These transgenic mice overexpress the mouse galanin protein under the direction of the human dopamine beta-hydroxylase promoter. Mice that are homozygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. In situ hybridization analysis of brain detects a 5-fold increase in galanin mRNA levels in the locus coeruleus region. Radioimmunoassay reveals a 2-fold increase in gene product peptide level in the forebrain. An increase of galanin-like immunoreactive staining and fiber density is also detected. The number of basal forebrain cholinergic neurons is decreased. Transgenic mice have impaired learning and memory as assessed by the Morris spatial navigational test and the social transmission of food preference test. Resistance to seizures induced by perforant path stimulation or administration of kainic acid is increased. Mutant mice exhibit increased afterdischarge (AD) induction threshold and diminished glutamate release after depolarization. Treatment with M35, a galanin receptor antagonist, rescues abnormal seizure response. Perforant path-dentate gyrus long-term potentiation is impaired. This mutant mouse strain represents a model that may be useful in studies of Alzheimer's disease and epileptic seizures.

These GalOE mice express a transgene containing the mouse galanin protein under the direction of the human dopamine beta-hydroxylase promoter and have impaired learning and memory with an increase of galanin in the brain.

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B6.Cg-Tg(DBH-Gal)1923Stei/J Frozen Embryos