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STOP knockout and NMDA NR1 hypomorphic mice exhibit deficits in sensorimotor gating
Rosa L Fradley1, Gillian F O'Meara, Richard J Newman
1Merck, Sharp and Dohme Research Laboratories, Neuroscience Research Centre, Terlings Park, Harlow, Essex, UK. rosa_fradley@merck.com
Behavioural Brain Research
|July 28, 2005
Summary
Mice lacking the stable tubule-only polypeptide (STOP) or N-methyl-D-aspartate (NMDA) NR1 gene showed schizophrenic-like behaviors. Clozapine treatment reversed hyperlocomotion but not sensorimotor gating deficits.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Schizophrenia is a neurodevelopmental disorder.
- Stable tubule-only polypeptide (STOP) and N-methyl-D-aspartate (NMDA) NR1 are crucial for neuronal development.
- Transgenic mice lacking STOP or NMDA NR1 may exhibit schizophrenic-like phenotypes.
Purpose of the Study:
- To investigate schizophrenic-like behaviors in STOP knockout and NMDA NR1 hypomorphic mice.
- To assess sensorimotor gating (prepulse inhibition) and hyperlocomotion.
- To determine the effect of clozapine on these behaviors.
Main Methods:
- STOP knockout and NMDA NR1 hypomorphic mouse models were used.
- Prepulse inhibition (PPI) was measured to assess sensorimotor gating.
- Hyperlocomotion was measured in STOP knockout mice.
- Mice were treated with clozapine (1 mg/kg, i.p.) to assess antipsychotic effects.
Main Results:
- Both STOP knockout and NMDA NR1 hypomorphic mice exhibited PPI deficits.
- STOP knockout mice showed hyperlocomotion.
- Clozapine reversed hyperlocomotion in STOP knockout mice.
- Clozapine did not reverse the PPI deficit in either mouse model.
Conclusions:
- STOP and NMDA NR1 genes are implicated in schizophrenic-like behaviors.
- Sensorimotor gating deficits in these models are not responsive to acute clozapine treatment.
- Hyperlocomotion is a potential therapeutic target for antipsychotics like clozapine.
