Fig. 1.

ORM reconsolidation is mediated by a Gs protein-independent β₁-AR signaling pathway. Mice trained with object A and object B were reexposed to both objects (A+B) for memory reactivation (RA) 24 h later. Drug injection was given within 2 min after memory reactivation. Memory retention was tested by exposure to object A and object C (A+C). Values in the bar indicate number of mice per group. (A and E) Postreactivation i.p. injection of propranolol (Prop, 10 mg/kg) or betaxolol (Bet; 1.0 mg/kg) inhibited reconsolidation, whereas ICI 118,551 (ICI; 10 mg/kg), carvedilol (Car; 3.0 mg/kg), alprenolol (Alp; 10 mg/kg), or vehicle (Veh; 4.0 mL/kg) did not. **P < 0.01, ***P < 0.001 vs. RA (A+B) with the same drug treatment. (B and F) Administration of Bet (1.0 mg/kg, i.p.) before Car (10 µg i.c.v.) or Alp (10 µg, i.c.v.) decreased preference index, whereas injection of Car or Alp alone did not. **P < 0.01, ***P < 0.001 vs. (A+B) with same drug treatment. (C and D) Injection of Car (3.0 mg/kg, i.p. or 10.0 µg, i.c.v., within 2 min after memory reactivation) decreased cAMP level and PKA activity in the Enc as determined 5 min after RA. Data are expressed as percentage of basal level determined before reactivation. *P < 0.05, **P < 0.01 vs. Veh, t test. (G) ORM retention was tested 2 d after training. β-Blockers were given 1 d after training without memory reactivation. *P < 0.05, **P < 0.01 vs. Training (A+B) with same drug treatment. (H) ORM retention was tested 1 h after memory reactivation. *P < 0.05, **P < 0.01, ***P < 0.001 vs. RA (A+B) within same treatment.