Title:Mechanisms Involved in Neuroprotective Effects of Transcranial Magnetic
Stimulation
Volume: 21
Issue: 7
Author(s): Javier Caballero-Villarraso*, Francisco J. Medina, Begoña M. Escribano, Eduardo Agüera, Abel Santamaría, Alvaro Pascual-Leone and Isaac Túnez*
Affiliation:
- Departamento de Bioquímica y Biología Molecular, Facultad de Medicina y Enfermería, Universidad de Cordoba,
Cordoba, Spain
- Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Cordoba, Spain
- UGC Análisis Clínicos, Hospital Universitario Reina Sofía, Córdoba, Cordoba, Spain
- Departamento de Bioquímica y Biología Molecular, Facultad de Medicina y Enfermería, Universidad de Cordoba,
Cordoba, Spain
- Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Cordoba, Spain
Keywords:
Neurochemical mechanisms, biochemical pathways, cell processes, neuroplasticity, transcranial magnetic stimulation, psychiatric disorders.
Abstract: Transcranial Magnetic Stimulation (TMS) is widely used in neurophysiology to study
cortical excitability. Research over the last few decades has highlighted its added value as a potential
therapeutic tool in the treatment of a broad range of psychiatric disorders. More recently, a number
of studies have reported beneficial and therapeutic effects for TMS in neurodegenerative conditions
and strokes. Yet, despite its recognised clinical applications and considerable research using
animal models, the molecular and physiological mechanisms through which TMS exerts its beneficial
and therapeutic effects remain unclear. They are thought to involve biochemical-molecular
events affecting membrane potential and gene expression. In this aspect, the dopaminergic system
plays a special role. This is the most directly and selectively modulated neurotransmitter system,
producing an increase in the flux of dopamine (DA) in various areas of the brain after the application
of repetitive TMS (rTMS). Other neurotransmitters, such as glutamate and gamma-aminobutyric
acid (GABA) have shown a paradoxical response to rTMS. In this way, their levels increased
in the hippocampus and striatum but decreased in the hypothalamus and remained unchanged in
the mesencephalon. Similarly, there are sufficient evidence that TMS up-regulates the gene expression
of BDNF (one of the main brain neurotrophins). Something similar occurs with the expression
of genes such as c-Fos and zif268 that encode trophic and regenerative action neuropeptides. Consequently,
the application of TMS can promote the release of molecules involved in neuronal genesis
and maintenance. This capacity may mean that TMS becomes a useful therapeutic resource to antagonize
processes that underlie the previously mentioned neurodegenerative conditions.
