TY - JOUR
T1 - Lack of effect of an early stressful life event on sensorimotor gating in adult rats
AU - Lehmann, Julia
AU - Pryce, Christopher R.
AU - Feldon, Joram
N1 - Funding Information:
This work was supported by a grant from the Swiss Federal Institute of Technology Zürich. We thank Animal Services for the maintenance and care of the animals.
PY - 2000/1/21
Y1 - 2000/1/21
N2 - Hypotheses of the etiology of schizophrenia emphasize the important role of perinatal insults in predisposing individuals to the development of the disease, so that an animal model in which a discrete postnatal manipulation of the infant social environment yields schizophrenia-like behavior in adulthood would be valuable in terms of the study of the neural substrate and treatment of schizophrenia. Schizophrenics demonstrate a deficit in sensorimotor gating (prepulse inhibition), and a similar phenomenon has been described in adult rats following the administration of direct and indirect dopamine agonists. Recently it has been reported that a 24 h separation of rat pups from the mother results in a disruption of prepulse inhibition at adulthood. Here we report a study which investigated the same phenomenon but which, in contrast to the previous study, utilized unrelated subjects all derived from different dams. Maternal separation was conducted for 24 h with pups aged 4, 9 or 18 days and these subjects, together with non-separated controls, were tested at age 3 months in terms of their prepulse inhibition in the acoustic startle response paradigm. Maternal separation did not disrupt prepulse inhibition. Comparison of males and females (with a maximum of one opposite-sex sibling) demonstrated that acoustic startle response and prepulse inhibition of this response was enhanced in males relative to females. This study indicates that 24 h maternal separation does not provide a robust model for studying the effects of early environmental insults on the long-term abnormal development of sensorimotor gating. (C) 2000 Elsevier Science B.V. All rights reserved.
AB - Hypotheses of the etiology of schizophrenia emphasize the important role of perinatal insults in predisposing individuals to the development of the disease, so that an animal model in which a discrete postnatal manipulation of the infant social environment yields schizophrenia-like behavior in adulthood would be valuable in terms of the study of the neural substrate and treatment of schizophrenia. Schizophrenics demonstrate a deficit in sensorimotor gating (prepulse inhibition), and a similar phenomenon has been described in adult rats following the administration of direct and indirect dopamine agonists. Recently it has been reported that a 24 h separation of rat pups from the mother results in a disruption of prepulse inhibition at adulthood. Here we report a study which investigated the same phenomenon but which, in contrast to the previous study, utilized unrelated subjects all derived from different dams. Maternal separation was conducted for 24 h with pups aged 4, 9 or 18 days and these subjects, together with non-separated controls, were tested at age 3 months in terms of their prepulse inhibition in the acoustic startle response paradigm. Maternal separation did not disrupt prepulse inhibition. Comparison of males and females (with a maximum of one opposite-sex sibling) demonstrated that acoustic startle response and prepulse inhibition of this response was enhanced in males relative to females. This study indicates that 24 h maternal separation does not provide a robust model for studying the effects of early environmental insults on the long-term abnormal development of sensorimotor gating. (C) 2000 Elsevier Science B.V. All rights reserved.
KW - Litter effects
KW - Long-term development
KW - Maternal separation
KW - Rat model
KW - Schizophrenia
KW - Sensorimotor gating
UR - http://www.scopus.com/inward/record.url?scp=0033980112&partnerID=8YFLogxK
U2 - 10.1016/S0920-9964(99)00080-8
DO - 10.1016/S0920-9964(99)00080-8
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AN - SCOPUS:0033980112
SN - 0920-9964
VL - 41
SP - 365
EP - 371
JO - Schizophrenia Research
JF - Schizophrenia Research
IS - 2
ER -