Long-term memory, unlike short-term memory, is dependent upon the construction of new proteins.[30] This occurs within the cellular body, and concerns in particular transmitters, receptors, and new synapse pathways that reinforce the communicative strength between neurons. The production of new proteins devoted to synapse reinforcement is triggered after the release of certain signaling substances (such as calcium within hippocampal neurons) in the cell. In the case of hippocampal cells, this release is dependent upon the expulsion of magnesium (a binding molecule) that is expelled after significant and repetitive synaptic signaling. The temporary expulsion of magnesium frees NMDA receptors to release calcium in the cell, a signal that leads to gene transcription and the construction of reinforcing proteins.[31] For more information, see long-term potentiation (LTP).
One of the newly synthesized proteins in LTP is also critical for maintaining long-term memory. This protein is an autonomously active form of the enzyme protein kinase C (PKC), known as PKMζ. PKMζ maintains the activity-dependent enhancement of synaptic strength and inhibiting PKMζ erases established long-term memories, without affecting short-term memory or, once the inhibitor is eliminated, the ability to encode and store new long-term memories is restored.
Also, BDNF is important for the persistence of long-term memories.[32]
What I worry about being confused on when reading the literature is the distinction between forming memories in the first place, and actually encoding for memory.
Another critical distinction is that, proteins that are needed to prevent degradation of memories over time (which get lots of research and emphasis in the literature due to their role in preventing degenerative diseases) aren’t necessarily the ones directly encoding for the memories.
So in subjects I know a lot about, I have dealt with many people who pick up strange notions by filling in the gaps from google and wikipedia with a weak foundation. The work required to effectively figure out what specific damage to the specific proteins you mentioned could be done by desiccation of a cell is beyond my knowledge base, so I leave it to someone more knowledgeable than myself(perhaps you?) to step in.
What open/closed states does PKMζ have? What regulates those open/closed states? Are the open/closed states important to its roll (it looks like yes given the notion of the inhibitor?)?
Yes, it’s important to build a strong foundation before establishing firm opinions. Also, in this particular case note that science appears to have recently changed it’s mind based on further evidence, which goes to show that you have to be careful when reading wikipedia. Apparently the protein in question is not so likely to underlie LTM after all, as transgenic mice lacking it still have LTM (exhibiting maze memory, LTP, etc). The erasure of memory is linked to zeta inhibitory peptide (ZIP), which incidentally happens in the transgenic mice as well.
ETA: Apparently PKMzeta can be used to restore faded memories erased with ZIP.
Here we have moved far past my ability to even speculate.
Presumably you can use google and wikipedia to fill in the gaps just like the rest of us.
Wikipedia: Long-term memory
What I worry about being confused on when reading the literature is the distinction between forming memories in the first place, and actually encoding for memory.
Another critical distinction is that, proteins that are needed to prevent degradation of memories over time (which get lots of research and emphasis in the literature due to their role in preventing degenerative diseases) aren’t necessarily the ones directly encoding for the memories.
So in subjects I know a lot about, I have dealt with many people who pick up strange notions by filling in the gaps from google and wikipedia with a weak foundation. The work required to effectively figure out what specific damage to the specific proteins you mentioned could be done by desiccation of a cell is beyond my knowledge base, so I leave it to someone more knowledgeable than myself(perhaps you?) to step in.
What open/closed states does PKMζ have? What regulates those open/closed states? Are the open/closed states important to its roll (it looks like yes given the notion of the inhibitor?)?
Yes, it’s important to build a strong foundation before establishing firm opinions. Also, in this particular case note that science appears to have recently changed it’s mind based on further evidence, which goes to show that you have to be careful when reading wikipedia. Apparently the protein in question is not so likely to underlie LTM after all, as transgenic mice lacking it still have LTM (exhibiting maze memory, LTP, etc). The erasure of memory is linked to zeta inhibitory peptide (ZIP), which incidentally happens in the transgenic mice as well.
ETA: Apparently PKMzeta can be used to restore faded memories erased with ZIP.