this nucleus.

The work of Mircea Steriade demonstrated that the neocortex could synchronize large regions of the thalamus within 10−100 msec. Unlike the synchrony generated by the cortex, the retinal afferents synchronize a restricted group of neighboring thalamic neurons with <1-msec precision. Here, we use a large sample (n = 372) of simultaneous recordings from neighboring neurons in the lateral geniculate nucleus (LGN) to illustrate the high specificity of the synchrony generated by retinal afferents and its dependency on sensory stimulation. First, we demonstrate that cells sharing a retinal afferent show a balanced receptive field diversity: although slight receptive field mismatches are common, the largest mismatches in a specific property (e.g. receptive field size) are restricted to cells that are precisely matched in other properties (e.g. receptive field overlap). Second, we show that these receptive field mismatches are functionally important and can lead to a 5-fold variation in the percentage of synchronous spikes driven by the shared retinal afferent under different stimulus conditions. Based on these and other findings, we speculate that the precise synchronous firing of cells sharing a retinal afferent might serve to amplify local stimuli that might be too brief and small to generate a large number of thalamic spikes.

Enlargement of the forebrain, including elaboration of the thalamus, has occurred independently within different groups of vertebrates. Dorsal and ventral thalamic territories can be identified in most vertebrates, with variations in the presence of GABAergic neuronal components. An inhibitory thalamic reticular nucleus-like input to the dorsal thalamus might be a common feature, as might the organizational plan of two divisions of the dorsal thalamus, the lemnothalamus and collothalamus. Differential, independent elaboration of these divisions occurred in mammals and sauropsids (reptiles and birds), making their evolutionary relationships challenging to discern. Not all of the crucial features identified for mammalian thalamocortical circuitry are present in other vertebrates, but birds share the most features identified to date. These include specific and nonspecific thalamic relay neurons, reciprocal pallial projections, and a GABAergic thalamic reticular nucleus with some but not all hodological features. Because birds share many higher-level cognitive abilities and, thus, possibly higher-level consciousness, with mammals, comparison of the thalamocortical (thalamopallial) circuitry might prove a fruitful resource for testing functional hypotheses. Comparisons with selected other vertebrates that likewise have relatively large brain:body ratios and also exhibit some cognitively sophisticated behaviors, such as cichlid fish, might also prove valuable.

Anterior thalamic lesions are thought to produce ‘covert pathology’ in retrosplenial cortex, but the causes are unknown. Using microarray analyses we tested the hypothesis that thalamic damage causes a chronic, hypofunction of metabolic and plasticity-related pathways (Experiment 1). Rats with unilateral, anterior thalamic lesions were exposed to a novel environment for 20 min, and granular retrosplenial tissue sampled from both hemispheres 30 min, 2 hours and 8 hours later. Complementary statistical approaches (analyses of variance, predictive patterning and gene set-enrichment analysis) revealed pervasive gene expression differences between retrosplenial cortex ipsilateral to the thalamic lesion and contralateral to the lesion. Selected gene differences were validated by QPCR, immunohistochemistry (Experiment 1) and in situ hybridization (Experiment 2). Following thalamic lesions, the retrosplenial cortex undergoes profuse cellular transcriptome changes including lower relative levels of specific mRNAs that are involved in energy metabolism and neuronal plasticity. These changes in functional gene expression might be driven largely by decreases in the expression of genes encoding transcription factors including brd8, c-fos, fra-2, klf5, nfix, nr4a1, smad3, smarcc2 and zfp9, with far fewer (nfat5, neuroD1 and RXRγ) showing increases. These findings have implications for conditions such as diencephalic amnesia and Alzheimer's disease in which both anterior thalamic pathology and retrosplenial cortex hypometabolism are prominent.

The seminal in vivo work of Mircea Steriade and his colleagues has, as is always the case with the most insightful and creative scientists, raised many serious questions: questions, for example, of the detailed cellular and molecular mechanisms of the phenomena they discovered. In our tribute to this great investigator, we shall present some examples, based on our in vitro and modeling work, that shed light on some of his remarkable breakthroughs: the slow oscillation of sleep (<1 Hz); the several types of fast oscillations that are superimposed on the intracellular depolarizing, or active, phases of the slow oscillation; and the transition from slow oscillation to seizure via a period of very fast (>70 Hz) oscillations.