"Robust LTP which lasted for over 25 h"
LTP for one day is not really LTP
It would be called TRANSIENT
it certainly doesn't account for supposed LTC that persists for weeks
Please stop with the BULLSHIT
I think you're confusing learning that is supported by "persistent" processes like LTP and genuinely "transient" memory such as working memory. If a rodent runs a maze a couple of times, wakes up the next day and runs the maze even faster, its because there was LTP. Whether or not there is continued
reinforcement of this memory/learning determines whether or not the memory will go extinct given enough time.
If there is continued reinforcement of something like the name or face of a friend, the memory won't go extinct. If the original learning period is strong enough, ie memories of trauma in PTSD, they won't go extinct. But even consciously recalling the memory would be enough to strengthen it again and delay its extinction/LTD.
That doesn't mean that there aren't benefits to having someone with PTSD recall their trauma (exposure therapy) but the benefits of techniques are centered more around loss of the strong emotional response rather than immediate loss of the objective recollection of the details - once the strong emotional response is subdued, the memory can then begin to go extinct (fear enhances the formation of aversive memories, a process facilitated by the amygdala acting in concert with the hippocampus).
So your idea that strengthening the response of an individual synapse for 24 hours doesn't have a persistent effect shows complete disregard for the idea that the brain is a
network.
Funny how they don't state how long the the "network state" persists.
It's because it is quite transient.
This research is about using brainwave entrainment to enhance the STORAGE of new memories. It requires the new information to be sensed DURING the ENTRAINMENT period.
....Gamma oscillations are natural network oscillations that allow neurons to communicate with each other by synchronizing activity (UP/DOWN states), these oscillations are produced by a resonant loop between pyramidal cells and inhibitory interneurons. Gamma oscillations are very important in higher cognition and memory, this isn't something just artificially induced in a laboratory that has no relevance to in vivo...
I wouldn't view gamma oscillations as inherently carrying the relevant info that is to be encoded into long term memory, but rather the network oscillations are playing a permissive role in allowing communication between brain cells by timing their firing.
(From that study) "Changes in the strength of synapses – the connections between neurons – form the basis of learning and memory. This process, which is known as synaptic plasticity, incorporates transient experiences into persistent memory traces. However, a single synapse should not be viewed in isolation. Neurons typically belong to extensive networks made up of large numbers of cells, which show coordinated patterns of activity. The synchronized firing of the neurons in such a network is referred to as a network oscillation.
~Analysis of the underlying molecular, cellular and synaptic mechanisms in vitro slice preparations showed changes in SWR-associated excitatory synaptic strength between pyramidal cells (PC) that are mediated postsynaptically and depend on metabotropic glutamate receptor-5 (mGluR5) activation. In stark contrast to excitation, alteration of inhibitory synaptic strength was independent of postsynaptic activation and less pronounced, reflecting an IN-specific, directionally biased synaptic plasticity, as demonstrated in our study for two major GABAergic inhibitory cell types, PV- and CCK-expressing INs.
Our results suggest that gamma frequency oscillations represent a network state that promotes the formation of long-lasting synaptic plasticity in the hippocampal area CA3, leading to modification of synaptic strengths in a cell-specific manner."
Here is from Stanford
http://www.nature.com/npp/journal/v33/n1/full/1301559a.html - "Experiences, whether they be learning in a classroom, a stressful event,
or ingestion of a psychoactive substance, impact the brain by modifying the activity and organization of specific neural circuitry.
A major mechanism by which the neural activity generated by an experience modifies brain function is via modifications of synaptic transmission; that is, synaptic plasticity. Here, we review current understanding of the mechanisms of the major forms of synaptic plasticity at excitatory synapses in the mammalian brain. We also provide examples of the possible developmental and behavioral functions of synaptic plasticity and how maladaptive synaptic plasticity may contribute to neuropsychiatric disorders."
"Furthermore,
administration of a single dose of several different classes of drugs of abuse causes a significant increase in synaptic strength at excitatory synapses onto dopamine cells in the VTA (
Faleiro et al, 2004;
Saal et al, 2003;
Ungless et al, 2001). This increase shares mechanisms with LTP in the VTA and appears to involve upregulation of AMPARs (
Ungless et al, 2001). This drug-induced ‘LTP’ appears to play a functional role in triggering or mediating some drug-induced behavioral adaptations, as both conditioned place preference and behavioral sensitization are blocked by injection of glutamate receptor antagonists into the VTA (
Harris and Aston-Jones, 2003;
Vanderschuren and Kalivas, 2000)."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669702/ "Sensitizing Regimens of MDMA (Ecstasy) Elicit Enduring and Differential Structural Alterations in the Brain Motive Circuit of the Rat"
"Following a 4-week drug-free period, MDMA-pretreated rats displayed behavioral sensitization, as well as large increases in spine density and the number of multiple-headed spines on medium spiny neurons in core and shell subregions of nucleus accumbens. In medial prefrontal cortex, the prelimbic subregion showed increased spine density on distal dendrites of layer V pyramidal neurons, while the anterior cingulate subregion showed a change in the distribution of dendritic material instead.
Collectively, our results show that long-lasting locomotor sensitization to MDMA is accompanied by reorganization of synaptic connectivity in limbic-cortico-striatal circuitry. The differential plasticity in cortical subregions, moreover, suggests that drug-induced structural changes are not homogeneous and may be specific to the circuitry underlying long-term changes in drug-seeking and drug-taking behavior."
Here are the neuroplastic changes to dendrites in the NAcc of rats 4 weeks after a 3 week sensitizing treatment protocol with MDMA.
To the OP: I'm sorry about all the debating
Just to be clear, I'm not saying any of this debate is relevant to you, I still think you could be having problems with chronic deconditioning etc and that cardio is your best bet.
