Reorganization After Deafferentations

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Partial deafferentations commonly occur in humans as a result of minor cuts and accidents. Almost everyone has sustained an injury that cut a peripheral nerve, often leaving part of a skin surface numb or insensitive to light touch. More profound deafferentations follow amputations of a digit or limb, and spinal cord injuries that damage ascending afferents in the spinal cord. In the auditory system, individuals lose high-frequency hearing as they age due to a loss of sensory hair cells of the inner ear. This loss can occur earlier in life with exposure to loud, enduring sounds. Parts of the retina also degenerate as certain clinical conditions interfere with retinal blood circulation. Thus, partial losses of afferents are common, and we should know what happens to a sensory system when some of the inputs are lost.

Since the partial loss of sensory afferents can produce dramatic alterations in the organizations of sensory representations (see below), such partial deafferenta-tions usefully demonstrate the potential for brain plasticity, especially in adults where the capacity for such plasticity has been doubted. In addition, reliable methods for producing extensive and easily measured brain plasticity provide an opportunity for discovering how plasticity is mediated. Some or many of the mechanisms of plasticity that are evoked after deafferentations may play a role in other types of brain reorganizations.

Since afferents from the skin, eye, or ear project to sensory nuclei or structures in the brainstem in an orderly almost point-to-point fashion, and this pattern of input is relayed onward to other structures in the system, partial deafferentations deprive parts of representations in every part of the system of their normal sources of activation. If the deafferentation is limited, or the receptive fields for neurons are large, as in higher-order cortical areas, the differentiation may remove only part of the normal sources of activation, and the deprived neurons might only have smaller, reduced receptive fields. Such a change does not reflect any plasticity, only the activity of the preserved inputs. Instead, plasticity is demonstrated by the appearance of inputs that were not apparent before. In most experiments, this means that the neurons acquire receptive fields in new locations on the receptor sheet, although the emergence of new receptive field properties could be considered as evidence for plasticity as well.

With deafferentations, cortical neurons commonly acquire new receptive fields. Early evidence for this came from our studies of the reorganization of area 3b of somatosensory cortex (S1) of monkeys after section of the median nerve to the thumb half of the glaborous hand (Merzenich et al., 1983). The median nerve at the level of the wrist is a sensory nerve with no motor component. Thus, this procedure deprives about half of the hand representation in cortex of activating inputs without eliminating motor control. When neurons in deprived somatosensory cortex are studied with microelectrodes some weeks after the nerve section, the neurons respond to remaining inputs on the dorsal hairy surface of the hand, which is innervated by the intact radial nerve. The change in receptive field locations from the front to the back of the hand is dramatic and obvious. Clearly, neurons do acquire new receptive fields, and the system is plastic, even in the mature brain. These early findings have been confirmed repeatedly in subsequent studies (e.g., Wall et al., 1993; Garraghty et al., 1994), so the results are not in doubt. In addition, similar reorganizations have been observed in area 3b of monkeys (Merzenich et al., 1984; Jain et al., 1998) and S1 of other mammals (see Zarzecki et al., 1993) after the loss of a digit. If digit 3 is lost, for example, cortical neurons that formerly had receptive fields on digit 3 come to have receptive fields on digits 2 or 4, or the adjoining pads of the palm.

Such reorganizations of sensory representations after a limited loss of sensory inputs also occur in the auditory and visual systems. After a partial hearing loss that is restricted to a limited frequency range, cortical neurons that formerly responded to tones in the damaged part of the cochlea came to respond to new tones that were lower or higher than those in the missing range (Rajan et al., 1993; Schwaber et al., 1993; Robertson and Irvine, 1989). After a restricted retinal lesion in cats or monkeys, deprived portions of primary visual cortex came to be activated by surrounding intact portions of the retina (Kaas et a!., 1990; Gilbert and Wiesel, 1992; Darian-Smith and Gilbert, 1995; Chino et al., 1992; Heinen and Skavenski, 1991; Schmid et al., 1996).

Extremely extensive reorganizations have been found in somatosensory cortex of monkeys after major but long-standing deafferentations. The loss of a forelimb, the afferents from a complete arm, or the afferents relayed from the arm and lower body by damage in the spinal cord all extensively deprive much of the body surface representation in area 3b of monkeys. While the lateral-most portion of area 3b that represents the face and mouth retains its normal source of activation, the more medial deprived parts of area 3b slowly become responsive to the face, and any preserved area inputs from the stump (Florence and Kaas, 1995; Pons et al., 1991; Jain et al., 1997). Comparable changes appear to occur in humans with amputations or spinal cord injury (see Flor et al., 1998). Because the extensive reorganizations take months to emerge (Jain et al., 1997), it seems likely that they depend on the growth of new connections (see below).

Finally, deafferentations have been shown to produce rather extensive reorganizations in the ventroposterior nucleus of the somatosensory thalamus of monkeys (Garraghty and Kaas, 1991; Jones and Pons, 1998; Florence et al., 2000) and humans (Davis et al., 1997). Limited recoveries have also been reported in the cuneate nucleus of the brainstem (Xu and Wall, 1997). However, only very limited recoveries have been reported in the visual thalamus after retinal lesions (Eysel, 1982; Darian-Smith and Gilbert, 1995). Reorganization in the auditory thalamus has not yet been adequately studied.

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