HTR1A and Anxiety: Collectively, our results suggest that enhancing Gi signaling in forebrain excitatory neurons during the postnatal window does not influence the programming of anxiety- and mood-related behaviors in both male and female mice; however, it is vital to keep in mind that this is not the same as driving enhanced Gi signaling via a specific GPCR, such as the 5-HT1A receptor, and indeed it is possible that a more targeted approach to selectively enhance 5-HT1A receptor signaling in forebrain excitatory neurons in this developmental window could exert a role in programming changes in emotionality.