Conventional approaches to behavioral correction, aimed at curbing addictive behaviors, often involve methods like electric shocks, which, while effective, pose a risk of harm due to induced nociceptive pain. Recent findings show that calcitonin gene-related peptide in the parabrachial nucleus (CGRPPBN) provides affective pain signals and generates general alarm signals. Here we investigated whether stimulating CGRPPBN neurons could replicate the behavioral correction effects of electrical shock, thereby suppressing addictive behavior without causing physical harm. Using Calca-Cre::DAT-Cre mice with channelrhodopsin-2 (ChR2) expressed in midbrain dopamine and CGRPPBN neurons, we first trained animals to press a lever for optical stimulation of dopamine cells (1s, 20Hz) until they developed addictive lever-pressing behavior (>400 lever presses/hour). Then, each lever press triggered optical stimulation in the CGRPPBN neurons (3s, 30Hz) instead of the stimulation of dopamine cells. Upon activation of CGRPPBN neurons, the mice exhibited a significant reduction in lever-pressing behavior compared to control animals without ChR2 expression in CGRPPBN neurons. This also impacted long-term memory, as the suppression effect of addictive-like behavior remained even 10 days after the last stimulation of CGRPPBN. Next, we investigated whether activating CGRPPBN could also suppress addictive behavior in the context of actual drug use. We trained animals to self-administer cocaine intravenously for over 10 days. Upon switching to CGRPPBN activation, we observed a similar reduction in lever-pressing, which was sustained even after a 14-day abstinence period. Collectively, these results indicate CGRPPBN generates alarm signals in the brain that strongly curb addictive behavior and effectively halt ongoing behavior.