AHCODA-DB

Experiment name: Epileptiform Activity and Cognitive Deficits in SNAP-25 Heterozygous Mice are Normalized by Antiepileptic Drugs. (Corradini 2012)
LSID: http://syli.cz/urn:lsid:public.sylics.com:experiment:5B6A-9DE7-G724

TreatmentAmountAdministration routeAdministration time


Treatment info:
Order of behavioural testing
PhenoTyper Spontaneous Behaviour
PhenoTyper Appetitive Conditioning
PhenoTyper Avoidance Learning

Novel Object Recognition

Published in Cerebral Cortex 2012:
http://cercor.oxfordjournals.org/content/24/2/364.long

Epileptiform activity and cognitive deficits in SNAP-25(+/-) mice are normalized by antiepileptic drugs.
Corradini I1, Donzelli A, Antonucci F, Welzl H, Loos M, Martucci R, De Astis S, Pattini L, Inverardi F, Wolfer D, Caleo M, Bozzi Y, Verderio C, Frassoni C, Braida D, Clerici M, Lipp HP, Sala M, Matteoli M.

Abstract
Synaptosomal-associated protein of 25 kDa (SNAP-25) is a protein that participates in the regulation of synaptic vesicle exocytosis through the formation of the soluble NSF attachment protein receptor complex and modulates voltage-gated calcium channels activity. The Snap25 gene has been associated with schizophrenia, attention deficit hyperactivity disorder, and bipolar disorder, and lower levels of SNAP-25 have been described in patients with schizophrenia. We used SNAP-25 heterozygous (SNAP-25(+/-)) mice to investigate at which extent the reduction of the protein levels affects neuronal network function and mouse behavior. As interactions of genotype with the specific laboratory conditions may impact behavioral results, the study was performed through a multilaboratory study in which behavioral tests were replicated in at least 2 of 3 distinct European laboratories. Reductions of SNAP-25 levels were associated with a moderate hyperactivity, which disappeared in the adult animals, and with impaired associative learning and memory. Electroencephalographic recordings revealed the occurrence of frequent spikes, suggesting a diffuse network hyperexcitability. Consistently, SNAP-25(+/-) mice displayed higher susceptibility to kainate-induced seizures, paralleled by degeneration of hilar neurons. Notably, both EEG profile and cognitive defects were improved by antiepileptic drugs. These results indicate that reduction of SNAP-25 expression is associated to generation of epileptiform discharges and cognitive dysfunctions, which can be effectively treated by antiepileptic drugs.

Mouse info:
Mouse ID Strain Coat color Genotype Ear tag Internal ID Sex Date of Birth Sub experiment 1 Sub experiment 2 Sub experiment 3
PH03944 Snap25 unknown hetro male 00-00-0000
PH03945 Snap25 unknown hetro male 00-00-0000
PH03946 Snap25 unknown hetro male 00-00-0000
PH03947 Snap25 unknown hetro male 00-00-0000
PH03948 Snap25 unknown WT male 00-00-0000
PH03949 Snap25 unknown hetro male 00-00-0000
PH03950 Snap25 unknown hetro male 00-00-0000
PH03951 Snap25 unknown WT male 00-00-0000
PH03952 Snap25 unknown hetro male 00-00-0000
PH03953 Snap25 unknown WT male 00-00-0000
PH03954 Snap25 unknown WT male 00-00-0000
PH03955 Snap25 unknown hetro male 00-00-0000
PH03956 Snap25 unknown WT male 00-00-0000
PH03957 Snap25 unknown hetro male 00-00-0000
PH03958 Snap25 unknown WT male 00-00-0000
PH03959 Snap25 unknown WT male 00-00-0000
PH03960 Snap25 unknown WT male 00-00-0000
PH03961 Snap25 unknown WT male 00-00-0000
PH03962 Snap25 unknown hetro male 00-00-0000
PH03963 Snap25 unknown WT male 00-00-0000
PH03964 Snap25 unknown hetro male 00-00-0000
PH03965 Snap25 unknown WT male 00-00-0000
PH03966 Snap25 unknown hetro male 00-00-0000
PH03967 Snap25 unknown WT male 00-00-0000