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 sonnatosensory cortex

    Authors

    C. Herrera-Rincon;F. Panetsos

    Comments

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    Abbreviated Journal Title

    Front. Cell. Neurosci.

    Keywords

    magnocellular basal nucleus; acetylcholine; plasticity; barrel cortex; BMI; auditory cortex; visual cortex; basal forebrain; SOMATOSENSORY CORTICAL PLASTICITY; EXPERIENCE-DEPENDENT PLASTICITY; RAT; CEREBRAL-CORTEX; VASOACTIVE INTESTINAL POLYPEPTIDE; AUDITORY-CORTEX; ACETYLCHOLINE-RELEASE; NUCLEUS BASALIS; ADULT-RAT; VISUAL-CORTEX; BARREL; CORTEX; Neurosciences

    Abstract

    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.

    Journal Title

    Frontiers in Cellular Neuroscience

    Volume

    8

    Publication Date

    1-1-2014

    Document Type

    Article

    Language

    English

    First Page

    16

    WOS Identifier

    WOS:000345841400001

    ISSN

    1662-5102

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