Neural cell adhesion molecule-null mice are not deficient in prepulse inhibition of the startle response.
Mice constitutively deficient in the neural cell adhesion molecule have morphological changes in the brain, which are hallmarks of schizophrenia. Schizophrenic patients are impaired in sensorimotor processing indicated by a deficit in prepulse inhibition of the acoustic startle response. Here we tested whether prepulse inhibition and prepulse facilitation are changed in neural cell adhesion molecule-deficient mice compared with their wild-type littermates. Neither prepulse inhibition nor prepulse facilitation (which occurred only at the lowest prepulse intensity used and was weak) was altered. This result is discussed in the light of the 'two-hit' hypothesis of schizophrenia, suggesting that in neural cell adhesion molecule-deficient mice, a prepulse inhibition deficit may become apparent only after treatment with a 'second hit' (such as increased stress).
Plappert
Claudia F
CF
Universität Tübingen, Zoologisches Institut, Fakultät fur Biologie, Universität Tübingen, Morgenstelle 28, 72076 Tübingen, Germany. claudia.plappert@uni-tuebingen.de
Schachner
Melitta
M
Pilz
Peter K D
PK
D000161:Acoustic Stimulation / Q000379:methods; D000704:Analysis of Variance; D000818:Animals; D004307:Dose-Response Relationship, Radiation; D007266:Inhibition, Psychological; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout / Q000502:physiology; D019006:Neural Cell Adhesion Molecules / Q000172:deficiency* / Q000502:physiology; D013216:Reflex, Startle / Q000235:genetics* / Q000528:radiation effects; D013997:Time Factors
D019006:Neural Cell Adhesion Molecules