Presynaptic dopaminergic agonists increased gripping-generated immobility episodes in the myelin-mutant taiep rat

Eguibar, José R.; Cortés, Ma. del Carmen; Lara-Lozano, Manuel

doi:10.1016/j.neulet.2010.07.086

Cited by 5 publications

(2 citation statements)

References 21 publications

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“…It was previously shown that taiep myelin mutant rats develop REM sleep abnormalities and cataplexy-like episodes and share pharmacological alterations similar to the canine model of narcolepsy; this suggests that abnormalities in myelination can lead to a narcolepsy-like phenotype. 32 Interestingly, the phenotype of taiep rats was linked to microtubule alterations in the cytoplasm of oligodendrocytes that lead to deficits in myelin membrane formation. 33 In this context it should be noted that MOG deficient mice (MOGÀ/À) have been extensively investigated for CNS-directed immune responses 34 but have not been examined for possible sleep phenotypes.…”

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confidence: 99%

A Missense Mutation in Myelin Oligodendrocyte Glycoprotein as a Cause of Familial Narcolepsy with Cataplexy

Hor

Bartesaghi

Kutalik

et al. 2011

The American Journal of Human Genetics

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Narcolepsy is a rare sleep disorder characterized by excessive daytime sleepiness and cataplexy. Familial narcolepsy accounts for less than 10% of all narcolepsy cases. However, documented multiplex families are very rare and causative mutations have not been identified to date. To identify a causative mutation in familial narcolepsy, we performed linkage analysis in the largest ever reported family, which has 12 affected members, and sequenced coding regions of the genome (exome sequencing) of three affected members with narcolepsy and cataplexy. We successfully mapped a candidate locus on chromosomal region 6p22.1 (LOD score ¼ 3.85) by linkage analysis. Exome sequencing identified a missense mutation in the second exon of MOG within the linkage region. A c.398C>G mutation was present in all affected family members but absent in unaffected members and 775 unrelated control subjects. Transient expression of mutant myelin oligodendrocyte glycoprotein (MOG) in mouse oligodendrocytes showed abnormal subcellular localization, suggesting an altered function of the mutant MOG. MOG has recently been linked to various neuropsychiatric disorders and is considered as a key autoantigen in multiple sclerosis and in its animal model, experimental autoimmune encephalitis. Our finding of a pathogenic MOG mutation highlights a major role for myelin and oligodendrocytes in narcolepsy and further emphasizes glial involvement in neurodegeneration and neurobehavioral disorders. [corrected].

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confidence: 99%

A Missense Mutation in Myelin Oligodendrocyte Glycoprotein as a Cause of Familial Narcolepsy with Cataplexy

Hor

Bartesaghi

Kutalik

et al. 2011

The American Journal of Human Genetics

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“…It is tempting to speculate that the treatment with a dopamine agonist might have facilitated the manifestation of cataplexy in our patient. In accordance, in a canine model of narcolepsy, the systemic administration of D(2)-dopaminergic agonists increased the frequency of cataplexies 10 . Even more, Burgess et al 11 showed that a D1 receptor mechanism can suppress sleep attacks and a D2 receptor mechanism can regulate cataplexy.…”

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confidence: 55%

Cataplexy in a patient treated for prolactinoma: Case report

et al. 2017

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Introduction. Isolated cataplexy, without the presence of narcolepsy, is a relatively rare condition, and can be regarded as attacks of motor inhibition with loss of muscle tone and areflexia. The diagnosis of cataplexy relies on the clinical presentation and medical history and it is rarely confirmed by video-polygraph. We here described a female patient treated for prolactinoma who developed isolated cataplexy. Case report. A 53-year-old female treated with bromocriptine for a macroprolactinoma presented with sudden episodes of weakness and toneless legs leading to falls and injuries on several occasions. Cardiovascular evaluation was completely normal. Psychiatric evaluation showed no psychotic phenomenology or suicidal ideas. Pituitary imaging showed empty sella with a remnant sellar mass with infra-and parasellar extension. Neurological examination revealed mild obstructive sleep hypopnea/apnea. Electroencephalographic monitoring during sleep and awakening did not show appearance of epi potentials. HLA haplotyping was positive for HLA-DR3,16;DR51;DQ1 allele, confirming a diagnosis of isolated cataplexy. Treatment included tricyclic antidepressants and reduction of bromocriptine dosage with resolution of cataplexy. Conclusion. We reported the first case of isolated cataplexy most probably associated with dopamine agonist treatment for prolactinoma.

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Long-term taurine administration improves motor skills in a tubulinopathy rat model by decreasing oxidative stress and promoting myelination

Vargas-Castro¹,

Gomez-Diaz²,

Blanco-Álvarez³

et al. 2021

Molecular and Cellular Neuroscience

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Presynaptic dopaminergic agonists increased gripping-generated immobility episodes in the myelin-mutant taiep rat

Cited by 5 publications

References 21 publications

A Missense Mutation in Myelin Oligodendrocyte Glycoprotein as a Cause of Familial Narcolepsy with Cataplexy

A Missense Mutation in Myelin Oligodendrocyte Glycoprotein as a Cause of Familial Narcolepsy with Cataplexy

Cataplexy in a patient treated for prolactinoma: Case report

Long-term taurine administration improves motor skills in a tubulinopathy rat model by decreasing oxidative stress and promoting myelination

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