The Brain Body Institute
The Brain Body Institute
Sidor M.M.,McMaster University |
Sidor M.M.,The Brain Body Institute |
Rilett K.,McMaster University |
Rilett K.,The Brain Body Institute |
And 2 more authors.
Journal of Neuroscience Methods | Year: 2010
The elevated plus maze (EPM) is one of the most widely used and established tests to assess anxiety-related behaviours and has been validated for use in both mice and rats. Although relatively quick and simple to conduct, there always exists the potential for observer bias during data collection. The KinderScientific EPM system uses a series of apparatus-embedded photobeams to collect spatiotemporal measures such as the amount of time spent in each zone of the maze (centre, open and closed arms), and the frequency of arm entries. Risk assessment behaviours, such as head dips and protected stretches, are also measured which represents a unique feature of this system over other automated EPM systems. We compared observer derived spatiotemporal and risk assessment measurements with automated generated data to test the reliability and accuracy of the automated system. Data were manually collected using different zone entry/exit criteria (2 vs. 4 paws). Automated data were generated using both the default zone map provided with the system and a user-modified zone map. We show that the automated EPM provides accurate and reliable measurements of both spatiotemporal and risk assessment behaviours. In addition, we show that the default zone map overestimated visually observed arm entries while our modified zone map generated data comparable to manually generated data using a 4 paws open arm entry criteria which is most consistently used to define arm entry in the literature. The KinderScientific automated EPM system represents a reliable tool for collection of a wide range of anxiety-related behavioural measures. © 2010 Elsevier B.V.
Roullet F.I.,McMaster University |
Roullet F.I.,The Brain Body Institute |
Wollaston L.,McMaster University |
Wollaston L.,The Brain Body Institute |
And 3 more authors.
Neuroscience | Year: 2010
Experiments in rodents have indicated that maternal valproic acid (VPA) exposure has permanent adverse effects upon neurological and behavioral development. In humans, prenatal exposure to VPA can induce fetal valproate syndrome, which has been associated with autism. The present study examined mouse pups exposed in utero to VPA, measuring physical development, olfactory discrimination, and social behavior as well as expression of plasticity-related genes, brain derived neurotrophic factor (BDNF) and NMDA receptor subunits NR2A and NR2B. VPA-exposed mice showed delayed physical development, impaired olfactory discrimination, and dysfunctional pre-weaning social behavior. In situ hybridization experiments revealed lower cortical expression of BDNF mRNA in VPA animals. These results support the validity of the VPA mouse model for human autism and suggest that alterations in plasticity-related genes may contribute to the behavioral phenotype. © 2010 IBRO.
Hall G.B.C.,McMaster University |
Hall G.B.C.,The Brain Body Institute |
Doyle K.A.R.,McMaster University |
Goldberg J.,McMaster University |
And 2 more authors.
PLoS ONE | Year: 2010
Current theoretical models of autism spectrum disorders (ASD) have proposed that impairments in the processing of social/ emotional information may be linked to amygdala dysfunction. However, the extent to which amygdala functions are compromised in ASD has become a topic of debate in recent years. In a jittered functional magnetic resonance imaging study, sub-threshold presentations of anxious faces permitted an examination of amygdala recruitment in 12 high functioning adult males with ASD and 12 matched controls. We found heightened neural activation of the amygdala in both high functioning adults with ASD and matched controls. Neither the intensity nor the time-course of amygdala activation differed between the groups. However, the adults with ASD showed significantly lower levels of fusiform activation during the trials compared to controls. Our findings suggest that in ASD, the transmission of socially salient information along subcortical pathways is intact: and yet the signaling of this information to structures downstream may be impoverished, and the pathways that facilitate subsequent processing deficient. © 2010 Hall et al.