TY - JOUR T1 - Cortical inhibition, facilitation and plasticity in late-life depression: effects of venlafaxine pharmacotherapy JF - Journal of Psychiatry and Neuroscience JO - JPN SP - E88 LP - E96 DO - 10.1503/jpn.200001 VL - 46 IS - 1 AU - Jennifer I. Lissemore AU - Benoit H. Mulsant AU - Tarek K. Rajji AU - Jordan F. Karp AU - Charles F. Reynolds III AU - Eric J. Lenze AU - Jonathan Downar AU - Robert Chen AU - Zafiris J. Daskalakis AU - Daniel M. Blumberger Y1 - 2021/01/01 UR - http://jpn.ca/content/46/1/E88.abstract N2 - Background Late-life depression is often associated with non-response or relapse following conventional antidepressant treatment. The pathophysiology of late-life depression likely involves a complex interplay between aging and depression, and may include abnormalities in cortical inhibition and plasticity. However, the extent to which these cortical processes are modifiable by antidepressant pharmacotherapy is unknown.Methods Sixty-eight patients with late-life depression received 12 weeks of treatment with open-label venlafaxine, a serotonin-norepinephrine reuptake inhibitor (≤ 300 mg/d). We combined transcranial magnetic stimulation of the left motor cortex with electromyography recordings from the right hand to measure cortical inhibition using contralateral cortical silent period and paired-pulse short-interval intracortical inhibition paradigms; cortical facilitation using a paired-pulse intracortical facilitation paradigm; and short-term cortical plasticity using a paired associative stimulation paradigm. All measures were collected at baseline, 1 week into treatment (n = 23) and after approximately 12 weeks of treatment.Results Venlafaxine did not significantly alter cortical inhibition, facilitation or plasticity after 1 or 12 weeks of treatment. Improvements in depressive symptoms during treatment were not associated with changes in cortical physiology.Limitations The results presented here are specific to the motor cortex. Future work should investigate whether these findings extend to cortical areas more closely associated with depression, such as the dorsolateral prefrontal cortex.Conclusion These findings suggest that antidepressant treatment with venlafaxine does not exert meaningful changes in motor cortical inhibition or plasticity in late-life depression. The absence of changes in motor cortical physiology, alongside improvements in depressive symptoms, suggests that age-related changes may play a role in previously identified abnormalities in motor cortical processes in late-life depression, and that venlafaxine treatment does not target these abnormalities. ER -