Data and code from: Cholecystokinin modulates age-dependent thalamocortical neuroplasticity

The thalamocortical pathways exhibit neuroplasticity not only during the
critical period but also in adulthood. In this study, we investigated how
cholecystokinin (CCK) modulates age-dependent thalamocortical plasticity.
Our findings demonstrated that CCK is expressed in thalamocortical neurons
and that high-frequency stimulation (HFS) of the thalamocortical pathway
triggers the release of CCK in auditory cortex (ACx), as detected by a CCK
sensor. HFS of the medial geniculate body (MGB) induced thalamocortical
long-term potentiation (LTP) in wild-type young adult mice. However,
knockdown of Cck expression in MGB neurons or blockade of the CCK-B
receptor (CCKBR) in the ACx abolished HFS-induced LTP. Interestingly, this
LTP could not be elicited in juvenile (3-week-old) or aged mice (over
18-month-old) due to distinct mechanisms: the absence of CCKBR in
juveniles and the inability to release CCK in aged mice. Notably,
exogenous administration of CCK into the ACx rescued LTP in aged mice and
significantly improved frequency discrimination. These findings highlight
the potential of CCK as a therapeutic intervention for ameliorating
neuroplasticity deficits associated with thalamocortical connectivity.