Somatosensory cortical plasticity: recruiting silenced barrels by active whiskers

Erzurumlu, Reha S.

doi:10.1016/s0014-4886(03)00396-0

Cited by 3 publications

(3 citation statements)

References 69 publications

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“…Using this experimental paradigm, the barrels corresponding to the spared whiskers expand their activity to the neighboring barrels and such expansion can reach the entire barrel field, probably due to potentiation or sprouting of horizontal connections in layers II/III and/or IV (Maier et al ., ). Our results give support to layer IV cortical connections as the main pathway for such cortical plasticity (in adult animals plastic changes are intracortically mediated; for a review, see Erzurumlu, ).…”

Section: Discussionsupporting

confidence: 71%

Chronic electrical stimulation of transected peripheral nerves preserves anatomy and function in the primary somatosensory cortex

Herrera-Rincon

Torets

Sánchez‐Jiménez

et al. 2012

Eur J of Neuroscience

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The structure and function of the central nervous system strongly depend on the organization and efficacy of the incoming sensory input. A disruption of somesthetic input severely alters the metabolic activity, electrophysiological properties and even gross anatomical features of the primary somatosensory cortex. Here we examined, in the rat somatosensory cortex, the neuroprotective and therapeutic effects of artificial sensory stimulation after irreversible unilateral transection of a peripheral sensory nerve (the infraorbital branch of the trigeminal nerve). The proximal stump of the nerve was inserted into a silicon tube with stimulating electrodes, through which continuous electrical stimulation was applied for 12 h/day (square pulses of 100 μs, 3.0 V, at 20 Hz) for 4 weeks. Deafferented animals showed significant decreases in cortical evoked potentials, cytochrome oxidase staining intensity (layers II-IV), cortical volume (layer IV) and number of parvalbumin-expressing (layers II-IV) and calbindin-D28k-expressing (layers II/III) interneurons. These deafferentation-dependent effects were largely absent in the nerve-stimulated animals. Together, these results provide evidence that chronic electrical stimulation has a neuroprotective and preservative effect on the sensory cortex, and raise the possibility that, by controlling the physical parameters of an artificial sensory input to a sectioned peripheral nerve, chronically deafferented brain regions could be maintained at near-'normal' conditions. Our findings could be important for the design of sensory neuroprostheses and for therapeutic purposes in brain lesions or neural degenerative processes.

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Section: Discussionsupporting

confidence: 71%

Chronic electrical stimulation of transected peripheral nerves preserves anatomy and function in the primary somatosensory cortex

Herrera-Rincon

Torets

Sánchez‐Jiménez

et al. 2012

Eur J of Neuroscience

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“…This hypothesis emerges from the observation that somatosensory representations in cortex are plastic and can be modified by Hebb-like processes. [103][104][105][106][107][108][109][110][111][112][113] For example, if a neuron receives nearly simultaneous inputs from a weak and a strong sensory synapse, the weak synapse will gain in strength. In the normal primary somatosensory cortex, area 3b, there is a precise differentiation of the representation of the fingers.…”

Section: Focal Hand Dystoniamentioning

confidence: 99%

Animal models of focal dystonia

Evinger

2005

Neurotherapeutics

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Summary: Animal models indicate that the abnormal movements of focal dystonia result from disordered sensorimotor integration. Sensorimotor integration involves a comparison of sensory information resulting from a movement with the sensory information expected from the movement. Unanticipated sensory signals identified by sensorimotor processing serve as signals to modify the ongoing movement or the planning for subsequent movements. Normally, this process is an effective mechanism to modify neural commands for ongoing movement or for movement planning. Animal models of the focal dystonias spasmodic torticollis, writer's cramp, and benign essential blepharospasm reveal different dysfunctions of sensorimotor integration through which dystonia can arise. Animal models of spasmodic torticollis demonstrate that modifications in a variety of regions are capable of creating abnormal head postures. These data indicate that disruption of neural signals in one structure may mutate the activity pattern of other elements of the neural circuits for movement. The animal model of writer's cramp demonstrates the importance of abnormal sensory processing in generating dystonic movements. Animal models of blepharospasm illustrate how disrupting motor adaptation can produce dystonia. Together, these models show mechanisms by which disruptions in sensorimotor integration can create dystonic movements.

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“…The best candidate was the acetylcholine (ACh) because it is heavily involved in plastic reorganization of the sensory and motor cortices and because it downregulates after peripheral deafferentation. ACh is mainly provided to the cortex by the “diffuse” corticopetal cholinergic system originated in the basal forebrain in magnocellular basal nucleus-MBN, the analogous to Meynert nucleus in primates (Mesulam et al, 1983b ; Verdier and Dykes, 2001 ; Erzurumlu, 2003 ; Kamke et al, 2005 ; Conner et al, 2010 ; Saper, 2011 ). ACh participates in the functional reorganization of adult rat, cat and primate sensory, and motor cortices (Celesia and Jasper, 1966 ; Casamenti et al, 1986 ; Rasmusson and Dykes, 1988 ; Sachdev et al, 1998 ; Thiel et al, 2002 ; Golmayo et al, 2003 ; Weinberger, 2004 ).…”

Section: Introductionmentioning

confidence: 99%

Substitution of natural sensory input by artificial neurostimulation of an amputated trigeminal nerve does not prevent the degeneration of basal forebrain cholinergic circuits projecting to the somatosensory cortex

Herrera-Rincon

Panetsos

2014

Front. Cell. Neurosci.

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Peripheral deafferentation downregulates acetylcholine (ACh) synthesis in sensory cortices. However, the responsible neural circuits and processes are not known. We irreversibly transected the rat infraorbital nerve and implanted neuroprosthetic microdevices for proximal stump stimulation, and assessed cytochrome-oxidase and choline- acetyl-transferase (ChAT) in somatosensory, auditory and visual cortices; estimated the number and density of ACh-neurons in the magnocellular basal nucleus (MBN); and localized down-regulated ACh-neurons in basal forebrain using retrograde labeling from deafferented cortices. Here we show that nerve transection, causes down regulation of MBN cholinergic neurons. Stimulation of the cut nerve reverses the metabolic decline but does not affect the decrease in cholinergic fibers in cortex or cholinergic neurons in basal forebrain. Artifical stimulation of the nerve also has no affect of ACh-innervation of other cortices. Cortical ChAT depletion is due to loss of corticopetal MBN ChAT-expressing neurons. MBN ChAT downregulation is not due to a decrease of afferent activity or to a failure of trophic support. Basalocortical ACh circuits are sensory specific, ACh is provided to each sensory cortex “on demand” by dedicated circuits. Our data support the existence of a modality-specific cortex-MBN-cortex circuit for cognitive information processing.

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Somatosensory cortical plasticity: recruiting silenced barrels by active whiskers

Cited by 3 publications

References 69 publications

Chronic electrical stimulation of transected peripheral nerves preserves anatomy and function in the primary somatosensory cortex

Chronic electrical stimulation of transected peripheral nerves preserves anatomy and function in the primary somatosensory cortex

Animal models of focal dystonia

Substitution of natural sensory input by artificial neurostimulation of an amputated trigeminal nerve does not prevent the degeneration of basal forebrain cholinergic circuits projecting to the somatosensory cortex

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