Abstract:The inhibitory gamma-aminobutyric acid (GABA) system is involved in the etiology of most psychiatric disorders, including schizophrenia, autism spectrum disorder (ASD) and major depressive disorder (MDD). It is therefore not surprising that proton magnetic resonance spectroscopy ((1) H-MRS) is increasingly used to investigate in vivo brain GABA levels. However, integration of the evidence for altered in vivo GABA levels across psychiatric disorders is lacking. We therefore systematically searched the clinical … Show more
“…In our opinion it would be advisable to include psychiatric comparison groups. Schür et al[100] pointed out that the inhibitory GABA system is thought to be involved in the etiology of several psychiatric disorders. The authors therefore performed a meta-analysis including a total of 40 MRS studies in seven different psychiatric disorders ( n = 1.591).…”
Section: Resultsmentioning
confidence: 99%
“…Decreased GABAergic inhibition was reported in limbic, frontal, temporal, and respectively insular regions[15,98,99]. Unfortunately, the findings regarding the GABAergic system are partly inconsistent and may not be specific for PD[100]. …”
AIMTo provide an overview of the current research in the functional neuroanatomy of panic disorder.METHODSPanic disorder (PD) is a frequent psychiatric disease. Gorman et al (1989; 2000) proposed a comprehensive neuroanatomical model of PD, which suggested that fear- and anxiety-related responses are mediated by a so-called “fear network” which is centered in the amygdala and includes the hippocampus, thalamus, hypothalamus, periaqueductal gray region, locus coeruleus and other brainstem sites. We performed a systematic search by the electronic database PubMed. Thereby, the main focus was laid on recent neurofunctional, neurostructural, and neurochemical studies (from the period between January 2012 and April 2016). Within this frame, special attention was given to the emerging field of imaging genetics.RESULTSWe noted that many neuroimaging studies have reinforced the role of the “fear network” regions in the pathophysiology of panic disorder. However, recent functional studies suggest abnormal activation mainly in an extended fear network comprising brainstem, anterior and midcingulate cortex (ACC and MCC), insula, and lateral as well as medial parts of the prefrontal cortex. Interestingly, differences in the amygdala activation were not as consistently reported as one would predict from the hypothesis of Gorman et al (2000). Indeed, amygdala hyperactivation seems to strongly depend on stimuli and experimental paradigms, sample heterogeneity and size, as well as on limitations of neuroimaging techniques. Advanced neurochemical studies have substantiated the major role of serotonergic, noradrenergic and glutamatergic neurotransmission in the pathophysiology of PD. However, alterations of GABAergic function in PD are still a matter of debate and also their specificity remains questionable. A promising new research approach is “imaging genetics”. Imaging genetic studies are designed to evaluate the impact of genetic variations (polymorphisms) on cerebral function in regions critical for PD. Most recently, imaging genetic studies have not only confirmed the importance of serotonergic and noradrenergic transmission in the etiology of PD but also indicated the significance of neuropeptide S receptor, CRH receptor, human TransMEMbrane protein (TMEM123D), and amiloride-sensitive cation channel 2 (ACCN2) genes.CONCLUSIONIn light of these findings it is conceivable that in the near future this research will lead to the development of clinically useful tools like predictive biomarkers or novel treatment options.
“…In our opinion it would be advisable to include psychiatric comparison groups. Schür et al[100] pointed out that the inhibitory GABA system is thought to be involved in the etiology of several psychiatric disorders. The authors therefore performed a meta-analysis including a total of 40 MRS studies in seven different psychiatric disorders ( n = 1.591).…”
Section: Resultsmentioning
confidence: 99%
“…Decreased GABAergic inhibition was reported in limbic, frontal, temporal, and respectively insular regions[15,98,99]. Unfortunately, the findings regarding the GABAergic system are partly inconsistent and may not be specific for PD[100]. …”
AIMTo provide an overview of the current research in the functional neuroanatomy of panic disorder.METHODSPanic disorder (PD) is a frequent psychiatric disease. Gorman et al (1989; 2000) proposed a comprehensive neuroanatomical model of PD, which suggested that fear- and anxiety-related responses are mediated by a so-called “fear network” which is centered in the amygdala and includes the hippocampus, thalamus, hypothalamus, periaqueductal gray region, locus coeruleus and other brainstem sites. We performed a systematic search by the electronic database PubMed. Thereby, the main focus was laid on recent neurofunctional, neurostructural, and neurochemical studies (from the period between January 2012 and April 2016). Within this frame, special attention was given to the emerging field of imaging genetics.RESULTSWe noted that many neuroimaging studies have reinforced the role of the “fear network” regions in the pathophysiology of panic disorder. However, recent functional studies suggest abnormal activation mainly in an extended fear network comprising brainstem, anterior and midcingulate cortex (ACC and MCC), insula, and lateral as well as medial parts of the prefrontal cortex. Interestingly, differences in the amygdala activation were not as consistently reported as one would predict from the hypothesis of Gorman et al (2000). Indeed, amygdala hyperactivation seems to strongly depend on stimuli and experimental paradigms, sample heterogeneity and size, as well as on limitations of neuroimaging techniques. Advanced neurochemical studies have substantiated the major role of serotonergic, noradrenergic and glutamatergic neurotransmission in the pathophysiology of PD. However, alterations of GABAergic function in PD are still a matter of debate and also their specificity remains questionable. A promising new research approach is “imaging genetics”. Imaging genetic studies are designed to evaluate the impact of genetic variations (polymorphisms) on cerebral function in regions critical for PD. Most recently, imaging genetic studies have not only confirmed the importance of serotonergic and noradrenergic transmission in the etiology of PD but also indicated the significance of neuropeptide S receptor, CRH receptor, human TransMEMbrane protein (TMEM123D), and amiloride-sensitive cation channel 2 (ACCN2) genes.CONCLUSIONIn light of these findings it is conceivable that in the near future this research will lead to the development of clinically useful tools like predictive biomarkers or novel treatment options.
“…Cr is often used as a denominator in signal ratio because Cr is in chemical equilibrium and comparatively unaffected by neurodegenerative processes [68]. GABA levels have also been examined using editing techniques such as MEGA-PRESS that allows for detecting brain GABA independently from other metabolites with overlapping resonances [69]. In most of the 1 H-MRS studies of PTSD, the ACC and temporal lobe structures including the hippocampus, which play an important role in the development and maintenance of PTSD symptoms, were investigated as regions of interest (ROIs) [7071727374].…”
Section: Mrs Studies Of Neurochemical Metabolitesmentioning
confidence: 99%
“…In contrast, GABA levels were lowered in the insula [102], parieto-occipital cortex [96], and medial temporal cortex [96] of patients with PTSD than healthy controls. Although the number of studies was limited, a recent meta-analysis has reported no significant alterations in GABA levels related to PTSD [69]. …”
Section: Mrs Studies Of Neurochemical Metabolitesmentioning
Over the past decade, an increasing number of neuroimaging studies have provided insight into the neurobiological mechanisms of posttraumatic stress disorder (PSTD). In particular, molecular neuroimaging techniques have been employed in examining metabolic and neurochemical processes in PTSD. This article reviews molecular neuroimaging studies in PTSD and focuses on findings using three imaging modalities including positron emission tomography (PET), single photon emission computed tomography (SPECT), and magnetic resonance spectroscopy (MRS). Although there were some inconsistences in the findings, patients with PTSD showed altered cerebral metabolism and perfusion, receptor bindings, and metabolite profiles in the limbic regions, medial prefrontal cortex, and temporal cortex. Studies that have investigated brain correlates of treatment response are also reviewed. Lastly, the limitations of the molecular neuroimaging studies and potential future research directions are discussed.
“…in vivo GABA rate (3). To the best of our knowledge, no research has been conducted on the immediate response of the human brain, especially in adolescents, after caffeine intake.…”
In adolescents, sleep deprivation problem is getting worse, and increased caffeine consumption is considered to relieve the stress caused by sleep deprivation and academic burden. In this study, immediate neurologic effects of caffeine intake on adolescents were evaluated in three high school students using the γ-aminobutyric acid (GABA)/creatine ratio on magnetic resonance spectroscopy (MRS). MEGA-PRESS MRS and TE 135 ms single voxel MRS were performed in the anterior cingulate cortex before and after drinking a cup of coffee, which contained 104 mg of caffeine. GABA and creatine were measured on LCModel 6.3, respectively. In all three students, GABA/creatine ratios were decreased after caffeine intake. The GABA/creatine ratios obtained before caffeine intake were decreased after caffeine intake in all the three adolescents. In this preliminary study, caffeine intake caused an immediate decrease in the GABA/creatine ratio in the brain and it may be related to the neurologic effects of caffeine on an adolescent's brain.
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