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The delineation of dopamine dysfunction in the mentally ill has been a long-standing quest of biological psychiatry. The present study focuses on a recently recognized group of dopamine receptor-interacting proteins as possible novel sites of dysfunction in schizophrenic and bipolar patients. We demonstrate that the dorsolateral prefrontal cortex in(More)
It has recently been reported that melatonin protects neuronal cells from damage by enhancing Akt activation, thus mediating antiapoptosis signals. However, there is little information regarding the effects of melatonin on the activation of genes further downstream in the Akt signaling pathway in ischemic brain injury. This study investigated whether(More)
Melatonin plays a neuroprotective role against brain injury through the activation of Akt and the inhibition of apoptotic cell death. This study investigated whether melatonin modulates the anti-apoptotic signal through the activation of Akt and its downstream targets, FKHR, AFX, and 14-3-3. Adult male rats were treated with melatonin (5 mg/kg) prior to(More)
  • Phil-Ok Koh
  • The Journal of veterinary medical science
  • 2008
Melatonin prevents neuronal cell death in ischemic brain injury. This study investigated whether melatonin inhibits the apoptotic signal through the activation of Raf-MEK-ERK and its downstream targets, including 90 ribosomal S6 kinase (p90RSK) and Bad. Adult male rats were treated with melatonin (5 mg/kg) or vehicle prior to middle cerebral artery(More)
Melatonin is a potent scavenger of reactive oxygen species and a strong antioxidant. Melatonin exerts protective effects against damage by the enhancing the Akt signal pathway, thus regulating apoptotic cell death. Akt phosphorylates pro-apoptotic proteins such as Bad and FoxO1 and inhibits the pro-apoptotic functions of these proteins. This study(More)
Intracellular calcium overload is a critical pathophysiological factor in ischemic injury. Hippocalcin is a neuronal calcium sensor protein that buffers intracellular calcium levels and protects cells from apoptotic stimuli. Ferulic acid exerts a neuroprotective effect in cerebral ischemia through its anti-oxidant and anti-inflammation activity. This study(More)
The recently cloned protein, calcyon, potentiates crosstalk between G(s)-coupled dopamine D1 receptors and heterologous G(q/11)-coupled receptors allowing dopamine D1 receptors to stimulate intracellular Ca(2+) release, in addition to cAMP production. This crosstalk also requires the participating G(q/11)-coupled receptors to be primed by their agonists. We(More)
  • Phil-Ok Koh
  • The Journal of veterinary medical science
  • 2008
Nitric oxide (NO) is produced by three NO synthases (NOS), iNOS, eNOS, and nNOS. Production of NO by iNOS plays key roles in neurodegeneration, while eNOS is a protective enzyme. This study investigated the neuroprotective effect of melatonin and the levels of NOS isoforms induced by melatonin in ischemic brain injury. Adult male rats were treated with(More)
Most of the known actions of angiotensin II have been considered primarily to be the result of angiotensin II subtype 1 receptor activation. However, recent data suggest that the angiotensin II subtype 2 receptor (AT2R) may modulate key processes linked to atherosclerosis. The aim of this study was to investigate the role of AT2R in diabetes-associated(More)
  • Phil-Ok Koh
  • The Journal of veterinary medical science
  • 2007
Diabetic disease is known to suppress male reproductive activity in laboratory animals and humans. The present study was designed to evaluate whether streptozotocin-induced diabetes increases apoptotic cell death in rat testes through activation of the JNK and Bax pathway. Diabetes was induced by a single intravenous injection of streptozotocin (40 mg/kg)(More)