Social odor discrimination and its enhancement by associative learning in the hippocampal CA2 region.

Although the hippocampus is crucial for social memory, how social sensory information is combined with contextual information to form episodic social memories remains unknown. Here, we investigated the mechanisms for social sensory information processing using two-photon calcium imaging from hippocampal CA2 pyramidal neurons (PNs)-which are crucial for social memory-in awake head-fixed mice exposed to social and non-social odors. We found that CA2 PNs represent social odors of individual conspecifics and that these representations are refined during associative social odor-reward learning to enhance the discrimination of rewarded compared with unrewarded odors.

Age-Dependent Specific Changes in Area CA2 of the Hippocampus and Social Memory Deficit in a Mouse Model of the 22q11.2 Deletion Syndrome.

Several neuropsychiatric disorders are associated with cognitive and social dysfunction. Postmortem studies of patients with schizophrenia have revealed specific changes in area CA2, a long-overlooked region of the hippocampus recently found to be critical for social memory formation. To examine how area CA2 is altered in psychiatric illness, we used the Df(16)A(+/-) mouse model of the 22q11.

Sick sinus syndrome in HCN1-deficient mice.

Background: Sinus node dysfunction (SND) is a major clinically relevant disease that is associated with sudden cardiac death and requires surgical implantation of electric pacemaker devices. Frequently, SND occurs in heart failure and hypertension, conditions that lead to electric instability of the heart. Although the pathologies of acquired SND have been studied extensively, little is known about the molecular and cellular mechanisms that cause congenital SND.