Our unconfessed sins hang over us like a dark cloud, but God promises to sweep them away like the rising sin burns away the morning mist Isa. God casts hurls our sins into the sea, where they sink like a stone. God not only erases our sin debt, He destroys the document on which our debt was recorded by nailing it to the cross. We are forgiven because of the cross of Jesus. My sin—oh, the bliss of this glorious thought! Notify me of follow-up comments by email. Notify me of new posts by email.
Comments This is wonderful. God forgives and forgets. He died for all of my sins. Thank you Jesus. Amen to that! Thank you Dan for your comment. Leave a Reply Cancel reply Your email address will not be published. Comment Name Email Website Notify me of follow-up comments by email.
In this magnified slice of rodent brain tissue enhanced with a fluorescent protein, the green glow reveals which cells in the hippocampus seem to be storing the engram, or physical trace, of an experimentally induced memory. Going along with all that variety is now a growing appreciation that forgetting — the functional loss of memories — may also come in diverse forms.
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This forgetting process could involve the spontaneous decay of connections between neurons that encode a memory, the random death of those neurons, the failure of systems that would normally help to consolidate and stabilize new memories, or the loss of context cues or other factors that might make it hard to retrieve a memory. One form of active forgetting that scientists formally identified in is called intrinsic forgetting. This idea emerged after Davis, a neuroscientist at the Scripps Research Institute in Jupiter, Florida, and his colleagues reported giving fruit flies mild electric shocks while exposing them to an odor.
The flies quickly learned to avoid the smell , associating it with the shock.
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Davis and his colleagues looked at a certain set of neurons in the brains of the fruit flies that continuously release the neurotransmitter dopamine onto others called mushroom body neurons. They found that dopamine plays a dual role in both forming and forgetting memories. The explanation that Davis and his team proposed is that after a new memory forms, the dopamine-based forgetting mechanism begins to erase it.
Davis thinks this erasure happens because the cells reverse the structural changes that created the memory engram. Then the engram is preserved through some sort of consolidation process, which maintains a balance between what is learned and forgotten.
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Somewhere in the brain, he noted, there may be some sort of judge that tells it to override the forgetting process when it comes across something worth remembering in the long run. Zhong, a neuroscientist at Tsinghua University in Beijing, and his team have also successfully manipulated forgetting in mice.
In they found that the inhibition of a specific protein called Rac1 in the hippocampal neurons prolonged the retention of memories from less than 72 hours to at least hours in many cases. Increasing the activity of Rac1 reduced the life of memories to less than 24 hours. As Davis and Zhong argued in their jointly written review , all those findings suggested that cellular processes mediated by dopamine and Rac1 constantly erode newly formed memories.
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Another cellular process that seems to cause its own form of forgetting is neurogenesis, the birth of new neurons in the brain. The connection of neurogenesis to memory and forgetting is complicated. Previous studies have shown that neurogenesis can be important to the formation of new memories: In tests on lab animals, drugs that inhibit neurogenesis in the hippocampus can interfere with new memory formation, and drugs that enhance neurogenesis seem to help with learning new tasks if they are given before the learning process. In their experiment , they first allowed the mice to create a memory by training at a task.
Hours later, with drugs, they raised the level of neurogenesis in the animals to test whether the integration of new neurons in the hippocampus would affect the stability of that already stored memory. Frankland suspects that neurogenesis can complicate the challenge of retrieving prior memories from the hippocampus.
If the added neural wiring overlaps with the circuitry holding older memories, it may damage the older engrams or make it harder to isolate the old memories from newer ones. One piece of evidence that supports his theory came from follow-up work published earlier this year which showed that the harmful effect of hippocampal neurogenesis is worse for relatively recent memories.
Much older memories do not seem to be hurt by it. Neurogenesis in the hippocampus today is therefore more disruptive for memories from a week ago than for those from months or years ago.
Indeed, Frankland noted that the forgetting produced by remodeling of the hippocampal circuits through neurogenesis happens more slowly than the intrinsic forgetting based on dopamine and Rac1 that Davis and Yi observed: It takes several weeks for newly formed neurons to create new connections — and to contribute to the forgetting processes at work. When memories are forgotten by whatever mechanism, what happens to them? Are all traces of them eliminated? Or do they persist in some form unavailable to us?
The pair, who have been studying how sea slugs form memories for a decade, recently switched their attention to the neurobiology of how the animals forget.