BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Talks.cam//talks.cam.ac.uk//
X-WR-CALNAME:Talks.cam
BEGIN:VEVENT
SUMMARY:Exploring the Mechanisms of Associative Plasticity  within and bet
 ween Hippocampal Areas CA1 and CA2 - Sreedharan Sajikumar\, Dept of Physio
 logy\, NUS\, Singapore
DTSTART:20231124T120000Z
DTEND:20231124T133000Z
UID:TALK205954@talks.cam.ac.uk
CONTACT:Susan Jones
DESCRIPTION:The hippocampus plays an integral role in episodic memory\, pr
 imarily through neurons in the CA1 subfield. Beyond the well-established c
 anonical circuitry\, the CA2 region is implicated in social memory. CA2 ne
 urons also display unique biochemical properties and are more resistant to
  plasticity. Our earlier studies observed metaplastic effects of neuromodu
 lators that permit plasticity in CA2 neurons.  Notably\, there are monosyn
 aptic connections from CA2 that innervate CA1\, the functional relevance o
 f which remains relatively unknown. Our study aims to investigate how thes
 e CA2-CA1 connections can modulate the maintenance of functional plasticit
 y models\, such as long-term potentiation (LTP) and long-term depression (
 LTD)\, within the Schaffer collateral (SC)-CA1 synapses. Subthreshold stim
 ulation of SC-CA1 synapses revealed an early form of LTP (early-LTP) but n
 ot the persistent late form (late-LTP). However\, when 'primed' by the act
 ivation of CA2\, SC-CA1 synapses exhibit protein synthesis-dependent late-
 LTP upon subthreshold stimulation within a temporal window that also promo
 tes associative plasticity\, such as synaptic tagging and capture (STC). M
 oreover\, CA2 'priming' does not disrupt the persistence of late forms of 
 LTD when SC-CA1 synapses are stimulated by strong low-frequency stimulatio
 n. In fact\, weak low-frequency stimulation can promote protein synthesis-
 dependent late-LTD in CA2-primed SC-CA1 synapses. Lastly\, we established 
 a behavioral model wherein social novelty\, which activates CA2\, can enha
 nce the persistence of CA1-dependent memory via the weak inhibitory avoida
 nce task. Combining a chemogenetics approach with behavioral assays also c
 onfirmed the role of CA2 in enhancing CA1-dependent memory. This set of re
 sults demonstrates that CA2 connections onto CA1 can influence the synapti
 c plasticity of CA1\, suggesting possible implications for how social beha
 vioral states can modulate the persistence of memory.
LOCATION:Bryan Matthews Seminar Room\, Physiology Buiding\, Department of 
 Physiology\, Development and Neuroscience University of Cambridge
END:VEVENT
END:VCALENDAR