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Rescue of prepulse inhibition deficit and brain mitochondrial dysfunction by pharmacological stimulation of the central serotonin receptor 7 in a mouse model of CDKL5 Deficiency Disorder.

Abstract：

:Mutations in the X-linked cyclin-dependent kinase-like 5 (CDKL5) gene cause CDKL5 Deficiency Disorder (CDD), a rare neurodevelopmental syndrome characterized by severe behavioural and physiological symptoms. No cure is available for CDD. CDKL5 is a kinase that is abundantly expressed in the brain and plays a critical role in neurodevelopmental processes, such as neuronal morphogenesis and plasticity. This study provides the first characterization of the neurobehavioural phenotype of 1 year old Cdkl5-null mice and demonstrates that stimulation of the serotonin receptor 7 (5-HT7R) with the agonist molecule LP-211 (0.25 mg/kg once/day for 7 days) partially rescues the abnormal phenotype and brain molecular alterations in Cdkl5-null male mice. In particular, LP-211 treatment completely normalizes the prepulse inhibition defects observed in Cdkl5-null mice and, at a molecular level, restores the abnormal cortical phosphorylation of rpS6, a downstream target of mTOR and S6 kinase, which plays a direct role in regulating protein synthesis. Moreover, we demonstrate for the first time that mitochondria show prominent functional abnormalities in Cdkl5-null mouse brains that can be restored by pharmacological stimulation of brain 5-HT7R.

journal_name

Neuropharmacology

journal_title

Neuropharmacology

authors

Vigli D,Rusconi L,Valenti D,La Montanara P,Cosentino L,Lacivita E,Leopoldo M,Amendola E,Gross C,Landsberger N,Laviola G,Kilstrup-Nielsen C,Vacca RA,De Filippis B

doi

10.1016/j.neuropharm.2018.10.018

subject

Has Abstract

pub_date

2019-01-01 00:00:00

pages

104-114

eissn

0028-3908

issn

1873-7064

pii

S0028-3908(18)30802-5

journal_volume

144

pub_type

杂志文章

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