Many changes occur in brain while an individual experience a depressive episode. This include alterations in cortical activity,shrinkage of neurones, changes in connectivity and loss of volume.Some of these changes are shown to correlate with depression severity .It is assumed that reduced neural plasticity could be fundamental to these changes. The counter argument is that the loss of motivation and effort is key to the observed changes.
Normann et al ( 2007) used changes in visual evoked potentials (VEP) in response to repeated visual stimuli as a means of examining changes in synaptic plasticity in depression and showed that increases in VEP amplitude were significantly smaller in depressed subjects compared with healthy controls.
Michael J Player and team of researchers from Australia under took the present study to assess neuroplasticity in depressed subjects compared with controls using a brain stimulation protocol (PAS:Paired Associative Stimulation) that induces temporary neuroplastic changes independent of subject effort. EMG was recorded from right first dorsal interosseous muscle.Motor evoked potentials (MEPs) were elicited by Transcranial Magnetic Stimuation (TMS). TMS to the left motor cortex was combined with electrical stimuli to the right ulnar nerve proximal to the wrist. Two hundred pairs of stimuli (TMS and ulnar nerve) were given.A motor learning task was added to see whether neuroplasticity as measured by the PAS protocol was related to functional ability.
The expected increase in cortical excitability with PAS is considered to be at least partially dependent on associative long-term potentiation.LTP is crucial for neural plasticity.
Both groups were similar to start with.There was a significant increase in the amplitude of motor evoked potentials (MEP) after PAS for the control group , whereas there was no change for the depression group .The amplitude decreased as depression severity increased.However the PAS results did not correlate with motor learning, nor appear to be related to BDNF measures.
Limitations: The majority of depressed subjects were on antidepressant medications ( i.e. what would be their effect?). To understand whether it is a state or trait phenomenon, neuroplasticity need to be measured while depressed as well as during remission. Neuroplasticity was assessed in the motor cortex, which is not considered the primary site of cerebral dysfunction in depression.
Conclusion: There is deficit of neuroplasticity in depressed subjects. It is possible that the mechanisms underlying LTP induction were impaired in the motor cortex in depression.
Summary of the study:
Player MJ, Taylor JL, Weickert CS, Alonzo A, Sachdev P, Martin D, Mitchell PB, Loo CK. Neuropsychopharmacology. 2013 Oct;38(11):2101-8.