Somatosensory Cortex

The somatosensory cortex of mammals has a number of subdivisions or processing areas. Although the number varies by species, each cerebral hemisphere in all mammals contains at least two systematic representations of the tactile receptors of the contralateral body surface, the primary somatic area SI, and the secondary somatic area SII. Neurons throughout these representations can be activated by stimuli on restricted portions of the body surface, the receptive fields of the neurons. These two representations have fairly consistent organizations from individual to individual within a species and conform to a general plan across species. Yet the organizations of the maps of the body surface can be altered in developing or adult mammals by removing or changing the significance of some of the inputs, or by damaging parts of maps. These changes in map organizations result from neurons losing their original receptive fields and acquiring new ones on different body parts. Thus, the organization of somatosensory cortex can change. Best documented in primates and rats, such changes have also been observed in humans.

Plasticity in the somatosensory cortex may be important in development by allowing the sensory systems of individuals to adjust to bodily growth through the use of information from the environment. Plasticity in adults may also be important in reassigning neurons to new roles after damage to the system in order to promote recovery. Following amputations, researchers have noted changes in patients' somatosensory cortex that often correlate with phantom pains. After a stroke, recovery of function is also related to changes in cortical organization.

The plasticity of the somatosensory cortex is probably most important for allowing adjustments in the neural network that may be critical in learning sensorimotor skills. Monkeys trained in various types of tactile discrimination tasks exhibit changes in the cortical organization of the trained skin surfaces that reflect the temporal and spatial structure of the trained stimuli. In humans, training for skilled motor behaviors evinces changes in SI. For example, trained violinists have larger SI representations of the hand used to finger the instrument than that used to bow it, and both representations are larger than in untrained subjects.

Researchers have used two dominant experimental methods to examine mechanisms underlying somatosensory plasticity. In one, they induce plasticity by cutting the sensory nerves to part of the skin or by dorsal rhizotomy. For example, over several weeks, neurons in the somatosensory cortex formerly activated by inputs from the denervated hand of a monkey acquire new receptive fields on adjoining parts of the hand that have intact sensory afferents. Some reactivation may occur sooner, within seconds or hours of the nerve section. In the other method, they induce plasticity by manipulating the patterns of use of the skin surface, thus obviating the need for a destructive lesion. For example, trimming all but two adjacent whiskers in a rat strengthens those whiskers' abilities to excite SI, both in their own somatotopic territory and in that of the other untrimmed whisker. Overall, there are likely to be several different cellular mechanisms of cortical plasticity with different intervals.

It is not clear how the cortex reorganizes, but there are several obvious possibilities. In both adult and developing brains, plasticity, particularly its initial stages, seems to result from alterations in the effectiveness of anatomical connections. Indeed, changes in synaptic efficacies of thalamocortical and intracortical projections have been detected after whisker pairing in intact animals and in brain slices. Such changes are likely based on Hebbian processes such as long-term potentiation (LTP) and depression (LTD), both of which can be elicited in SI. There is more evidence for these types of mechanisms: Blockade of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor, which is necessary for the induction of cortical LTP, can also block plasticity of SI.

In addition to Hebbian processes, some immediate recovery of cortical responsiveness might be due to a reduction in the lateral spread of inhibition of excitatory pathways, a result of removal of a source of activation for the inhibitory neurons. Other changes might be due to a reduction in the production of inhibitory or neuromodulatory (such as acetylcholine, norepinephrine, or serotonin) neurotransmitters in the deprived zones of cortex. Over longer times, new connections are likely to be formed, such as those observed in the hindbrain nuclei and cortex. Increases in the number, size, or strength of excitatory synaptic contacts probably play a major role, and this could involve the formation of new synapses and the elaboration of axon arbors, dendrites, and dendritic spines.

The changes in the cortex reflect, in part, adjustments made in the relays of sensory information in the brain stem and thalamus before they reach the cortex. There is evidence for changes in the receptive fields of spinal cord neurons after section or anesthetic block of peripheral nerves. Other changes, particularly sprouting of new connections after early lesions and transneuronal atrophy, have occurred in the hindbrain and thalamus and undoubtedly contribute to cortical reorganization. Probably all the mechanisms cited above underlie the plasticity in these sub-cortical somatosensory areas. There is evidence for purely cortical changes, however, including observations of receptive field changes in cortex that are not observed in thalamus, reorganization of SII after partial lesions of SI (which provides the only input to SII), and changes in isolated slices of cortex after reorganization. Interestingly, rats implanted with multielect-rode arrays demonstrate rapid changes at all levels of the somatosensory pathway in response to anesthetic block of peripheral nerves; the dynamics of these changes suggest that the changes are relayed from the cortex to thalamus and hindbrain, not just in the ascending direction.

Plasticity of sensory representation in cortex has been most extensively studied for the somatosensory cortex, but reorganizations occur after partial removals of inputs for visual, auditory and motor areas as well. Thus, plasticity is a basic feature of important systems throughout the brain.

Bibliography

Buonomano, D. V., and Merzenich, M. M. (1998). Cortical plasticity: From synapses to maps. Annual Review of Neuroscience 21, 149-186.

Ebner, F. F., Rema, V., Sachdev, R., and Symons, F. J. (1997). Activity-dependent plasticity in adult somatic sensory cortex. Seminars in Neuroscience 9, 47-58.

Jones, E. G. (2000). Cortical and subcortical contributions to activity-dependent plasticity in primate somatosensory cortex. Annual Review of Neuroscience 23, 1-37.

Kaas, J. H. (1991). Plasticity of sensory and motor maps in adult mammals. Annual Review of Neuroscience 14, 137-167.

Jon H.Kaas

Revised byPeter W.Hickmott