We
found previously that fear conditioning by combined stimulation
of a row B facial vibrissae (conditioned stimulus, CS) with a tail
shock (unconditioned stimulus, UCS) leads to expansion of the cortical
representation of the “trained” row, labeled with 2-deoxyglucose
(2DG), in the layer IIIb/IV of the adult mouse the primary somatosensory
cortex (S1) 24 h later. We have observed that these learning-dependent
plastic changes are manifested by increased expression of somatostatin,
cholecystokinin (SST+, CCK+) but not parvalbumin (PV+) immunopositive
interneurons We have expanded this research and quantified a numerical
value of CB1-expressing and PV-expressing GABAergic axon terminals
(CB1+ and PV+ immunopositive puncta) that innervate different segments
of postsynaptic cells in the barrel hollows of S1 cortex. We used
3D microscopy to identify the CB+ and PV+ puncta in the barrel cortex
“trained” and the control hemispheres CS+UCS group and
in controls: Pseudoconditioned, CS-only, UCS-only, and naive animals.
We have identified that (i) the association between whisker-shock
“trained” barrel B hollows and CB1+, but not PV+ puncta
expression remained significant after Bonferroni correction, (ii)
CS+UCS has had a significant increasing effect on expression of CB1+
but not PV+ puncta in barrel cortex “trained” hemisphere,
and (iii) the pseudoconditioning had a significant decreasing effect
on expression of CB1+, but not on PV+ puncta in barrel cortex, both
trained and untrained hemispheres. It is correlated to disturbing
behaviors. The results suggest that CB1+ puncta regulation is specifically
linked with mechanisms leading to learning-dependent plasticity in
S1 cortex
