Funding for this site is provided by readers like you.
Memory and the brain
How Memory Works

HelpNew Players in the Molecular Basis of Memory and LearningNew laser method reveals high-density information storage in the brainGlutamate Receptors - Structures and Functions
Why We Remember Important Things And Forget Trivia: Neuron's Synapses Remodel Themselves
David Linden, Ph.D : Cellular Substrates of Memory

Many studies are producing more and more evidence that the nervous system and the immune system interact continuously. For example, certain proteins that act as extra-cellular messengers in the immune system have also been identified in various parts of the brain, including the hippocampus, where they appear to play a role in neuromodulation.

This is the case for cytokines–molecules that are involved in inflammation–such as interleukin-1, interleukin-6, and TNF alpha. Recent data show that these cytokines appear to reduce LTP, and perhaps LTD as well. A causal link between certain bacterial or viral infections and cognitive functions thus becomes conceivable.

Experiment Module: Lipopolysaccharide Inhibits Long-Term Potentiation and Glutamate Release in Rat Dentate GyrusLinked Module: Evidence That Increased Hippocampal Expression of the Cytokine Interleukin-1 Is a Common Trigger for Age- and Stress-Induced Impairments in Long-Term PotentiationLinked Module: Interleukin-1 beta exerts a myriad of effects in the brain and in particular in the hippocampus: analysis of some of these actionsResearcher Module: Patterson Lab Home Page: Introduction

Long-term depression (LTD) may be regarded as a complementary mechanism to long-term potentiation (LTP). In the hippocampus, the role of LTD is thought to be to return synapses that have been potentiated by LTP to a normal level so that they will be available to store new information. But elsewhere in the brain, LTD may be actively responsible for the storage of new information, as in the cerebellum.

LTD develops when a presynaptic neuron is active at low frequencies (1 to 5 Hz) without the postsynaptic neuron’s being subjected to strong depolarization, as it is with LTP. This lack of association between the two neurons raises the concentration of calcium in the postsynaptic neuron, but much less than in LTP.

Consequently, instead of proteins such as CaM kinase II or kinase A being activated, enzymes called phosphatases are activated. These enzymes remove certain phosphate groups from the AMPA receptors; in other words, they dephosphorylate them.

The AMPA receptor GluR1 subunit, which has two sites that can be phosphorylated (Ser831, phosphorylated by CaM kinase II, and Ser845, phosphorylated by PKA), appears to be the target for phosphatases 1, 2A, and 2B. In the hippocampus, the effect of this dephosphorylation of the AMPA receptor would be to reduce the amplitude of the postsynaptic potential to the normal level where it was before LTP.

It is also believed that the number of AMPA receptors decreases during LTD. These receptors would be removed from the postsynaptic membrane and placed in reserve: in short, the opposite of what happens in LTP, when additional receptors are inserted into the membrane.


  Presentations | Credits | Contact | Copyleft