Abstract
Previous studies have identified the beneficial effects of electroacupuncture (EA) on motor behaviors in Parkinson's disease (PD). However, the role and potential mechanisms of EA in PD-associated depression remain unclear. In the present study, a rat model of PD with unilateral 6-hydroxydopamine (6-OHDA) lesions in the medial forebrain bundle was treated using EA for 4 weeks. We found that 100 Hz EA improved several motor phenotypes. In addition, tyrosine hydroxylase (TH) immunohistochemical analysis showed that EA had a minimal impact on the TH-positive profiles of the ipsilateral ventral tegmental area. Compared with the 6-OHDA group, long-term EA stimulation significantly increased sucrose solution consumption and decreased immobility time in the forced swim test. EA treatment did not alter dopamine, norepinephrine, and serotonin levels in the striatum and hippocampus. Noticeably, EA treatment reversed the 6-OHDA-induced abnormal expression of brain-derived neurotrophic factor (BDNF) and tropomyosin-related kinase B (TrkB) in the midbrain and hippocampus. These results demonstrate that EA at 100-Hz possesses the ability to improve depressive-like symptoms in PD rats, which is, at least in part, due to the distinct effect of EA on the mesostriatal and mesocorticolimbic dopaminergic pathways. Moreover, BDNF seems to participate in the effect of EA in PD.
Highlights
Parkinson’s disease (PD) is generally recognized as a progressive neurodegenerative disorder characterized by motor dysfunction
In the unilateral PD model used in the present study, almost all the dopaminergic neurons were lost in the SNc and the DA level was depleted 7-fold in the ipsilateral striatum after 6-OHDA lesions were induced in the medial forebrain bundle (MFB)
We found that 6-OHDA induced a marked reduction in the levels of DA, 5-HT, and NE in both the striatum and hippocampus, which suggests that dysfunctions in these neurotransmitters may contribute to many nonmotor symptoms of PD
Summary
Parkinson’s disease (PD) is generally recognized as a progressive neurodegenerative disorder characterized by motor dysfunction. Accumulating evidence indicates that nonmotor symptoms of PD, such as sensory dysfunction, sleep disturbance, and psychiatric complications (depression, anxiety, apathy, and cognitive impairment), are more detrimental to well-being and functional ability than motor symptoms [1,2,3]. As one of the most common comorbidities, depression affects approximately 40–50% of PD patients [4] and might account for substantial disability and poor quality of life. The efficacy of antidepressant treatment in PD remains unclear [5]. Polypharmacy, with antidepressant and antiparkinsonian treatments, may produce unexpected drug interactions and complicate disease development [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
