Function Of Cerebral Cortex Research Articles

Cerebellar Function: Multiple Topographic Maps of Visual Space

New evidence from the Human Connectome Project has revealed multiple maps of visual space in human cerebellum. While some features of these maps adhere to the topographic organizational principles shared among the multiple maps in cerebral cortex, some properties appear idiosyncratic.

Body maps on the human genome.

BackgroundChromosomes have territories, or preferred locales, in the cell nucleus. When these sites are taken into account, some large-scale structure of the human genome emerges.ResultsThe synoptic picture is that genes highly expressed in particular topologically compact tissues are not randomly distributed on the genome. Rather, such tissue-specific genes tend to map somatotopically onto the complete chromosome set. They seem to form a “genome homunculus”: a multi-dimensional, genome-wide body representation extending across chromosome territories of the entire spermcell nucleus. The antero-posterior axis of the body significantly corresponds to the head-tail axis of the nucleus, and the dorso-ventral body axis to the central-peripheral nucleus axis.ConclusionsThis large-scale genomic structure includes thousands of genes. One rationale for a homuncular genome structure would be to minimize connection costs in genetic networks. Somatotopic maps in cerebral cortex have been reported for over a century.

Compromise of Auditory Cortical Tuning and Topography after Cross-Modal Invasion by Visual Inputs

Brain damage resulting in loss of sensory stimulation can induce reorganization of sensory maps in cerebral cortex. Previous research on recovery from brain damage has focused primarily on adaptive plasticity within the affected modality. Less attention has been paid to maladaptive plasticity that may arise as a result of ectopic innervation from other modalities. Using ferrets in which neonatal midbrain damage results in diversion of retinal projections to the auditory thalamus, we investigated how auditory cortical function is impacted by the resulting ectopic visual activation. We found that, although auditory neurons in cross-modal auditory cortex (XMAC) retained sound frequency tuning, their thresholds were increased, their tuning was broader, and tonotopic order in their frequency maps was disturbed. Multisensory neurons in XMAC also exhibited frequency tuning, but they had longer latencies than normal auditory neurons, suggesting they arise from multisynaptic, non-geniculocortical sources. In a control group of animals with neonatal deafferentation of auditory thalamus but without redirection of retinal axons, tonotopic order and sharp tuning curves were seen, indicating that this aspect of auditory function had developed normally. This result shows that the compromised auditory function in XMAC results from invasion by ectopic visual inputs and not from deafferentation. These findings suggest that the cross-modal plasticity that commonly occurs after loss of sensory input can significantly interfere with recovery from brain damage and that mitigation of maladaptive effects is critical to maximizing the potential for recovery.

Parallel Regulation of Feedforward Inhibition and Excitation during Whisker Map Plasticity

Sensory experience drives robust plasticity of sensory maps in cerebral cortex, but the role of inhibitory circuits in this process is not fully understood. We show that classical deprivation-induced whisker map plasticity in layer 2/3 (L2/3) of rat somatosensory (S1) cortex involves robust weakening of L4-L2/3 feedforward inhibition. This weakening was caused by reduced L4 excitation onto L2/3 fast-spiking (FS) interneurons, which mediate sensitive feedforward inhibition and was partially offset by strengthening of unitary FS to L2/3 pyramidal cell synapses. Weakening of feedforward inhibition paralleled the known weakening of feedforward excitation. As a result, mean excitation-inhibition balance and timing onto L2/3 pyramidal cells were preserved. Thus, reduced feedforward inhibition is a covert compensatory process that can maintain excitatory-inhibitory balance during classical deprivation-induced Hebbian map plasticity.

Transforming sensory perceptions into motor commands: evidence from programming of eye movements.

The visual stimulus for a saccadic eye movement is encoded in place-coded maps in cerebral cortex and the dorsal superior colliculus. In contrast, the motor command for the saccade is encoded by the temporal discharge properties of ocular motoneurons and premotor burst neurons in the brain-stem reticular formation. Thus, there is need for a spatial-temporal transformation of neural signals, and recent findings suggest that the superior colliculus might contribute to this process. The ventral, output layers of the superior colliculus encode the metric of the desired saccade in polar coordinates. However, premotor neurons in the pontine and mesencephalic reticular formation are organized to generate horizontal and vertical saccades, respectively. Studies of oblique saccades in patients with slow vertical components--due to Niemann-Pick type C disease--support the interpretation that the saccadic command from the reticular formation is encoded in Cartesian coordinates. Currently, saccades are thought to be generated under local, brain-stem feedback control in which current eye displacement is continuously subtracted from desired eye displacement to compute motor error--the remaining movement required for the eye to acquire the target. If the superior colliculus is positioned in the feedback loop, then there is a need for transformation of premotor signals back into a place-coded version of motor error. Recent studies suggest that, during the saccade, this might be achieved by a wave of activity spreading rostrally, which traverses the collicular map in a direction corresponding to progressively smaller movements and finally activates a group of neurons concerned with fixation. These new hypotheses are ripe for testing by basic and clinical studies. By confronting the issue of what signal transformations are required to program visually guided saccades, new experimental approaches have emerged. Such computational approaches offer insights into how the brain controls behavior not just by measuring stimulus and response, but by asking what "currency" is being used by interacting populations of neurons at any stage in the process.

Chronic deafferentation in monkeys differentially affects nociceptive and nonnociceptive pathways distinguished by specific calcium-binding proteins and down-regulates gamma-aminobutyric acid type A receptors at thalamic levels.

Chronic deafferentation of skin and peripheral tissues is associated with plasticity of representational maps in cerebral cortex and with perturbations of sensory experience that include severe "central" pain. This study shows that in normal monkeys the nonnociceptive, lemniscal component of the somatosensory pathways at spinal, brainstem, and thalamic levels is distinguished by cells and fibers immunoreactive for the calcium-binding protein parvalbumin, whereas cells of the nociceptive component at these levels are distinguished by immunoreactivity for 28-kDa calbindin. Long-term dorsal rhizotomies in monkeys lead to transneuronal degeneration of parvalbumin cells at brainstem and thalamic sites accompanied in the thalamus by a down-regulation of gamma-aminobutyric acid type A receptors and an apparent increase in activity of calbindin cells preferentially innervated by central pain pathways. Release from inhibition and imbalance in patterns of somatosensory inputs from thalamus to cerebral cortex may constitute subcortical mechanisms for inducing changes in representational maps and perturbations of sensory perception, including central pain.