These H2-IFNB transgenic mice have the murine interferon beta 1 (Ifnb1) coding sequence driven by a fragment of the murine histocompatibility 2, K1, K region (H2-K1) promoter. The transgene integrated into the X-linked monoamine oxidase A (Maoa) gene, replacing exons 2-3 and abolishing Maoa gene function. Hemizygous males and homozygous females are viable, and fertile until at least 6 months. MAOA is a mitochondrial enzyme that oxidizes monoamine neurotransmitters and dietary monoamines. These mutants lack MAOA activity resulting in increased levels of serotonin, dopamine, and norepinephrine. Excess serotonin in these mice causes abnormal development of certain neural circuits, such as in the barrelfield. During the first two postnatal weeks, these mice successively exhibit increased trembling and head nodding, frantic running and falling over. Adult males exhibit increased aggression towards subordinate males, male intruders, and females during courtship. These changes are not attributable to expression of the Ifnb1 transgene. These mice may be useful for studying MAOA-related aggression and abnormal development of neural circuits under excess serotonin.

These H2-IFNB transgenic mice have the murine interferon beta 1 (Ifnb1) gene driven by a fragment of the histocompatibility 2, K1, K region (H2-K1) promoter. The transgene integrated into the X-linked monoamine oxidase A (Maoa) gene, replacing exons 2-3 and abolishing Maoa gene function. These mice may be useful for studying MAOA-related aggression and abnormal development of neural circuits under excess serotonin.

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