Developmental delays and reduced pup ultrasonic vocalizations but normal sociability in mice lacking the postsynaptic cell adhesion protein neuroligin2

Markus Wöhr, Jill L Silverman, Maria L. Scattoni, Sarah M. Turner, Mark J. Harris, Roheeni Saxena, Jacqueline Crawley

Research output: Contribution to journalArticle

60 Citations (Scopus)

Abstract

Mutations in neurexin and neuroligin genes have been associated with neurodevelopmental disabilities including autism. Autism spectrum disorder is diagnosed by aberrant reciprocal social interactions, deficits in social communication, and repetitive, stereotyped patterns of behaviors, along with narrow restricted interests. Mouse models have been successfully used to study physiological and behavioral outcomes of mutations in the trans-synaptic neurexin-neuroligin complex. To further understand the behavioral consequences of Neuroligin2 (NLGN2) mutations, we assessed several behavioral phenotypes relevant to autism in neuroligin2 null (Nlgn2-/-), heterozygote (Nlgn2+/-), and wildtype (Nlgn2+/+) littermate control mice. Reduced breeding efficiency and high reactivity to handling was observed in Nlgn2-/- mice, resulting in low numbers of adult mice available for behavioral assessment. Consistent with previous findings, Nlgn2-/- mice displayed normal social behaviors, concomitant with reduced exploratory activity, impaired rotarod performance, and delays on several developmental milestones. No spontaneous stereotypies or repetitive behaviors were detected. Acoustic, tactile, and olfactory sensory information processing as well as sensorimotor gating were not affected. Nlgn2-/- pups isolated from mother and littermates emitted fewer ultrasonic vocalizations and spent less time calling than Nlgn2+/+ littermate controls. The present findings add to the growing literature on the role of neurexins and neuroligins in physiology and behavior relevant to neurodevelopmental disorders.

Original languageEnglish (US)
Pages (from-to)50-64
Number of pages15
JournalBehavioural Brain Research
Volume251
DOIs
StatePublished - Aug 15 2013
Externally publishedYes

Fingerprint

Cell Adhesion
Ultrasonics
Autistic Disorder
Proteins
Mutation
Sensory Gating
Stereotyped Behavior
Social Behavior
Touch
Interpersonal Relations
Heterozygote
Automatic Data Processing
Acoustics
Breeding
Communication
Mothers
Phenotype
Genes

Keywords

  • Anxiety
  • Autism
  • Communication
  • GABA
  • Inhibition
  • Neuroligin
  • Schizophrenia
  • Social behavior
  • Ultrasonic vocalization

ASJC Scopus subject areas

  • Behavioral Neuroscience

Cite this

Developmental delays and reduced pup ultrasonic vocalizations but normal sociability in mice lacking the postsynaptic cell adhesion protein neuroligin2. / Wöhr, Markus; Silverman, Jill L; Scattoni, Maria L.; Turner, Sarah M.; Harris, Mark J.; Saxena, Roheeni; Crawley, Jacqueline.

In: Behavioural Brain Research, Vol. 251, 15.08.2013, p. 50-64.

Research output: Contribution to journalArticle

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