Decrease of motor cortex excitability following exposure to a 20 Hz magnetic field as generated by a rotating permanent magnet.

OBJECTIVES: Rotation of a static magnet over the motor cortex (MC) generates a transcranial alternating magnetic field (tAMF), and a linked alternating electrical field. The aim of this transcranial magnetic stimulation (TMS) study is to investigate whether such fields are able to influence MC excitability, and whether there are parallels to tACS induced effects. METHODS: Fourteen healthy volunteers received 20 Hz tAMF stimulation over the MC, over the vertex, and 20 Hz tACS over the MC, each with a duration of 15 min. TMS assessments were performed before and after the interventions. Changes in motor evoked potentials (MEP), short interval intra-cortical inhibition (SICI) and intra-cortical facilitation (ICF) were evaluated. RESULTS: The tACS and the tAMF stimulation over the MC affected cortical excitability in a different way. After tAMF stimulation MEP amplitudes and ICF decreased and the effect of SICI increased. After tACS MEP amplitudes increased and there were no effects on SICI and ICF. CONCLUSIONS: The recorded single and paired pulse MEPs indicate a general decrease of MC excitability following 15 min of tAMF stimulation. SIGNIFICANCE: The effects demonstrate that devices based on rotating magnets are potentially suited to become a novel brain stimulation tool in clinical neurophysiology.

Increased expression of retinoic acid-induced gene 1 in the dorsolateral prefrontal cortex in schizophrenia, bipolar disorder, and major depression.

BACKGROUND: Retinoids regulate gene expression in different cells and tissues at the transcriptional level. Retinoic acid transcriptionally regulates downstream regulatory molecules, including enzymes, transcription factors, cytokines, and cytokine receptors. Animal models indicate an involvement of retinoid signaling pathways in the regulation of synaptic plasticity and learning, especially in the hippocampus. Retinoic acid-inducible or induced gene 1 (RAI-1) is induced during neuronal differentiation, and was associated with the severity of the phenotype and response to medication in schizophrenic patients. METHODS: In the present study, we used immunohistochemistry to investigate the expression of RAI-1 in 60 brains from the Stanley Neuropathology Consortium (15 cases each from controls and from patients with schizophrenia, bipolar disorder, and major depression). Rating scores for density and intensity were determined in the dorsolateral prefrontal cortex. RESULTS: All four groups showed high interindividual variation. RAI-1-positive cells were identified as neurons and astrocytes. Significantly increased intensities in cortical neurons were noted in all three major psychiatric groups compared with controls. The density of RAI-1-positive neurons was increased (P=0.06) in schizophrenia and bipolar disorder. In bipolar disorder, RAI-1-positive astrocytes in gray matter showed a significantly increased intensity and compound value. Thus, a significant increase in the parameters measured was found in schizophrenia, bipolar disorder, and major depression. CONCLUSION: Our study shows a significant increase in expression of RAI-1 in the brains from patients with schizophrenia, bipolar disorder, or major depression. The increased expression might reflect altered signaling pathways, like that for retinoic acid. The underlying mechanisms leading to the increased expression and its functional consequences are so far unknown, and remain to be investigated in future studies.