The study has implications for understanding cognitive deficits in a variety of brain disorders, including schizophrenia, age-related cognitive decline and Alzheimer's, and for the treatment of cognitive deficits, researchers said.
Neurons in the brain interact by sending each other chemical messages, so-called 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 - a part of the brain that sits within our temporal lobes - plays a major role in our everyday memory of events and of where and when they happen.
The research has shown that a lack of restraint in the neural firing within the hippocampus disrupts hippocampus-dependent memory.
In addition, such aberrant neuron firing within the hippocampus also disrupted attention - a cognitive function that does not normally require the hippocampus.
"The finding that faulty inhibition disrupts memory suggests that memory depends on well-balanced neural activity within the hippocampus, with both too much and too little causing impairments," he said.
"This is an important finding because traditionally, memory impairments have mainly been associated with reduced activity or lesions of the hippocampus," said Bast.
"Our second important finding is that faulty inhibition leading to increased neural activity within the hippocampus disrupts attention, a cognitive function that does not normally require the hippocampus, but depends on the prefrontal cortex," he said.
"Our finding suggests that aberrant hippocampal activity has a knock-on effect on the prefrontal cortex, thereby disrupting attention," he said.
"Overall, our new findings show that increased activity of a brain region, due to faulty inhibitory neurotransmission, can be more detrimental to cognitive function than reduced activity or a lesion," he added.
The research was published in the journal Cerebral Cortex.
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