ABSTRACT
Severe acute respiratory syndrome coronavirus 2, or coronavirus disease 2019 (COVID-19), vaccine hesitancy, defined as a behavioral phenomenon whereby individuals neither fully accept nor fully reject the COVID-19 vaccine, presents a major health threat in the midst of the current pandemic. Traditional approaches for addressing vaccine hesitancy in health care lack empirical support and, in some instances, have actually increased vaccine hesitancy. Thus, there is an urgent need for approaches that effectively address COVID-19 vaccine hesitancy, especially in health care settings. The current article highlights the need for and importance of motivational interviewing (MI), which emphasizes collaborative communication between physicians and patients, in addressing vaccine hesitancy. We describe a 3-step process for addressing COVID-19 vaccine hesitancy that includes using a guiding style, using the MI toolbox, and responding mindfully and skillfully to the individual's degree of hesitancy. The discussion concludes with a consideration of possible challenges in implementing these steps when addressing and resolving COVID-19 vaccine hesitancy.
Subject(s)
COVID-19 , Motivational Interviewing , Vaccines , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Vaccines/therapeutic use , Health Knowledge, Attitudes, Practice , Humans , Patient Acceptance of Health Care , Vaccination , Vaccination HesitancyABSTRACT
New antidepressant pharmacotherapies that provide rapid relief of depressive symptoms are needed. The NMDA receptor antagonist ketamine exerts rapid antidepressant actions in depressed patients but also side effects that complicate its clinical utility. Ketamine promotes excitatory synaptic strength, likely by producing high-frequency correlated activity in mood-relevant regions of the forebrain. Negative allosteric modulators of GABA-A receptors containing α5 subunits (α5 GABA-NAMs) should also promote high-frequency correlated electroencephalogram (EEG) activity and should therefore exert rapid antidepressant responses. Because α5 subunits display a restricted expression in the forebrain, we predicted that α5 GABA-NAMs would produce activation of principle neurons but exert fewer side effects than ketamine. We tested this hypothesis in male mice and observed that the α5 GABA-NAM MRK-016 exerted an antidepressant-like response in the forced swim test at 1 and 24 h after administration and an anti-anhedonic response after chronic stress in the female urine sniffing test (FUST). Like ketamine, MRK-016 produced a transient increase in EEG γ power, and both the increase in γ power and its antidepressant effects in the forced swim test were blocked by prior administration of the AMPA-type glutamate receptor antagonist 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX). Unlike ketamine, however, MRK-016 produced no impairment of rota-rod performance, no reduction of prepulse inhibition (PPI), no conditioned-place preference (CPP), and no change in locomotion. α5 GABA-NAMs, thus reproduce the rapid antidepressant-like actions of ketamine, perhaps via an AMPA receptor (AMPAR)-dependent increase in coherent neuronal activity, but display fewer potential negative side effects. These compounds thus demonstrate promise as clinically useful fast-acting antidepressants.
