Bidirectional Synaptic Plasticity and Spatial Memory Flexibility Require Ca2+-Stimulated Adenylyl Cyclases

• DOI: 10.1523/jneurosci.0009-11.2011
• Publication Date: 2011-07-13T16:43:01Z
• Authors: M. Zhang; D. R. Storm; H. Wang
• Keywords: Mice, Knockout; Neurons; 0301 basic medicine; Neuronal Plasticity; Hippocampus; Electric Stimulation; Electrophysiology; Mice; 03 medical and health sciences; Mental Recall; Synapses; Animals; Calcium; Maze Learning; Adenylyl Cyclases

When certain memory becomes obsolete, effective suppression of the previously established is essential for animals to adapt changing environment. At cellular level, reversal synaptic potentiation may be important neurons acquire new information and prevent saturation. Here, we investigated function Ca²⁺-stimulated cAMP signaling in regulation bidirectional plasticity spatial formation double knock-out mice (DKO) lacking both type 1 8 adenylyl cyclases (ACs). In anesthetized animals, DKO mutants showed defective long-term (LTP) after a single high-frequency stimulation (HFS) or two spaced HFSs at 100 Hz. However, normal LTP HFS 200 Hz compressed Interestingly, as well <i>de novo</i> depression was impaired mice. Morris water maze, acquisition retention, although deficits could attenuated by overtraining trainings with shorter intertrial interval. platform test, were relearning old suppression. Furthermore, extinction not efficient These data demonstrate that AC activity only but also memory.