Science, Space and Technology News 2024
A recent study involving computational modeling by researchers from four Boston institutions has provided new insights into how ketamine affects brain function, particularly in treatment-resistant depression. By detailing the drug’s interaction with NMDA receptors in the brain’s cortex and simulating its impact on neural activity, the research offers a clearer understanding of the mechanisms behind ketamine’s altered arousal states and potential therapeutic benefits.
“This modeling work has helped decipher likely mechanisms through which ketamine produces altered arousal states as well as its therapeutic benefits for treating depression,” co-senior author Emery N.
Blocking slows the voltage build-up across the neuron’s membrane that eventually leads a neuron to “spike,” or send an electrochemical message to other neurons. The NMDA doorway becomes unblocked when the voltage gets high. This interdependence between voltage, spiking and blocking can equip NMDA receptors with faster activity than its slow closing speed might suggest.
With their model, the scientists simulated how different doses of ketamine affecting NMDA receptors would alter the activity of a model brain network. The simulated network included key neuron types found in the cortex: one excitatory type and two inhibitory types. It distinguishes between “tonic” interneurons that tamp down network activity and “phasic” interneurons that react more to excitatory neurons.
Another prediction is that these bursts become synchronized into the gamma frequency waves seen with ketamine. How? The team found that the phasic inhibitory interneurons become stimulated by lots of input of the neurotransmitter glutamate from the excitatory neurons and vigorously spike, or fire.
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