Activity in the parabrachial calcitonin gene-related peptide to bed nucleus of the stria terminalis circuit associates with anxiety-like behavior. To test whether heightened anxiety induces neuronal adaptations in parabrachial to bed nucleus of the stria terminalis circuit, C57 mice were exposed to 4 days of daily forced swim stress. The novelty suppressed feeding test demonstrated the forced swim stress model increased anxiety-like behavior and induced hyperphagia. To assess if forced swim stress potentiates anxiety-like behavior in mice with baseline dysregulated affect, mice received chronic intermittent ethanol vapor and forced swim stress in alcohol-abstinence. Anxiety-like behavior measured by the novelty suppressed feeding test was potentiated and hyperphagia was induced by forced swim stress in alcohol-abstinence. To measure anxiety-related neuroadaptations, CalcaCRE mice, with of CRE-dependent hM3D(Gq) DREADDs in the parabrachial nucleus and the Ca2+ sensor GCaMP7f in the bed nucleus of the stria terminalis, were exposed to forced swim stress. Neurotransmission was measured by recording GCaMP7f fluorescence in ex vivo bed nucleus of the stria terminalis slices. hM3D(Gq) DREADDs in parabrachial projections expressing calcitonin gene-related peptide were activated via bath application of clozapine-n-oxide. Excitatory drive by parabrachial calcitonin gene-related peptide projections decreased GCaMP7f spike frequency and amplitude in the bed nucleus of the stria terminalis. Forced swim stress potentiated excitatory drive of parabrachial calcitonin gene-related peptide projections as the decrease in GCaMP frequency was potentiated. In summary repeated exposure to stress induces heightened anxiety and hyperphagia that is associated with potentiated parabrachial to bed nucleus of the stria terminalis circuit activity.