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J Neurophysiol 89: 684-690, 2003; doi:10.1152/jn.01041.2001
0022-3077/03 $5.00
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J Neurophysiol (February 1, 2003). 10.1152/jn.01041.2001
Submitted on Submitted 21 December 2001; accepted in final form 25 September 2002

Protein Phosphatases Mediate Depotentiation Induced by High-Intensity Theta-Burst Stimulation

Maeng-Hee Kang-Park,1 Meredith A. Sarda,1 Katherine H. Jones,1 Scott D. Moore,2,3 Shirish Shenolikar,1 Suzanne Clark,3 and Wilkie A. Wilson1,3

 1Department of Pharmacology and Cancer Biology and  2Department of Psychiatry, Duke University Medical Center, Durham, North Carolina 27710; and  3Neurology Research Laboratory, Veterans Administration Medical Center, Durham, North Carolina 27705

Kang-Park, Maeng-Hee, Meredith A. Sarda, Katherine H. Jones, Scott D. Moore, Shirish Shenolikar, Suzanne Clark, and Wilkie A. Wilson. Protein Phosphatases Mediate Depotentiation Induced by High-Intensity Theta-Burst Stimulation. J. Neurophysiol. 89: 684-690, 2003. We have previously reported that varying stimulus intensity produces qualitatively different types of synaptic plasticity in area CA1 of hippocampal slices: brief low-intensity (LI) theta-burst (TB) stimuli induce long-term potentiation (LTP), but if the stimulus intensity is increased (to mimic conditions that may exist during seizures), LTP is not induced; instead, high-intensity (HI) TB stimuli erase previously induced LTP ("TB depotentiation"). We now have explored the mechanisms underlying TB depotentiation using extracellular field recordings with pharmacological manipulations. We found that TB depotentiation was blocked by okadaic acid and calyculin A (inhibitors of serine/threonine protein phosphatases PP1 and PP2A), FK506 (a specific blocker of calcineurin, a Ca2+/calmodulin (CaM) protein phosphatase), and 8-Br-cAMP (an activator of protein kinase A) with 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase inhibitor). These results suggest that protein phosphatase pathways are involved in the TB depotentiation similar to other type of down-regulating synaptic plasticity such as low-frequency stimulation (LFS)-induced long-term depression (LTD) and depotentiation in the rat hippocampus. However, TB depotentiation and LFS depotentiation could have differential functional significance.




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