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| Pinpointing Neurons In Memory Formation |
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| SciMed - Neuroscience | ||||||
| TS-Si News Service | ||||||
| Friday, 14 September 2007 20:00 | ||||||
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Findings could help evaluate various neurological conditions
 The
 amygdala (Gr. almond) is a small structure in the medial temporal lobe of the brain, a few inches from either ear. The left and right amygdalae are not physically identical. Neuroimaging studies suggest that the right amygdala has a larger volume than the left. Additionally, the two are functionally asymmetrical as well.
Recent research points to the circuits, not just the structure. The nerves coursing through the amygdala connect it to a number of important brain centers, including the
neocortex and visual cortex. Specifically, the left amygdala appears to be consistently activated in response to negative, withdrawal-related stimuli. The right amygdala seems to be involved in autonomic responses (heart rate, skin responses, blood pressure, etc.).
Amygdala activation can be driven by one's own emotional experiences. It has long been linked with a person's mental and emotional state, playing a critical role in several emotional behaviors.
These include the evaluation of and response to emotionally salient information, anxiety disorders, depression, and the arousal-related components of drug abuse.
The fact that the amygdala influences diverse emotional responses suggests that it serves an important emotional function. It likely influences perception and arousal responses before higher-level, cognitive analysis of the stimuli. Working with a unique breed of transgenic mice, the new study has shown for the first time that the same neurons activated during fear conditioning are, in fact, reactivated during memory retrieval.
The new results suggest that the affected neurons evolved stable synaptic changes, giving them a capacity for reactivation by conditioned stimulus for at least three days. The study concluded that the reactivated neurons were likely a component of a stable engram or memory trace for conditioned fear.
The findings could potentially be used to uncover precisely how drugs such as antidepressants work in the brain, allowing clinicians to more accurately evaluate various treatment options.
"Our study provides the answers to some basic questions," said Mark Mayford, whose laboratory conducted the groundbreaking study.
Memories are presumably stored in subgroups of neurons that are activated in response to various sensory experiences, the study said. Previously, some encoding of memories in complex neuronal networks had been identified with electrophysiological recordings, and similar approaches have identified neurons with firing properties temporally linked to various aspects of learned task performance.
But, Mayford noted, this is like knowing only that a computer is turned on. The new study shows precisely which circuits are active during a specific memory formation.
"We found neurons in the basolateral amygdala that were activated during fear conditioning and were reactivated during memory retrieval," Mayford said. The basolateral amygdala is the part of the brain believed to be responsible for memories involving emotional arousal.
"The number of reactivated neurons correlated with the behavioral expression of that fear memory in the mice themselves, which indicates a stable correlation between these neurons and memory."
 The Mouse Innovator. The new study utilized a unique transgenic mouse (TetTag mouse) that enabled scientists to genetically tag individual neurons activated during a given time frame. The tag can be used for the direct comparison of neuronal activity at two distinct and widely spaced points in time.
This novel technology can be used with free roaming mice, enabling the scientists to record and measure the correlation between neuronal activity and any behavioral expression of a specific memory. Moreover, the study noted, the technology requires only basic laboratory equipment, which is generally available to most researchers.
"The TetTag mouse allows us to put genes into neurons that have been activated by an environmental stimulus," Mayford said. "Basically, we can put any gene we want into those neurons activated by fear, and this gives us genetic control over very specific circuits in the brain."
The reason fear and anxiety were used as the activating experience, Mayford said, is because fear is an ancient and fundamental emotion" "We know that mice feel fear; we don't know if they feel joy. In the wild, you can survive without joy, but you don't live very long without fear."
The ability to genetically manipulate these activated neurons should allow a better and more precise understanding of the underlying molecular mechanisms of memory encoding within a particular neuronal network.
This might one day translate into a clinical advantage for treating patients suffering from disorders such as depression, Mayford said.
"Antidepressants don't work the same in every individual," he said, "so our genetic tagging technique could potentially help clinicians evaluate treatment by showing how an individual's brain works at two different times during treatment — where and how the drug is affecting specific neurons."
The study was supported by the US National Institutes of Health (NIH).
Localization of a Stable Neural Correlate of Associative Memory. Leon G. Reijmers, Brian L. Perkins, Naoki Matsuo, Mark Mayford. Science 31 August 2007: Vol. 317. no. 5842, pp. 1230 - 1233. DOI: 10.1126/science.1143839.
| Abstract |
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