When a presynaptic neuron is experimentally stimulated at a high frequency, even for just a few seconds, the excitability of the synapse is enhanced—or potentiated—when this neuron pathway is subsequently stimulated. The improved efficacy of synaptic transmission may last for hours or even weeks and is called long-term potentiation (LTP). Long-term potentiation may favor transmission along frequently used neural pathways and thus may represent a mechanism of neural "learning." It is interesting in this regard that LTP has been observed in the hippocampus of the brain, which is an area implicated in memory storage (see chapter 8).
Most of the neural pathways in the hippocampus use glutamate as a neurotransmitter that activates NMDA receptors. This implicates glutamate and its NMDA receptors in learning and memory, and indeed, in a recent experiment, it was demonstrated that genetically altered mice with enhanced NMDA expression were smarter when tested in a maze. The association of NMDA receptors with synaptic changes during learning and memory is discussed more fully in chapter 8.
Although glutamate-mediated neurotransmission is necessary for normal brain function, excessive release of glutamate can cause epilepsy and neuronal cell death, a process termed excitotoxicity. This process has been implicated in the neuronal damage that occurs in stroke and traumatic damage to the CNS, and in the loss of neurons in various neurodegenerative diseases. Interestingly, the street drug known as PCP or angel dust blocks NMDA receptors, suggesting that the aberrant schizophrenia-like effects of this drug are produced by a reduction in glutamate stimulation of NMDA receptors.
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