Several lines of evidence implicate serotonin ( 5-HT ) as the mediator of this enhancement : ( 1 ) Tranyclypromine-enhanced nicotine reinforcement was blocked by the 5-HT₂ receptor antagonists , ritanserin and ketanserin ; ( 2 ) parachloroamphetamine ( PCA ) , a 5-HT releaser , also enhanced nicotine self-administration in animals in which MAO activity was inhibited ; ( 3 ) pretreatment with tranylcypromine increased PCA-induced 5-HT overflow in the nucleus accumbens .
Serotonergic mechanism underlying tranylcypromine enhancement of nicotine self-administration. Although nicotine is generally considered to be the main psychoactive component of tobacco, growing evidence highlights the importance of nonnicotine compounds in smoking reinforcement. Monoamine oxidase (MAO) inhibition is a major consequence of smoking and MAO inhibitors, such as tranylcypromine, increase nicotine reinforcement. tranylcypromine has multiple pharmacological effects, increasing monoamine release for a few hours immediately after its administration and blocking MAO activity for several days. To assess the relative role of these two actions, adult male rats were tested in consecutive daily 3-h sessions for self-administration of nicotine (3 μg kg⁻¹) inj⁻¹, i.v.) either 20 or 1 h following administration of tranylcypromine (3 mg kg⁻¹). Both paradigms were shown to produce highly significant inhibition of MAO activity. However, whereas animals readily acquired self-administration when pretreated with tranylcypromine 1 h prior to testing, they did not with the longer pretreatment interval. Such animals did immediately acquire nicotine self-administration when the tranylcypromine pretreatment interval was switched to 1 h prior to testing on Day 4, indicating that an acute effect of the MAO inhibitor was responsible for enhanced nicotine reinforcement. Several lines of evidence implicate serotonin ( 5-HT ) as the mediator of this enhancement : ( 1 ) Tranyclypromine-enhanced nicotine reinforcement was blocked by the 5-HT₂ receptor antagonists , ritanserin and ketanserin ; ( 2 ) parachloroamphetamine ( PCA ) , a 5-HT releaser , also enhanced nicotine self-administration in animals in which MAO activity was inhibited ; ( 3 ) pretreatment with tranylcypromine increased PCA-induced 5-HT overflow in the nucleus accumbens . These findings suggest that MAO inhibition enhances serotonergic transmission, which serves a critical role in the reinforcing effects of nicotine.
### Instruction:
            Given the context about compound efficacy for the given treatment mentioned within the input, mentioned the compounds 
            that can co-occur for the mentioned treatment

            ### Input:
            Serotonergic mechanism underlying tranylcypromine enhancement of nicotine self-administration. Although nicotine is generally considered to be the main psychoactive component of tobacco, growing evidence highlights the importance of nonnicotine compounds in smoking reinforcement. Monoamine oxidase (MAO) inhibition is a major consequence of smoking and MAO inhibitors, such as tranylcypromine, increase nicotine reinforcement. tranylcypromine has multiple pharmacological effects, increasing monoamine release for a few hours immediately after its administration and blocking MAO activity for several days. To assess the relative role of these two actions, adult male rats were tested in consecutive daily 3-h sessions for self-administration of nicotine (3 μg kg⁻¹) inj⁻¹, i.v.) either 20 or 1 h following administration of tranylcypromine (3 mg kg⁻¹). Both paradigms were shown to produce highly significant inhibition of MAO activity. However, whereas animals readily acquired self-administration when pretreated with tranylcypromine 1 h prior to testing, they did not with the longer pretreatment interval. Such animals did immediately acquire nicotine self-administration when the tranylcypromine pretreatment interval was switched to 1 h prior to testing on Day 4, indicating that an acute effect of the MAO inhibitor was responsible for enhanced nicotine reinforcement. Several lines of evidence implicate serotonin ( 5-HT ) as the mediator of this enhancement : ( 1 ) Tranyclypromine-enhanced nicotine reinforcement was blocked by the 5-HT₂ receptor antagonists , ritanserin and ketanserin ; ( 2 ) parachloroamphetamine ( PCA ) , a 5-HT releaser , also enhanced nicotine self-administration in animals in which MAO activity was inhibited ; ( 3 ) pretreatment with tranylcypromine increased PCA-induced 5-HT overflow in the nucleus accumbens . These findings suggest that MAO inhibition enhances serotonergic transmission, which serves a critical role in the reinforcing effects of nicotine.

            ### Response:
            nicotine, ketanserin, nicotine, tranylcypromine, parachloroamphetamine, ritanserin
            