Multisensory Integration

2008 ◽  
Vol 19 (10) ◽  
pp. 989-997 ◽  
Author(s):  
J.E. Lugo ◽  
R. Doti ◽  
Walter Wittich ◽  
Jocelyn Faubert

Multisensory integration in humans is thought to be essentially a brain phenomenon, but theories are silent as to the possible involvement of the peripheral nervous system. We provide evidence that this approach is insufficient. We report novel tactile-auditory and tactilevisual interactions in humans, demonstrating that a facilitating sound or visual stimulus that is exactly synchronous with an excitatory tactile signal presented at the lower leg increases the peripheral representation of that excitatory signal. These results demonstrate that during multisensory integration, the brain not only continuously binds information obtained from the senses, but also acts directly on that information by modulating activity at peripheral levels. We also discuss a theoretical framework to explain this novel interaction.

Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


Development ◽  
1998 ◽  
Vol 125 (4) ◽  
pp. 599-608 ◽  
Author(s):  
M.R. Hirsch ◽  
M.C. Tiveron ◽  
F. Guillemot ◽  
J.F. Brunet ◽  
C. Goridis

Mash1, a mammalian homologue of the Drosophila proneural genes of the achaete-scute complex, is transiently expressed throughout the developing peripheral autonomic nervous system and in subsets of cells in the neural tube. In the mouse, targeted mutation of Mash1 has revealed a role in the development of parts of the autonomic nervous system and of olfactory neurons, but no discernible phenotype in the brain has been reported. Here, we show that the adrenergic and noradrenergic centres of the brain are missing in Mash1 mutant embryos, whereas most other brainstem nuclei are preserved. Indeed, the present data together with the previous results show that, except in cranial sensory ganglia, Mash1 function is essential for the development of all central and peripheral neurons that express noradrenergic traits transiently or permanently. In particular, we show that, in the absence of MASH1, these neurons fail to initiate expression of the noradrenaline biosynthetic enzyme dopamine beta-hydroxylase. We had previously shown that all these neurons normally express the homeodomain transcription factor Phox2a, a positive regulator of the dopamine beta-hydroxylase gene and that a subset of them depend on it for their survival. We now report that expression of Phox2a is abolished or massively altered in the Mash1−/− mutants, both in the noradrenergic centres of the brain and in peripheral autonomic ganglia. These results suggest that MASH1 controls noradrenergic differentiation at least in part by controlling expression of Phox2a and point to fundamental homologies in the genetic circuits that determine the noradrenergic phenotype in the central and peripheral nervous system.


1875 ◽  
Vol 8 ◽  
pp. 136-137 ◽  
Author(s):  
P. D. Handyside

The author showed to the Society a small entire specimen of the P. gladius, and next described, from a larger opened and dissected one, and from part of an adult fish, the spinal cord, the brain, the organs of the senses, and other parts of its nervous system. He illustrated his remarks by exhibiting four large drawings and nine smaller ones, including six microscopic views, explanatory of his description of the structure and disposition of the spino-cerebral axis, the encephalon as viewed from above and below, the ramifications of the encephalic nerves, and more particularly the structures subserving the senses of smell, sight, and hearing.


2018 ◽  
Vol 29 (6) ◽  
pp. 926-935 ◽  
Author(s):  
Christopher C. Berger ◽  
H. Henrik Ehrsson

Can what we imagine in our minds change how we perceive the world in the future? A continuous process of multisensory integration and recalibration is responsible for maintaining a correspondence between the senses (e.g., vision, touch, audition) and, ultimately, a stable and coherent perception of our environment. This process depends on the plasticity of our sensory systems. The so-called ventriloquism aftereffect—a shift in the perceived localization of sounds presented alone after repeated exposure to spatially mismatched auditory and visual stimuli—is a clear example of this type of plasticity in the audiovisual domain. In a series of six studies with 24 participants each, we investigated an imagery-induced ventriloquism aftereffect in which imagining a visual stimulus elicits the same frequency-specific auditory aftereffect as actually seeing one. These results demonstrate that mental imagery can recalibrate the senses and induce the same cross-modal sensory plasticity as real sensory stimuli.


2019 ◽  
Vol 48 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Mark T. Butt

Many preclinical investigations limit the evaluation of the peripheral nervous system (PNS) to paraffin-embedded sections/hematoxylin and eosin–stained sections of the sciatic nerve. This limitation ignores several key mechanisms of toxicity and anatomic differences that may interfere with an accurate assessment of test article effects on the neurons/neurites peripheral to the brain and spinal cord. Ganglion neurons may be exposed to higher concentrations of the test article as compared to neurons in the brain or spinal cord due to differences in capillary permeability. Many peripheral neuropathies are length-dependent, meaning distal nerves may show morphological changes before they are evident in the mid-sciatic nerve. Paraffin-embedded nerves are not optimal to assess myelin changes, notably those leading to demyelination. Differentiating between axonal or myelin degeneration may not be possible from the examination of paraffin-embedded sections. A sampling strategy more consistent with known mechanisms of toxicity, atraumatic harvest of tissues, optimized fixation, and the use of resin and paraffin-embedded sections will greatly enhance the pathologist’s ability to observe and characterize effects in the PNS.


1998 ◽  
Vol 17 (3) ◽  
pp. 231-275 ◽  
Author(s):  
Marciavan Gemert ◽  
James Killeen

The diverse, structurally unrelated chemicals that cause toxic myelinopathies have been investigated and can be categorized into two types of primary demyelinators. Some demyelinating chemicals seem to leave intact the myeli-nating cells (oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system), while others damage the myelinating cells as well as the myelin. The significance between the two is that with the myelinating cells still in tact, repair of the myelin sheath can occur. However, if the myelinating cells are destroyed, repair and reversal of the neuropathy may not occur. Histologically, these chemicals produce an edema of the white matter of the brain, and in some cases the peripheral nervous system, that appears spongy by light microscopy. By electron microscopy, vacuoles can be seen in the myelin surrounding axons. These vacuoles are characterized as fluid-filled separations (splitting) of myelin lamellae at the intraperiod line. In some cases these vacuoles can degenerate further to full demyelination, affecting conduction through those axons. Regeneration of the myelin layers can occur, and in some cases occurs at the same time other axons are undergoing toxic demyelination. Several of these chemicals, however, have been shown to increase cerebrospinal fluid pressure in the brain, optic nerve, and spinal cord, and/or intraneuronal pressure in the perineurium surrounding the axons in the peripheral nervous system. This increased pressure has been correlated with decreased conduction capacity through the axon, ischemia to the neuronal tissue from decreased blood flow because of pressure against the blood vessels, and, if unrelieved, permanent axonal damage. Several of these chemicals havebeen shown to inhibit oxidative phosphorylation, while others uncouple oxidative phosphorylation. One chemical appears to inhibit an enzyme critical to cholesterol synthesis, thus destabilizing myelin. Another hypothesis for a mechanism of action may be in the ability of these compounds to alter membrane permeability.


1927 ◽  
Vol 23 (4) ◽  
pp. 464-464
Author(s):  
V. I. Znamensky

According to V. I. Znamensky indicated for treatment in Matsesta: 1) diseases of the peripheral nervous system, -neuralgia, neuritis; 2) diseases of the central nervous system connected with disorders of the cardiovascular system, - hemiplegia and hemiparesis due to thrombosis and embolism; (treatment of acute forms of the mentioned diseases, it goes without saying, is contraindicated); 3) Luetic diseases,-vascular syphilis of the brain, lues cerebrospinalis, meningo-myelitis, tabes dorsalis incipiens and Luetic radiculitis (here; baths, giving increase of metabolism and excretions, make possible mercury treatment with impunity); 4) remnants of lethargic encephalitis.


2010 ◽  
Vol 120 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Koichi Wakabayashi ◽  
Fumiaki Mori ◽  
Kunikazu Tanji ◽  
Satoshi Orimo ◽  
Hitoshi Takahashi

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