Bdnf-e2-/- mice have an EGFP-STOP cassette inserted upstream of the splice donor site of exon 2 of the brain derived neurotrophic factor (Bdnf) gene that results in disruption of production of BDNF from promoter 2, while leaving expression of BDNF from other promoters intact. During development, BDNF promotes the survival and differentiation of selected neuronal populations where it participates in axonal growth, pathfinding and in the modulation of dendritic growth and morphology. It is a major regulator of synaptic transmission and plasticity at adult synapses in many regions of the central nervous system (CNS). BDNF contributes to a range of adaptive neuronal responses including long-term potentiation (LTP), long-term depression (LTD), certain forms of short-term synaptic plasticity, as well as homeostatic regulation of intrinsic neuronal excitability. Loss of expression of this gene is associated with neurobehavioral alterations and several neuropsychiatric disorders including Alzheimer's, Parkinson's, and Huntington's disease. BDNF transcription is regulated by nine individual promoters, which drive expression of unique splice isoforms. Bdnf-e2 expression in these mice is decreased in the hypothalamus, prefrontal cortex, and hippocampus. These mutant males display heightened aggression with decreased attack latency and increased attack number. Aggression in these mice is accompanied by convergent expression changes in specific genes associated with serotonin signaling, which is associated with control of aggressive behavior. They show increases in expression of the serotonin transporter 5-HTT (Slc6a4) and the serotonin receptor 5-HT2A (Htr2a), accompanied by reduced 5-HT content. They have elevations in GABAergic interneuron marker expressions such as cortistatin (Cort), somatostatin (Sst), corticotropin-releasing factor-binding protein (Crhbp), and tachykinin (Tac1). They also show significant weight gain, lean mass, fat mass, and percent fat in both sexes, which is due to hyperphagia and not altered energy expenditure. Females exhibit reduced sexual receptivity and impaired maternal care, which is associated with decreased oxytocin (Oxt) expression during development. The donating investigator notes that homozygotes are viable, yet homozygous do not care for their young and do become obese. Heterozygous females can show some phenotypes in maternal care and do become obese, although more slowly than homozygotes. For generating homozygous experimental animals, heterozygous mice may be bred together, or heterozygous females may be bred to homozygous males. Of note, similar strains with BDNF transcription selectively disrupted from one of the other major promoters are available: Bdnf-e1-/- mice, with transcription from exon 1 disrupted, are available as Stock No. <a href="https://www.jax.org/strain/033941">033941</a>. Bdnf-e4-/- mice, with transcription from exon 4 disrupted, are available as Stock No. <a href="https://www.jax.org/strain/033943">033943</a>. Bdnf-e6-/- mice, with transcription from exon 6 disrupted, are available as Stock No. <a href="https://www.jax.org/strain/033944">033944</a>.

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Bdnf-e2-/- mice have an EGFP-STOP cassette inserted upstream of the splice donor site of exon 2 of the brain derived neurotrophic factor (Bdnf) gene. These mice may be useful when studying the functional role of BDNF production from unique promoters in aggression and serotonin signaling.

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