The synthetic predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) was used to induce innate fear in male GAD67 mice and behavioral changes were correlated with c-fos mRNA levels as marker for neuronal activation to reveal underlying activated fear circuits. Results show the same amount of increased freezing and decreased rearing and grooming behavior of TMT-exposed GAD67 mice and wild type littermates, and therefore suggest that heterozygous knock-in of GFP in the GAD67 gene that is associated with a fifty percent decreased GAD67 protein level in the brain, has no impact on TMT-induced behavioral effects. Exposure to TMT significantly increased the number of c-fos mRNA positive cells in the main olfactory bulb (MOB), the lateral septum (LS), the bed nucleus of the stria terminalis (BNST), the central amygdala (CeA), the anterior-ventral (MeAav), the anterior-dorsal (MeAad) and the posterior-ventral (MeApv) part of the medial amygdala in GAD67 mice. Thus, to further investigate the role of GABAergic neurons in TMT-induced uncontrollable stress responses GAD67 mice that provide the advantage of prelabeled GABAergic neurons through the GABA neuron specific expression of GFP could be a suitable model organism.
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