Brief Report: Self-Reported Medication Use in Individuals Diagnosed with Autism Spectrum Disorder in Adulthood: A U.S. Clinic Sample from 2012 to 2022.

PURPOSE: As the understanding of autism spectrum disorder (ASD) across the lifespan has increased, so has the number of individuals being identified with ASD for the first time in adulthood. Understanding co-occurring psychiatric conditions in this subset of the ASD population is a growing focus of research; however, little is known about the rate at which psychiatric medications are prescribed to adults with a first-time diagnosis of ASD. The purpose of this study was to examine self-reported medication use in persons diagnosed with ASD in adulthood in a clinic sample (2012-2022) in the United States. METHODS: The present study was a retrospective record review. Participants (n = 281) were drawn from an outpatient clinic specializing in the diagnosis of ASD in adults. Participants self-reported previous and current psychiatric medication prescription using a medication checklist. RESULTS: Approximately 50% of participants self-reported being prescribed at least one psychiatric medication at the time of their initial evaluation appointment. The most commonly prescribed psychiatric medications were antidepressants (23.8%), followed by stimulants (16.7%). CONCLUSION: Similar to individuals diagnosed with ASD in childhood, those identified with ASD for the first time in adulthood are prescribed psychiatric medication at a much higher rate than their same-age non-autistic peers. These results can inform future research and practice for improving outcomes for autistic adults, particularly those who were undiagnosed for much of their lives.

Hyperglycemia reduces functional expression of astrocytic Kir4.1 channels and glial glutamate uptake.

Diabetics are at risk for a number of serious health complications including an increased incidence of epilepsy and poorer recovery after ischemic stroke. Astrocytes play a critical role in protecting neurons by maintaining extracellular homeostasis and preventing neurotoxicity through glutamate uptake and potassium buffering. These functions are aided by the presence of potassium channels, such as Kir4.1 inwardly rectifying potassium channels, in the membranes of astrocytic glial cells. The purpose of the present study was to determine if hyperglycemia alters Kir4.1 potassium channel expression and homeostatic functions of astrocytes. We used q-PCR, Western blot, patch-clamp electrophysiology studying voltage and potassium step responses and a colorimetric glutamate clearance assay to assess Kir4.1 channel levels and homeostatic functions of rat astrocytes grown in normal and high glucose conditions. We found that astrocytes grown in high glucose (25 mM) had an approximately 50% reduction in Kir4.1 mRNA and protein expression as compared with those grown in normal glucose (5mM). These reductions occurred within 4-7 days of exposure to hyperglycemia, whereas reversal occurred between 7 and 14 days after return to normal glucose. The decrease in functional Kir channels in the astrocytic membrane was confirmed using barium to block Kir channels. In the presence of 100-µM barium, the currents recorded from astrocytes in response to voltage steps were reduced by 45%. Furthermore, inward currents induced by stepping extracellular [K(+)]o from 3 to 10mM (reflecting potassium uptake) were 50% reduced in astrocytes grown in high glucose. In addition, glutamate clearance by astrocytes grown in high glucose was significantly impaired. Taken together, our results suggest that down-regulation of astrocytic Kir4.1 channels by elevated glucose may contribute to the underlying pathophysiology of diabetes-induced CNS disorders and contribute to the poor prognosis after stroke.