| First Author | Tsokas P | Year | 2016 |
| Journal | Elife | Volume | 5 |
| PubMed ID | 27187150 | Mgi Jnum | J:234012 |
| Mgi Id | MGI:5788789 | Doi | 10.7554/eLife.14846 |
| Citation | Tsokas P, et al. (2016) Compensation for PKMzeta in long-term potentiation and spatial long-term memory in mutant mice. Elife 5:e14846 |
| abstractText | PKMzeta is a persistently active PKC isoform proposed to maintain late-LTP and long-term memory. But late-LTP and memory are maintained without PKMzeta in PKMzeta-null mice. Two hypotheses can account for these findings. First, PKMzeta is unimportant for LTP or memory. Second, PKMzeta is essential for late-LTP and long-term memory in wild-type mice, and PKMzeta-null mice recruit compensatory mechanisms. We find that whereas PKMzeta persistently increases in LTP maintenance in wild-type mice, PKCiota/lambda, a gene-product closely related to PKMzeta, persistently increases in LTP maintenance in PKMzeta-null mice. Using a pharmacogenetic approach, we find PKMzeta-antisense in hippocampus blocks late-LTP and spatial long-term memory in wild-type mice, but not in PKMzeta-null mice without the target mRNA. Conversely, a PKCiota/lambda-antagonist disrupts late-LTP and spatial memory in PKMzeta-null mice but not in wild-type mice. Thus, whereas PKMzeta is essential for wild-type LTP and long-term memory, persistent PKCiota/lambda activation compensates for PKMzeta loss in PKMzeta-null mice. |
