Sustained fentanyl exposure inhibits neuronal activity in dissociated striatal neuronal-glial co-cultures through actions independent of opioid receptors

This is the authors' abstract. We don't add key points for this paper.

Acute fentanyl exposure attenuated the activity of striatal medium spiny neurons (MSNs) in vitro and in dopamine D2, but not D1, receptor-expressing MSNs in ex vivo slices. By contrast, sustained fentanyl exposure suppressed the spontaneous activity of MSNs cocultured with glia through a nonopioid receptor-dependent mechanism modulated, in part, by α 1 -adrenoceptors. Fentanyl exposure can affect striatal function via a nonopioid receptor mechanism of action that appears mediated by α 1 -adrenoreceptor-expressing striatal neurons and/or astroglia.