Brain Cells Work Differently Than Previously Thought
Scientists know that information travels between brain cells along neuronal extensions called axons. For the first time, researchers have found that axons don’t just transmit information — they can turn the signal up or down with the right stimulation
This finding may help scientists develop treatments for psychiatric disorders such as depression and schizophrenia in which it is thought that different parts of the brain do not communicate correctly with each other.
“Until now, scientists have thought that in the brain’s cortex — where most cognitive processes occur — information was only processed in the cell body,” said Raju Metherate, author of the study, associate professor of neurobiology and behavior, and director of the Center for Hearing Research at UC Irvine. “The result of our study suggests that we must consider the axons as sites of information processing — and of potential problems when things go wrong.”
Increasingly, studies are beginning to show that complex information processing, and perhaps consciousness itself, may result from coordinated activity among many parts of the brain connected by bundles of long axons. Cognitive problems may occur when these areas don’t communicate properly with each other.
Cognitive function occurs when millions of brain cells communicate with each other at the same time. A brain cell has a network of branches called dendrites through which it receives and processes information from other cells. The body of the cell then relays the processed information along an axon to a terminal that links to another cell’s dendrites. At the terminal, chemicals called neurotransmitters are released, allowing the information to enter the receiving cell. Until now, scientists believed axons were just the wires between point A and point B.
“Axons, we thought, were like wires in a radio conveying signals, but we found that if you stimulate the axon, the signal can be altered, like turning the volume knob on the radio,” Metherate said.
Originally, Metherate and his colleagues had hoped to confirm the idea that the drug nicotine alters information that is processed in the cell body or terminal. Puzzled by several negative tests, they developed an experiment in which they could study the intervening axon.
In their experiment, they examined a section of mouse brain associated with hearing that contained a brain cell with an axon connecting to the cortex. Using nicotine, they stimulated the axon to determine how it would affect a signal the brain cell sent to the cortex. Without applying nicotine, about 35 percent of the messages sent by the brain cell reached the cortex. But when nicotine was applied to the axon, the success rate nearly doubled to about 70 percent.
“We looked for more conventional reasons why the response was enhanced, but the evidence just kept pointing to the axon. Nicotine activated the proteins that we think are on the axon,” Metherate said. “This is a completely new idea about how the brain works.”
Nat Neurosci. 2007 Aug 19; [Epub ahead of print]
Nicotinic control of axon excitability regulates thalamocortical transmission.
Kawai H, Lazar R, Metherate R.
Department of Neurobiology and Behavior and Center for Hearing Research, University of California, Irvine, 2205 McGaugh Hall, Irvine, California 92697-4550, USA.
The thalamocortical pathway, a bundle of myelinated axons that arises from thalamic relay neurons, carries sensory information to the neocortex. Because axon excitation is an obligatory step in the relay of information from the thalamus to the cortex, it represents a potential point of control. We now show that, in adult mice, the activation of nicotinic acetylcholine receptors (nAChRs) in the initial portion of the auditory thalamocortical pathway modulates thalamocortical transmission of information by regulating axon excitability. Exogenous nicotine enhanced the probability and synchrony of evoked action potential discharges along thalamocortical axons in vitro, but had little effect on synaptic release mechanisms. In vivo, the blockade of nAChRs in the thalamocortical pathway reduced sound-evoked cortical responses, especially those evoked by sounds near the acoustic threshold. These data indicate that endogenous acetylcholine activates nAChRs in the thalamocortical pathway to lower the threshold for thalamocortical transmission and to increase the magnitude of sensory-evoked cortical responses. Our results show that a neurotransmitter can modulate sensory processing by regulating conduction along myelinated thalamocortical axons.
PMID: 17704774 [PubMed – as supplied by publisher]