Figure 3.

Prerestraint systemic administration of the β-noradrenergic receptor antagonist, propranolol, blocked the decrease in VTA DA neuron population activity and prevented the attenuation of amphetamine-induced locomotor activity measured 24 h after restraint. a1–a3, For all rats restrained for a 2 h session, propranolol pretreatment (PRO; n = 8) significantly increased the DA neuron population activity compared with saline (SAL; n = 9) control (*p < 0.05) (a1), with no significant difference between mean firing rates (a2) or bursting activity (a3). DA neurons recorded: SAL (n = 42), PRO (n = 78). b1, b2, AMPH induced higher locomotor activity regardless pretreatment (b1, SAL; b2, PRO), with significantly higher locomotor activity produced in rats pretreated with PRO. (all ps < 0.05). Group sizes: SAL-SAL (n = 6), SAL-AMPH (n = 5), PRO-SAL (n = 5), and PRO-AMPH (n = 6).