GABA is the most important inhibitor of neurotransmitters in the central nervous system and is often dysfunctional in people with mood disorders. It has also been investigated in people with PTSD. GABA can be measured via peripheral levels in plasma, via central levels in cerebrospinal fluid, and in brain regions using proton magnetic resonance spectroscopy.

What is the evidence for changes in GABA in people with PTSD?

Moderate to low quality evidence found no significant differences in brain GABA levels between people with PTSD and controls.

August 2021

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Catecholamines are a group of neurotransmitters that include dopamine, norepinephrine, also called noradrenaline, and epinephrine, also called adrenaline. The sympathetic nervous system stimulates the release of catecholamines to mediate adaptive responses to acute stress. Catecholamines are also linked to long-term memory of events that induce strong emotions, including fear. Stress-responsive neurotransmitters released during emotional arousal are thought to enhance the consolidation of fear memory. Hyperresponsiveness in the dopaminergic system is common in individuals who have been exposed to stress, which was associated with PTSD symptoms such as restlessness, nightmares, fear memory, and impulsivity. Over activation of noradrenaline receptors could be associated with the flashbacks, and nightmares frequently experienced by those with persistence of PTSD symptoms.

What is the evidence for changes in catecholamines in people with PTSD?

Moderate to high quality evidence found a small increase in plasma or urinary norepinephrine levels in people with PTSD, with no differences in epinephrine or dopamine levels compared to controls without PTSD. Containing the epinephrine analysis to urine samples showed increased epinephrine in people with PTSD compared to controls.

August 2021

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The serotonergic system is a diffuse network in the central nervous system that plays a major role in mood regulation, particularly low mood and depression. The main agents for treating depression are antidepressants, including selective serotonin reuptake inhibitors or combined serotonin/noradrenaline reuptake inhibitors. The mechanisms of these antidepressants result in increased synaptic levels of serotonin and/or noradrenaline.

What is the evidence for serotonin changes in people with bipolar disorder?

Moderate quality evidence suggests increases in serotonin receptors (5-TH1R) in the hippocampus, parahippcampus, and amygdala of people with acute bipolar depression compared to controls. There were also increases in serotonin transporters (SERT) in the cingulate and insula of people with acute bipolar depression. Most patients were unmedicated.

Low quality evidence is unclear of changes in serotonin receptor or transporter levels in people with acute bipolar mania.

December 2021

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An N-methyl-d-aspartate (NMDA) receptor consists of several subunits; the NR1 subunits that bind coagonists glycine and d-serine, the NR2 subunits that bind the neurotransmitter glutamate, and the NR3 subunits that bind glycine. The NMDA receptor is activated by binding glutamate and a coagonist.

Glutamate is the major excitatory neurotransmitter in the brain and is crucial to normal brain function. In bipolar disorder, there may be changes in levels of glutamate and its metabolites (e.g. glutamine), and changes in levels or activity of mechanical components of the NMDA receptor system, such as the receptors that ‘receive’ glutamate, or the transporters that ‘remove’ it.

What is the evidence for changes in NMDA receptors in people with bipolar disorder?

Moderate to low quality evidence suggests significant, medium to large increases in glutamate+glutamine in people with bipolar disorder compared to controls across all brain regions, and in a separate analysis of frontal regions. Non-significant medium to large trend effects were also found for increased glutamate alone and glutamate+glutamine/creatine ratio across all brain regions combined, but no increases were found in the analysis of frontal regions. There were no differences between people with bipolar disorder and controls in glutamate/creatine ratio levels, or in any analyses contained to children and adolescents.

Moderate quality evidence suggests people with bipolar depression showed a medium-sized trend effect of higher glutamate+glutamine in the anterior cingulate cortex than controls, while people with unipolar depression showed a large, significant effect of lower glutamate+glutamine in the anterior cingulate cortex than controls.

December 2021

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Products of normal chemical metabolism may be altered in bipolar disorder. Changes in metabolite levels may be indicative of altered biochemical activity. Magnetic resonance spectroscopy (MRS) has been used to measure levels of metabolites, such as N-acetylaspartate (NAA), creatine (Cr), trimethylamines/ choline containing compounds (Cho) and glutamine (Gln). These derivatives are indirect indicators of biochemical activity. Alteration in levels of NAA/Cr is associated with the protective myelin sheath surrounding neurons, which is used as a marker of neural cell viability. Decreased levels of NAA are associated with neuron death, or injury to the part of the neuron that connects to other cells, the axon. Gln is a metabolite of the neurotransmitter, glutamate (Glu).

What is the evidence for changes in neurometabolites in people with bipolar disorder?

Moderate quality evidence suggests a medium-sized effect of decreased NAA levels in the basal ganglia, a large effect of decreased NAA/Cr ratio in the hippocampus, and a small trend effect of increased NAA levels in the frontal lobes of people with bipolar disorder compared to controls. There were no differences in Cr and Cho levels, or NAA and other ratios in any other brain region.

December 2021

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Gamma-aminobutyric acid (GABA) is one of the most important inhibitors of neurotransmitters in the central nervous system. GABA is thought to be dysfunctional in people with depression and other affective disorders, with reduced levels found in human postmortem studies. GABA can also be measured via peripheral levels in plasma, via central levels in cerebrospinal fluid, and in particular brain regions using proton magnetic resonance spectroscopy.

What is the evidence for changes in GABA levels in people with bipolar disorder?

Moderate to high quality evidence shows a medium-sized effect of reduced levels of GABA in plasma of people with bipolar disorder during a depression phase when compared to controls without bipolar disorder. Moderate quality evidence also suggests a medium-sized effect of reduced levels of GABA in plasma during a euthymic phase. There were no differences in GABA levels between bipolar disorder and controls when GABA was measured in cerebrospinal fluid or with magnetic resonance spectroscopy.

Compared to people with unipolar depression, people with bipolar depression showed higher GABA levels in cerebrospinal fluid, with no differences in plasma levels.

December 2021

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