scholarly journals Altered cerebellar response to somatosensory stimuli in the Cntnap2 mouse model of autism

2021 ◽  
Author(s):  
Marta Fernandez ◽  
Carlos A Sanchez-Leon ◽  
Javier Llorente ◽  
Teresa Sierra-Arregui ◽  
Shira Knafo ◽  
...  
Keyword(s):  
Mouse Model ◽  
Purkinje Cells ◽  
Sensory Information ◽  
Postmortem Brain ◽  
Cerebellar Malformations ◽  
Physiological Analysis ◽  
Sensory Evoked Potentials ◽  
Whisker Pad ◽  
Crus I ◽  
Sensory Evoked

Atypical sensory processing is currently included within the diagnostic criteria of autism. The cerebellum is known to integrate sensory inputs of different modalities through its connectivity to the cerebral cortex. Interestingly, cerebellar malformations are among the most replicated features found in postmortem brain of individuals with autism. We studied cerebellar integration of sensory information in a mouse model of autism, knockout for the Cntnap2 gene. Cntnap2 is widely expressed in Purkinje cells and has been recently reported to regulate their morphology. Further, individuals with CNTNAP2 mutations display cerebellar malformations and CNTNAP2 antibodies are associated with a mild form of cerebellar ataxia. Previous studies in this mouse model show an altered cerebellar sensory learning. However, a physiological analysis of cerebellar function has not been performed yet. We studied sensory evoked potentials in cerebellar Crus I/II region upon electrical stimulation of the whisker pad in alert mice and found striking differences between WT and Cntnap2 KO mice. In addition, single-cell recordings identified alterations in both sensory-evoked and spontaneous firing patterns of Purkinje cells. These alterations were accompanied by altered intrinsic properties and morphological features of these neurons. Together, these results indicate that the Cntnap2 mouse model could provide novel insight into the pathophysiological mechanisms of ASD core sensory deficits. 

Latencies of vagus sensory evoked potentials are prolonged in Parkinson's disease

2009 ◽  
Vol 36 (S 02) ◽  
Author(s):  
T Polak ◽  
D Weise ◽  
F Metzger ◽  
A Schramm ◽  
AJ Fallgatter ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Evoked Potentials ◽  
Sensory Evoked Potentials ◽  
Sensory Evoked

Comparison of sensory evoked potentials during neurosurgery under remimazolam anesthesia with those under propofol anesthesia

2021 ◽  
Author(s):  
Ryusuke TANAKA ◽  
Atsushi SATO ◽  
Kenji SHINOHARA ◽  
Tohru SHIRATORI ◽  
Chiaki KIUCHI ◽  
...  
Keyword(s):  
Evoked Potentials ◽  
Sensory Evoked Potentials ◽  
Sensory Evoked

119. Dermatomal sensory evoked potentials in sensory neuropathies of lower limb

2013 ◽  
Vol 124 (11) ◽  
pp. e215-e216
Author(s):  
G. de Scisciolo ◽  
R. Caramelli ◽  
V. Schiavone ◽  
F. Del Corso ◽  
A. Comanducci ◽  
...  
Keyword(s):  
Evoked Potentials ◽  
Lower Limb ◽  
Sensory Evoked Potentials ◽  
Sensory Evoked

scholarly journals Intra-operative neurophysiological monitoring

2015 ◽  
Vol 02 (03) ◽  
pp. 179-192
Author(s):  
Zulfiqar Ali ◽  
Parmod Bithal
Keyword(s):  
Evoked Potentials ◽  
Surgical Procedures ◽  
Complication Rate ◽  
Motor Evoked Potentials ◽  
Neurological Complication ◽  
Intraoperative Neurophysiological Monitoring ◽  
Neurophysiological Monitoring ◽  
Sensory Evoked Potentials ◽  
Sensory Evoked

AbstractIntraoperative neurophysiological monitoring has achieved importance due to complexity of cranio-spinal surgical procedures being performed frequently these days. Many studies have proven a decreased neurological complication rate after its introduction. It is broadly of two types: Sensory evoked potentials and motor evoked potentials which are further sub-divided. Its use during surgery requires a controlled anaesthesia technique with no or minimal influence on its recording. Its success depends upon three way communication among the surgeon the neurophysiologist and the anaesthesiologist.

scholarly journals Altered White Matter and Layer VIb Neurons in Heterozygous Disc1 Mutant, a Mouse Model of Schizophrenia

2020 ◽  
Vol 14 ◽  
Author(s):  
Shin-Hwa Tsai ◽  
Chih-Yu Tsao ◽  
Li-Jen Lee
Keyword(s):  
White Matter ◽  
Mouse Model ◽  
Pyramidal Neurons ◽  
Sensory Information ◽  
Morphological Characters ◽  
Cortical Layer ◽  
Type I ◽  
Brain Functions ◽  
Neuron Density ◽  
Subplate Neurons

Increased white matter neuron density has been associated with neuropsychiatric disorders including schizophrenia. However, the pathogenic features of these neurons are still largely unknown. Subplate neurons, the earliest generated neurons in the developing cortex have also been associated with schizophrenia and autism. The link between these neurons and mental disorders is also not well established. Since cortical layer VIb neurons are believed to be the remnant of subplate neurons in the adult rodent brain, in this study, we aimed to examine the cytoarchitecture of neurons in cortical layer VIb and the underlying white matter in heterozygous Disc1 mutant (Het) mice, a mouse model of schizophrenia. In the white matter, the number of NeuN-positive neurons was quite low in the external capsule; however, the density of these cells was found increased (54%) in Het mice compared with wildtype (WT) littermates. The density of PV-positive neurons was unchanged in the mutants. In the cortical layer VIb, the density of CTGF-positive neurons increased (21.5%) in Het mice, whereas the number of Cplx3-positive cells reduced (16.1%) in these mutants, compared with WT mice. Layer VIb neurons can be classified by their morphological characters. The morphology of Type I pyramidal neurons was comparable between genotypes while the dendritic length and complexity of Type II multipolar neurons were significantly reduced in Het mice. White matter neurons and layer VIb neurons receive synaptic inputs and modulate the process of sensory information and sleep/arousal pattern. Aberrances of these neurons in Disc1 mutants implies altered brain functions in these mice.

scholarly journals Human alpha-synuclein overexpressing MBP29 mice mimic functional and structural hallmarks of the cerebellar subtype of multiple system atrophy

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Lisa Mészáros ◽  
Markus J. Riemenschneider ◽  
Heiko Gassner ◽  
Franz Marxreiter ◽  
Stephan von Hörsten ◽  
...  
Keyword(s):  
Mouse Model ◽  
Multiple System Atrophy ◽  
Cerebellar Ataxia ◽  
Purkinje Cells ◽  
Alpha Synuclein ◽  
Significant Loss ◽  
Disease Stage ◽  
Cytoplasmic Inclusions ◽  
Unsteady Gait ◽  
Advanced Disease Stage

AbstractMultiple system atrophy (MSA) is a rare, but fatal atypical parkinsonian disorder. The prototypical pathological hallmark are oligodendroglial cytoplasmic inclusions (GCIs) containing alpha-synuclein (α-syn). Currently, two MSA phenotypes are classified: the parkinsonian (MSA-P) and the cerebellar subtype (MSA-C), clinically characterized by predominant parkinsonism or cerebellar ataxia, respectively. Previous studies have shown that the transgenic MSA mouse model overexpressing human α-syn controlled by the oligodendroglial myelin basic protein (MBP) promoter (MBP29-hα-syn mice) mirrors crucial characteristics of the MSA-P subtype. However, it remains elusive, whether this model recapitulates important features of the MSA-C-related phenotype. First, we examined MSA-C-associated cerebellar pathology using human post-mortem tissue of MSA-C patients and controls. We observed the prototypical GCI pathology and a preserved number of oligodendrocytes in the cerebellar white matter (cbw) accompanied by severe myelin deficit, microgliosis, and a profound loss of Purkinje cells. Secondly, we phenotypically characterized MBP29-hα-syn mice using a dual approach: structural analysis of the hindbrain and functional assessment of gait. Matching the neuropathological features of MSA-C, GCI pathology within the cbw of MBP29-hα-syn mice was accompanied by a severe myelin deficit despite an increased number of oligodendrocytes and a high number of myeloid cells even at an early disease stage. Intriguingly, MBP29-hα-syn mice developed a significant loss of Purkinje cells at a more advanced disease stage. Catwalk XT gait analysis revealed decreased walking speed, increased stride length and width between hind paws. In addition, less dual diagonal support was observed toward more dual lateral and three paw support. Taken together, this wide-based and unsteady gait reflects cerebellar ataxia presumably linked to the cerebellar pathology in MBP29-hα-syn mice. In conclusion, the present study strongly supports the notion that the MBP29-hα-syn mouse model mimics important characteristics of the MSA-C subtype providing a powerful preclinical tool for evaluating future interventional strategies.

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