*Understanding the Neuropathophysiology of Psychiatry Disorder Using Transcranial Magnetic… DOI: http://dx.doi.org/10.5772/intechopen.103748*

these cortical reactivity parameters. Gamma-aminobutyric acid (GABA) is one of the most important inhibitory neurotransmitters in the brain, widely distributed, and plays an important role in the modulation of cortical reactivity and neuroplasticity. GABAergic neurons represent between 20–40% of all neurons present in the central nervous system [3, 4] and they are present throughout all levels of the neuraxis, and play an important role to balance and fine-tune excitatory neurotransmission of various other neuronal systems including the cholinergic and monoaminergic projection to the area of the forebrain. Gamma-aminobutyric acid-ergic (GABAergic) deficit pathology is widely studied in various neuropsychiatric disorders [5, 6]. GABA shows its actions by interacting with two different subtypes of receptors a) GABAA receptors (GABAARs)-ionotropic b) GABAB receptor (GABABRs)-metabotropic. GABAARs are predominately responsible for anxiety and mood disorders, due to marked evidence suggesting altered GABAAR signaling in both disorders [7, 8]. Benzodiazepine act as an allosteric modulator of a major subset of GABAARs demonstrating potent anxiolytic activity and playing key control elements of anxiety state [7, 9]. GABAB Rs, Coded by GABA 1 gene and GABA 2 gene are members of the G-protein coupled receptor family and their role in the causation of affective disorder have been recently implicated in mice who demonstrated alerted anxiety and depression-related behavior after subjecting to pharmacological and genetic manipulations of these receptors [10]. The results from this study reflect that future development of therapeutic anxiolytic can be based on modulating GABAB receptors in the experimental study. In 2010, one review suggested that there are compelling evidence of both GABAA and GABAB inhibitory deficit in the pathophysiology of depressive disorder [11]. Both GABA-A and GABA-B receptors are involved in cortical inhibition with GABA-A mediating short interval cortical inhibition (SICI) and GABA B mediating cortical silent period (CSP), long interval cortical inhibition (LICI), interhemispheric inhibition (IHI) [12].
