RESUMEN
Background: ChatGPT is a generative artificial intelligence chatbot that uses natural language processing to understand and execute prompts in a human-like manner. While the chatbot has become popular as a source of information among the public, experts have expressed concerns about the number of false and misleading statements made by ChatGPT. Many people search online for information about self-managed medication abortion, which has become even more common following the overturning of Roe v. Wade. It is likely that ChatGPT is also being used as a source of this information; however, little is known about its accuracy. Objective: To assess the accuracy of ChatGPT responses to common questions regarding self-managed abortion safety and the process of using abortion pills. Methods: We prompted ChatGPT with 65 questions about self-managed medication abortion, which produced approximately 11,000 words of text. We qualitatively coded all data in MAXQDA and performed thematic analysis. Results: ChatGPT responses correctly described clinician-managed medication abortion as both safe and effective. In contrast, self-managed medication abortion was inaccurately described as dangerous and associated with an increase in the risk of complications, which was attributed to the lack of clinician supervision. Conclusion: ChatGPT repeatedly provided responses that overstated the risk of complications associated with self-managed medication abortion in ways that directly contradict the expansive body of evidence demonstrating that self-managed medication abortion is both safe and effective. The chatbot's tendency to perpetuate health misinformation and associated stigma regarding self-managed medication abortions poses a threat to public health and reproductive autonomy.
RESUMEN
OBJECTIVE: γ-Aminobutyric acid type A (GABAA ) receptor subunit gene mutations are significant causes of epilepsy, which are often accompanied by various neuropsychiatric comorbidities, but the underlying mechanisms are unclear. It has been suggested that the comorbidities are caused by seizures, as the comorbidities often present in severe epilepsy syndromes. However, findings from both humans and animal models argue against this conclusion. Mutations in the GABAA receptor γ2 subunit gene GABRG2 have been associated with anxiety alone or with severe epilepsy syndromes and comorbid anxiety, suggesting that a core molecular defect gives rise to the phenotypic spectrum. Here, we determined the pathophysiology of comorbid anxiety in GABRG2 loss-of-function epilepsy syndromes, identified the central nucleus of the amygdala (CeA) as a primary site for epilepsy comorbid anxiety, and demonstrated a potential rescue of comorbid anxiety via neuromodulation of CeA neurons. METHODS: We used brain slice recordings, subcellular fractionation with Western blot, immunohistochemistry, confocal microscopy, and a battery of behavior tests in combination with a chemogenetic approach to characterize anxiety and its underlying mechanisms in a Gabrg2+/Q390X knockin mouse and a Gabrg2+/- knockout mouse, each associated with a different epilepsy syndrome. RESULTS: We found that impaired GABAergic neurotransmission in CeA underlies anxiety in epilepsy, which is due to reduced GABAA receptor subunit expression resulting from the mutations. Impaired GABAA receptor expression reduced GABAergic neurotransmission in CeA, but not in basolateral amygdala. Activation or inactivation of inhibitory neurons using a chemogenetic approach in CeA alone modulated anxietylike behaviors. Similarly, pharmacological enhancement of GABAergic signaling via γ2 subunit-containing receptors relieved the anxiety. SIGNIFICANCE: Together, these data demonstrate the molecular basis for a comorbidity of epilepsy, anxiety, and suggest that impaired GABAA receptor function in CeA due to a loss-of-function mutation could at least contribute to anxiety. Modulation of CeA neurons could cause or suppress anxiety, suggesting a potential use of CeA neurons as therapeutic targets for treatment of anxiety in addition to traditional pharmacological approaches.
