Long-term potential activity

Long-term potentiation (LTP) is a synaptic plasticity phenomenon that corresponds to an increase in the synaptic strength (increase in the post-synaptic response observed for the same stimulation of the presynaptic terminals) observed after a high frequency stimulation (tetanus) of the afferent fibres. This increased response is still observed hours and even days after the tetanus. The phenomenon is often observed at glutamatergic synapses and involves, in most cases, the activation of the V-methyl D-aspartate (NMDA) subtype of ionotropic glutamate receptors. 

Despite the above precautions, it is still possible that NT spillover and extrasynaptic action may occur and indeed could be required in some instances. Thus the diffusion of glutamate beyond the synapse could activate extrasynaptic high-affinity NMDA or metabotropic receptors (Chapter 9) to produce long-lasting effects to maintain activity in a network. This may be important in long-term potentiation and memory effects. Crosstalk between synapses could also act as a back-up to ensure that a pathway functions properly (see Barbour and Hausser 1997). 

Histaminergic activation of ion channels may also occur through NMDA receptors [ 1 ]. This action occurs at the polyamine binding site on NR1/NR2B subunits and is sensitive to pH. Endogenous histamine may act at this site to facilitate the induction of long term potentiation, but this has not been established. Additional histamine receptors may still be discovered. 

COXs thus catalyze the same first committed step of the AA cascade (Fig. 33-2). COX-2, however, is expressed in response to mitogenic and inflammatory stimuli and encoded by an early-response gene. To date we do not understand how COX-3 expression is regulated. In contrast, COX-1 expression is not subject to short-term regulation. Neurons in the hippocampus, as well as in a few other brain regions, are unlike other cells in that they display basal COX-2 expression [36]. This expression is modulated by synaptic activity, such as long-term potentiation, and involves the NMDA glutamate receptors [36,40]. 

Kato, K., Clark, G. D., Bazan, N. G. and Zorumski, C. F. Platelet activating factor as a potential retrograde messenger in CA1 hippocampal long-term potentiation. Nature 367, 175-179,1994. 

Wieraszko, A., Li, G., Kornecki, E., Hogan, M. V. and Ehrlich, Y. H. Long-term potentiation in the hippocampus induced by platelet-activating factor. Neuron 10 553-557,1993. 

Kobayashi K, Ishii S, Kume K, Takahashi T, Shimizu T, Manabe T. (1999). Platelet-activating factor receptor is not required for long-term potentiation in the hippocampal CAl region. Eur J Neurosci. 11(4) 1313-16. 

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