Commonly understood as depression, bipolar disorder is really a mental disorder that causes alternate periods of deep depression and then periods of elevated mood. But now here is new research that suggests the key role played by the PLCγ1 protein in the process leading to bipolar disorder. This then actually is a breakthrough in attempting to understand bipolar disorder.
With countless people all over the world suffering from the condition, bipolar disorder is a debilitating mental illness. People living with the disease experience drastic changes in mood and energy levels to a degree that interferes with their daily activities. With this new information we now know that a protein deficiency is responsible and could be a step forward in future treatment options.
The sad truth is that an overwhelming majority of cases of bipolar disease are rather severe. The causes of the malaise are unknown but again research says it is a genetic disposition and that background could be the cause of the illness. The gene encoding the cellular protein phospholipase Cγ1 is linked to bipolar disease although the exact mechanism that causes the disorder was not known until now.
This new research comes from Ulsan National Institute of Science and Technology in Ulsan, South Korea. It has tested the role of phospholipase Cγ1 (PLCγ1) in mice and the findings are helping to explain the causative link between the protein and the disease. This study was published in the journal Molecular Psychiatry.
The studied undertook the premise about occurrences in synapses or the ends of neurons that facilitate electric signaling between two brain cells. Scientists noticed impairment in the inhibitory transmission and synaptic plasticity that is, the synapses’ ability to change their shape, function, or strength over time.
The brain-derived neurotrophic factor is a protein that regulates several synaptic functions, including the activity of PLCγ1. The crucial synapse formation in the brain deficits led to an imbalance between excitatory and inhibitory transmission between the brain cells’ synapses. PLCγ1-deprived mice displayed symptoms like hyperactivity, reduced anxiety-like behavior, abnormally high feelings of pleasure, excessive hunger and impaired learning and memory, as well as abnormally high startle responses. Researchers administered drug treatment for BD to these mice and this reduced their symptoms.
Thus it appears that a neurochemical chain reaction leads to the disease. The synapses that do not have enough PLCγ1 are unable to fulfill their inhibitory function properly in excitatory neurons, because the BDNF is not working properly either. This causes a disproportion between excitatory synapses and inhibitory ones, eventually leading to bipolar symptoms. Until now, although the PLCγ1 gene had been suggested to play a role, it was unclear exactly how PLCγ1 affected interneuronal signaling and how it caused mental illness.
After ten long years of research findings suggest evidence that PLCγ1 is critical for synaptic function and plasticity and that the loss of PLCγ1 from the forebrain results in manic-like behavior playing a major role in the onset of bipolar disorder. The breakthrough is likely to influence research into the treatment of the condition and its symptoms.