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Astrocytes and synaptic plasticity
October 13, 2008By mopping up excess neurotrophic factor from neuronal synapses, astrocytes may finely tune synaptic transmission to affect processes such as learning and memory, say Bergami et al.
The major cellular events of learning and memory are long-term potentiation (LTP) and long-term depression (LTD), both of which affect neurons' ability to communicate with one another. Neurons that have undergone LTP display a stronger electrical response to the same level of a stimulus, whereas neurons that have gone through LTD display a weaker response. These changes are thought to result from modifications of the neuronal synapses, such as alterations in the density of postsynaptic receptors, or downstream signaling events.
Secretion of the neurotrophic factor BDNF (brain-derived neurotrophic factor) has been implicated in long-term synaptic modification, and the function of BDNF on synaptic strength depends on its particular form: in its pro-BDNF form it is believed to promote LTD, and in its mature form it prompts LTP. Neurons were thought to secrete pro-BDNF, which then matured into BDNF in the synaptic space. However, a recent study suggests that only mature BDNF is secreted, pro-BDNF being processed intracellularly.
To get to the bottom of things, Bergami et al. investigated the fate of both forms after LTP induction in brain slices from the rat cortex. By fluorescent immunohistochemistry they showed that that neurons indeed secrete both mature and pro-BDNF, but that a large amount of the pro-BDNF is immediately taken up by astrocytes.
Astrocytes, previously thought to be unimportant in neuronal transmission, have recently been implicated in long-term modulation of neuronal synapses. For example, they release the neurotransmitter glutamate into the synapse prompting LTP. By specifically mopping up pro-BDNF, astrocytes seem to have another means to assist in LTP. However, while it's likely that most pro-BDNF gets degraded inside astrocytes, say the authors, some gets recycled and re-released, suggesting that astrocytes in fact fine-tune synaptic plasticity.
Rockefeller University Press
To get to the bottom of things, Bergami et al. investigated the fate of both forms after LTP induction in brain slices from the rat cortex. By fluorescent immunohistochemistry they showed that that neurons indeed secrete both mature and pro-BDNF, but that a large amount of the pro-BDNF is immediately taken up by astrocytes.
Astrocytes, previously thought to be unimportant in neuronal transmission, have recently been implicated in long-term modulation of neuronal synapses. For example, they release the neurotransmitter glutamate into the synapse prompting LTP. By specifically mopping up pro-BDNF, astrocytes seem to have another means to assist in LTP. However, while it's likely that most pro-BDNF gets degraded inside astrocytes, say the authors, some gets recycled and re-released, suggesting that astrocytes in fact fine-tune synaptic plasticity.
Rockefeller University Press
Astrocytes and synaptic plasticity
By mopping up excess neurotrophic factor from neuronal synapses, astrocytes may finely tune synaptic transmission to affect processes such as learning and memory, say Bergami et al.
New Brandeis research sheds light on memory by erasing it
For years, scientists have studied the molecular basis of memory storage, trying to find the molecules that store memory, just as DNA stores genetic memory.
Brains response to visual stimuli helps us to focus on what we should see, rather than all there is to see
Delving ever deeper into the intricate architecture of the brain, researchers at The Salk Institute have now described how two different types of nerve cells, called neurons, work together in tiny sub-networks to pass on just the right amount and the right kind of sensory information.
Hebrew University, German And British Researchers Develop Means To Help Post-Traumatic Stress Sufferers
Try as we may to suppress memories of highly stressful experiences, they nevertheless come back to bother us - even causing attacks of intense fear or other undesirable behavioral impairments. Now a group of German, Israeli and British scientists and students have found that a gene-based approach offers promise for development of a treatment that can suppress these reactions while not impairing memory itself. In an article appearing as the cover story in the current issue of Molecular Psychiatry, a team of researchers from the Silberman Institute of Life Sciences at the Hebrew University of Jerusalem and the Max Planck Institute for Experimental Medicine in Goettingen, Germany, describe the
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