Line Plot from Scientific Research

Mean calcium and eCB signals from the CA1PC layer during physiological (locomotion; left) and pathological (seizure; right) activity with pharmacological interrogation of the signal. Drugs to block the synthesis and degradation of AEA and 2-AG were used to determine if the eCB signal depended on either or both of these endogenous ligands. Under both physiological and pathological conditions, inhibiting 2-AG synthesis and degradation, but not AEA, was associated with the reduction and augmentation of the eCB signal, respectively, highlighting a key role for 2-AG in activity-dependent eCB dynamics. Notably, seizures were associated with a spreading wave that accompanied postictal flattening on the local field potential. This signal was ~350 times greater than physiological eCB signal changes.

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