A non−human model animal suffering from diseases caused by α<sb>1B</sb> Ca<sp>2+</sp> channel dysfunction which is useful in clarifying various pain transmission mechanisms and methods of inhibiting or treating neurodegenerative diseases, endogenous pain, chronic pain, autonomic diseases, emotional disturbance, etc.; a method of screening a preventive/a remedy for the above diseases with the use of the non−human model animal; and so on. The whole potential−dependent Ca<sp>2+</sp> channel α<sb>1B</sb> gene obtained from a mouse gene library or a fragment of this gene is replaced by a marker gene to thereby construct a targeting vector. After linearizing, the targeting vector is transferred into embryonic stem cells. Then the target embryonic stem cells lacking the potential−dependent Ca<sp>2+</sp> channel α<sb>1B</sb> gene function are microinjected into mouse blastocysts and returned into the womb of a host. Thus the non−human model animal suffering from diseases caused by α<sb>1B</sb> Ca<sp>2+</sp> channel dysfunction is constructed.
POTENTIAL−DEPENDENT CA<sp>2+</sp> CHANNEL A1B KNOCKOUT NON−HUMAN ANIMAL