New research revealed that over-activity in a specific part of the brain is linked to certain schizophrenia symptoms, opening up possibilities for targeted treatments.
Researchers from the University of Nottingham found that faulty inhibitory neurotransmission and abnormally increased activity in the hippocampus does not disrupt the ability to filter out irrelevant information, a key process that has shown to be deficient in patients with schizophrenia symptoms and is thought to cause hallucinations or delusions but does disrupt associative learning. Deficits in associative learning, such as Pavlovian fear conditioning, have been linked to the negative schizophrenia symptoms, which includes reduced motivation and disrupted emotional and reward processing.
Their findings have been published in eNeuro.
Brain over-activity and schizophrenia symptoms
Schizophrenia is a major illness. At any one time, about 220,000 people are being treated for this condition in the UK by the NHS. Schizophrenia symptoms exhibit themselves in three ways: negative symptoms such as lethargy, apathy and social withdrawal, positive symptoms such as hallucinations and delusions and cognitive symptoms such as impaired memory. Either or all three may be present in an individual simultaneously.
Neurons in the brain interact by sending each other chemical messages – neurotransmitters. Gamma-aminobutyric acid (GABA) is the most common inhibitory neurotransmitter, which is important to restrain neural activity, preventing neurons from getting too trigger-happy and from firing too much or responding to irrelevant stimuli.
The hippocampus is a part of the brain that sits within our temporal lobes and plays a major role in our memories and emotions. This latest research has implications for understanding how this part of the brain affects specific aspects of schizophrenia.
Developing new treatment for schizophrenia
The study was led by post-doctoral researcher Stuart Williams. He said: “We know that people with schizophrenia have increased hippocampal activity; we wanted to explore this further and find out exactly how this manifests itself. Through our research carried out in rats, we were able to ascertain the importance of GABAergic inhibition within the hippocampus in relation to certain symptoms associated with schizophrenia. Specifically, we found no evidence that faulty inhibition within the hippocampus disrupts behaviours related to the underlying cognitive processes which are thought to contribute to the onset of hallucinations or delusions but did find that it may contribute to some of the negative symptoms, disrupting associative learning in the form of conditioned fear.”
This study has important implications for developing treatments for schizophrenia symptoms that negatively affect the patient.
Stuart continued: “By revealing previously unknown detail about the role of aberrant activity in the hippocampus, we are providing insights into the behavioural consequences that disruption of specific neural structures, such as the hippocampus, have in schizophrenia. This could help to develop more targeted treatments that improve the management of specific aspects of schizophrenia symptomatology such as improving negative symptoms, potentially by dampening down this overactivity in the hippocampus.”
