scholarly journals Nicotine shifts the temporal activation of hippocampal protein kinase A and extracellular signal-regulated kinase 1/2 to enhance long-term, but not short-term, hippocampus-dependent memory

2014 ◽  
Vol 109 ◽  
pp. 151-159 ◽  
Author(s):  
Thomas J. Gould ◽  
Derek S. Wilkinson ◽  
Emre Yildirim ◽  
Rachel L.F. Poole ◽  
Prescott T. Leach ◽  
...  
Author(s):  
G. F. Stepanov ◽  
N. Y. Yasinenko ◽  
A. G. Vasylieva ◽  
V. L. Davydenko

Memory is provided by changes in synapses in neural circuits: short-term memory - by functional changes in a separate sensory neuron and a separate motor neuron, long-term memory - by structural changes (regrowth of new synapses).During the formation of short-term memory in synapses, cAMP, protein kinase A, are used, which act inside the cell and transmit a signal that cause the release of large amounts of the neurotransmitter glutamate. Two independent mechanisms are involved in the formation of long-term memory: - one triggers a long-term strengthening of synaptic connections, directing protein kinase A to the nucleus, which activates the CREB protein, thereby turning on the structural genes encoding proteins necessary for the growth of new synaptic connections; - the other reinforces the already formed memory, supporting the newly formed synaptic endings, which requires local synthesis of proteins.


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