Spencer, Jonathan P. and Murphy, Kerry P.S.J.
|DOI (Digital Object Identifier) Link:||http://dx.doi.org/10.1016/S0304-3940(02)00659-6|
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The induction of long-term potentiation (LTP) at corticostriatal synapses is dependent on the activation of postsynaptic NMDA receptors, but the mechanisms involved in the maintenance of LTP are not known. We report here that forskolin, an activator of adenylyl cyclase, induces a lasting enhancement of the corticostriatal synaptic response. This enhancement is associated with a lasting decrease in paired-pulse ratio, and is blocked by inhibitors of adenylyl cyclase and cyclic AMP-dependent protein kinase (PKA), but not by a PKA inhibitor injected into the postsynaptic cell. Tetanically-induced LTP is also associated with a decrease in paired-pulse ratio and partially occludes the subsequent action of forskolin. Our results suggest that activation of presynaptic PKA can enhance neurotransmission at corticostriatal synapses; a mechanism required for the expression of LTP at these synapses. Copyright 2002 Elsevier Science Ireland Ltd.
|Item Type:||Journal Article|
|Keywords:||Striatum; Long-term potentiation (LTP); Basal ganglia; Forskolin; Protein kinase; Presynaptic; Cyclic AMP; Glutamate|
|Academic Unit/Department:||Science > Life, Health and Chemical Sciences
|Interdisciplinary Research Centre:||Biomedical Research Network (BRN)|
|Depositing User:||Kerry Murphy|
|Date Deposited:||28 Jun 2006|
|Last Modified:||14 Jan 2016 15:56|
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