| Project/Area Number |
24659539
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Psychiatric science
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TODA Shigenobu 金沢大学, 大学病院, 講師 (00323006)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 脳神経疾患 / 死後脳研究 / 国際研究者交流 / 死後脳 |
|---|
| Research Abstract |
We tested our hypothesis that GABA neurotransmission by projection neurons in the substantia nigra pars reticulata (SNR) is reduced and dopamine neurons in the substantia nigra pars compacta (SNC) are hyperactive as the result. We analyzed gene expression for GAD67, an enzyme for GABA synthesis, tyrosine hydroxylase (TH), an enzyme for dopamine synthesis, and KCNS3 voltage-gated potassium channel subunit in the SNR and SNC of 14 pairs of control and sex- and age-matched schizophrenia subjects, using in situ hybridization. In the SNR, GAD67 mRNA levels did not differ between control and schizophrenia subjects. In contrast, TH and KCNS3 mRNA levels were significantly lower in the SNC of schizophrenia subjects. Our results did not support altered GABA neurotransmission by SNR neurons. However, decreased KCNS3 expression could enhance excitability of SNC dopamine neurons, contributing to positive symptoms. Lower TH levels might reflect a compensatory mechanism.
|
