Brain Plasticity And ‘Reliable Neurons’

Reliable neurons play role in synaptic strength

New research indicates that the history of communication between neurons plays a greater role than their current excitation in determining  how weakly or strongly they react to stimulation.

Plastic change occurs when the strength of the synaptic connections over prolonged periods lasts beyond the particular experience or activity (memory). Hitherto, scientists had believed that neurons at both ends of a signal (sending and receiving) can affect the outcome of the transmission with equal weight. Dr. Mike Friedlander, a professor and chair of the department of neuroscience at the Baylor College of Medicine, has demonstrated that this is not the case. Sometimes the sender neuron dominates the outcome while in some cases the receiver dominates it.

“Which one dominates the overall behavior of the connection is largely determined by the initial state of the synapses, or the reliability of the connection, based either on its past activity history or on some intrinsic factors not yet identified,” said Friedlander.

By examining the interactions of a group of neurons, Friedlander’s team showed that if the initial state of the synaptic connections was strong and the amount of neurotransmitter released reliable, the receiver neuron dominated the plasticity response. (Near simultaneous sender-receiver activation weakened the plastic response.) But if the initial state of the synaptic connections was weak and the amount of neurotransmitter released unreliable, the sender neuron dominated the receiver neuron’s plasticity response, growing in strength as the probability of neurotransmitter release by the sender increased.

The team also found a high degree of stability in about one-quarter of the connections between the cortical neurons, resulting in little capacity for plasticity.

“These ‘hard-wired’ cellular connections may represent an information-processing scaffold within the brain, playing a role in the stability of cortical microcircuits in the face of ongoing dynamic change during learning,” Friedlander said. “While basic in its nature for understanding the function of the normal cerebral cortex, this work provides fundamental new information regarding how the brain learns at a cellular microcircuit level that can provide new insights into disorders of learning and memory such as mental retardation and dementias of aging such as Alzheimer’s disease,” said Friedlander.

Funding for this study came from the The National Eye Institute, National Institutes of Health.

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