Coincidence detection in a neural correlate of classical conditioning is initiated by bidirectional 3-phosphoinositide-dependent kinase-1 signalling and modulated by adenosine receptors

摘要

Key points class="unordered" style="list-style-type:disc"> Signalling mechanisms for coincidence detection of paired stimuli during classical conditioning are fundamental for understanding the mechanisms of associative learning. Bidirectional 3-phosphoinositide-dependent kinase-1 (PDK1) activity is signalled by TrkB neurotrophin receptors for paired stimuli and p75^NTR for unpaired stimuli. Adenosine 2A receptors modulate PDK1 responses directly as G proteins and by transactivation of TrkB. Convergence of protein kinase A and PDK1 activity initiates signalling of paired stimuli during classical conditioning.