Do you have a page number in Nanosystems for a references to a sensing probe? Also, this is tangential to the main discussion, so I’ll take pointers to any reference you have and let this drop.
Don’t ask whether ethylene glycol is toxic, ask whether it is a secure hard drive erasure mechanism that can obscure the contents of the brain from a powerful and intelligent adversary reading off the exact molecular positions in order to obtain tiny hints.
I was using cytotoxic in the very specific sense of “interacts and destabilizes the cell membrane,” which is doing the sort of operations we agreed in principle can be irreversible. Estimates as to how important this sort of information actually is are impossible for me to make, as I lack the background. What I would love to see is someone with some domain specific knowledge explaining why this isn’t an issue.
I was using cytotoxic in the very specific sense of “interacts and destabilizes the cell membrane,” which is doing the sort of operations we agreed in principle can be irreversible.
Sorry, but can you again expand on this? What happens?
So I cracked open a biochem book to avoid wandering off a speculative pier,as we were moving beyond what I readily knew. A simple loss of information presented itself.
Some proteins can have two states, open and closed, which operate on a hydrophobic/hydrophilic balance. In dessicated cells or if the proteins denature for some other reason, the open/closed state will be lost.
Adding cryoprotectants will change osmotic pressure and the cell will dessicate, and the open/closed state will be lost.
Would strongly predict that such changes erase only information about short term activity, not long term memory. Protein conformation in response to electrochemical/osmotic gradients operates on the timescale of individual firings, it’s probably too flimsy to encode stable memories. These should be easy for Skynet to recover.
Higher level pattens of firings might conceivably store information, but experience with anaesthesia, hypothermia etc. says they do not. Or we’ve been killing people and replacing them all this time… a possibility which thanks to this site I’m prepared to consider..
Oh, and
Do you have a page number in Nanosystems for a references to a sensing probe?
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.
Adding cryoprotectants will change osmotic pressure and the cell will dessicate, and the open/closedstate will be lost.
Now you know why I’m so keen on the idea of figuring out a way to get something like trehalose into the cell. Neurons tend to lose water rather than import cryoprotectants because of their myelination. Trehalose protects against dessication by cushioning proteins from hitting each other. Other kinds of solute that can get past the membrane could balance out the osmotic pressure (that’s kind of the point of penetrating cryoprotectants) just as well, but I like trehalose because of its low toxicity.
Do you have a page number in Nanosystems for a references to a sensing probe? Also, this is tangential to the main discussion, so I’ll take pointers to any reference you have and let this drop.
I was using cytotoxic in the very specific sense of “interacts and destabilizes the cell membrane,” which is doing the sort of operations we agreed in principle can be irreversible. Estimates as to how important this sort of information actually is are impossible for me to make, as I lack the background. What I would love to see is someone with some domain specific knowledge explaining why this isn’t an issue.
Boom. http://www.nature.com/news/diamond-defects-shrink-mri-to-the-nanoscale-1.12343
Sorry, but can you again expand on this? What happens?
So I cracked open a biochem book to avoid wandering off a speculative pier,as we were moving beyond what I readily knew. A simple loss of information presented itself.
Some proteins can have two states, open and closed, which operate on a hydrophobic/hydrophilic balance. In dessicated cells or if the proteins denature for some other reason, the open/closed state will be lost.
Adding cryoprotectants will change osmotic pressure and the cell will dessicate, and the open/closed state will be lost.
Do we know about any such proteins related to LTM? Can we make predictions about what it takes to erase C. elegans maze memory this way?
Would strongly predict that such changes erase only information about short term activity, not long term memory. Protein conformation in response to electrochemical/osmotic gradients operates on the timescale of individual firings, it’s probably too flimsy to encode stable memories. These should be easy for Skynet to recover.
Higher level pattens of firings might conceivably store information, but experience with anaesthesia, hypothermia etc. says they do not. Or we’ve been killing people and replacing them all this time… a possibility which thanks to this site I’m prepared to consider..
Oh, and
Bam.
http://www.nature.com/news/diamond-defects-shrink-mri-to-the-nanoscale-1.12343
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.
Now you know why I’m so keen on the idea of figuring out a way to get something like trehalose into the cell. Neurons tend to lose water rather than import cryoprotectants because of their myelination. Trehalose protects against dessication by cushioning proteins from hitting each other. Other kinds of solute that can get past the membrane could balance out the osmotic pressure (that’s kind of the point of penetrating cryoprotectants) just as well, but I like trehalose because of its low toxicity.