Psychiatry Investig.
2019 Jul;16(7):558-564. 10.30773/pi.2019.04.22.
Restoration of Cdk5, TrkB and Soluble N-ethylmaleimide-Sensitive Factor Attachment Protein Receptor Proteins after Chronic Methylphenidate Treatment in Spontaneous Hypertensive Rats, a Model for Attention-Deficit Hyperactivity Disorder
- Affiliations
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- 1Department of Child and Adolescent Psychiatry, National Center for Mental Health, Seoul, Republic of Korea. yenikim@korea.kr
- 2Department of Biomedical Sciences, Center for Creative Biomedical Scientists at Chonnam National University, Gwangju, Republic of Korea.
- 3Department of Pharmacy, Sahmyook University, Uimyung Research Institute for Neuroscience, Seoul, Republic of Korea. cheongjh@syu.ac.kr
- 4Department of Pharmaceutical and Administrative Sciences, Loma Linda University Health, Loma Linda, CA, USA.
- 5Department of Psychiatry, Chung Ang University Hospital, Seoul, Republic of Korea.
- 6Division of Child & Adolescent Psychiatry, Department of Psychiatry and Institute of Human Behavioral Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
- KMID: 2454726
- DOI: http://doi.org/10.30773/pi.2019.04.22
Abstract
OBJECTIVE
Synaptic vesicle mobilization and neurite outgrowth regulation molecules were examined in modulation of effects of methylphenidate (MPH) in Spontaneous Hypertensive Rats (SHRs), a model for attention-deficit hyperactivity disorder (ADHD).
METHODS
We compared the changes in the protein expression level of Cyclin dependent kinase 5 (Cdk5) and molecular substrates of Cdk5; tropomyosin receptor kinase B (TrkB), syntaxin 1A (STX1A) and synaptosomal-associated protein 25 (SNAP25). Comparisons were made in prefrontal cortex of vehicle (distilled water i.p. for 7 days)-treated SHRs, vehicle-treated Wistar Kyoto Rats (WKYs) and MPH (2 mg/kg i.p. for 7 days) treated SHRs.
RESULTS
The Cdk5 level of vehicle-treated SHRs was significantly decreased compared to the Cdk5 level of vehicle-treated WKY rats, but was restored to the expression level of vehicle-treated WKYs in MPH-treated SHR. The ratio of p25/p35 was significantly decreased in MPH-treated SHR compared to vehicle-treated SHR. Moreover, TrkB, STX1A and SNAP25 of vehicle-treated SHRs were significantly decreased compared to vehicle-treated WKY rats, but were restored to the expression level of vehicle-treated WKYs in MPH-treated SHR.
CONCLUSION
The results show that Cdk5, TrkB, STX1A, and SNAP25 were involved in the modulation of MPH effects in prefrontal cortex of SHRs and play important role in treatment of ADHD.
Keyword
MeSH Terms
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Animals
Cyclin-Dependent Kinase 5
Methylphenidate*
Neurites
Phosphotransferases
Prefrontal Cortex
Rats*
Rats, Inbred WKY
Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins*
Synaptic Vesicles
Synaptosomal-Associated Protein 25
Syntaxin 1
Tropomyosin
Water
Cyclin-Dependent Kinase 5
Methylphenidate
Phosphotransferases
Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins
Synaptosomal-Associated Protein 25
Syntaxin 1
Tropomyosin
Water
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