Forskolin and Long Term Potentiation (LTP)

  1. Lightbulb Forskolin and Long Term Potentiation (LTP)

    This is a very intriguing topic. Has anybody tried Forskolin in combination with a natural supplement containing a PDE-IV inhibitor (Instead of Rolipram) to enhance long term memory potentiation? Perhaps Forskolin + Artichoke extract or Forskolin + Resveratrol?

    Forskolin-Induced LTP in the CA1 Hippocampal Region Is NMDA Receptor Dependent

    Chemically induced long-term potentiation (cLTP) could potentially work by directly stimulating the biochemical machinery that underlies synaptic plasticity, bypassing the need for synaptic activation. Previous reports suggested that agents that raise cAMP concentration might have this capability. We examined the cLTP induced in acute slices by application of Sp-cAMPS or a combination of the adenylyl cyclase activator, forskolin, and the phosphodiesterase inhibitor, rolipram. Under our conditions, cLTP was induced but only if inhibition was reduced. We found that this form of cLTP was blocked by a N-methyl-D-aspartate receptor (NMDAR) antagonist and required the low-frequency test stimulation typically used to monitor the strength of synapses. Interestingly, similar LTP could be induced by lowering the Mg2+ concentration of the ACSF during forskolin/rolipram or Sp-cAMPS application or even by just lowering Mg2+ concentration alone. This LTP was also NMDAR dependent and required only a few (∼5) low-frequency stimuli for its induction. The finding that even low-frequency synaptic stimulation was sufficient for LTP induction indicates that a highly sensitized plasticity state was generated. The fact that some stimulation was required means that potentiation is probably restricted to the stimulated axons, limiting the usefulness of this form of cLTP. However, when similar experiments were conducted using slice cultures, potentiation occurred without test stimuli, probably because the CA3–CA1 connections are extensive and because presynaptic spontaneous activity is sufficient to fulfill the activity requirement. As in acute slices, the potentiation was blocked by an NMDAR antagonist. Our general conclusion is that the induction of LTP caused by elevating cAMP requires presynaptic activity and NMDA channel opening. The method of inducing cLTP in slice cultures will be useful when it is desirable to produce NMDAR-dependent LTP in a large fraction of synapses.

    Long-term potentiation
    In neuroscience, long-term potentiation (LTP) is a long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously.[2] It is one of several phenomena underlying synaptic plasticity, the ability of chemical synapses to change their strength. As memories are thought to be encoded by modification of synaptic strength,[3] LTP is widely considered one of the major cellular mechanisms that underlies learning and memory.
    ^^ The reason I bring this topic up. Thoughts?


  2. I know someone on another popular bodybuilding forum has.. can't remember what he said overall about it.

  3. There are more effective ways to induce LTP, like DAA supplementation. Also, there are much better PDE IV inhibitors than those listed (either do your own search or *possibly* wait a long time )

  4. Quote Originally Posted by mr.cooper69 View Post
    There are more effective ways to induce LTP, like DAA supplementation.
    Do you have any articles handy showing DAA supplementation elevating cAMP in CA1-CA3 pyramidal neurons? I know it obviously is an NDMA receptor agonist. Just curious.

    I saw the rat study using orally administered Sodium D-aspartate . They correlated a significant increase ability to find the hidden platform in the Morris Water Maze to rats with elevated concentrations of hippocampal D-asp.

    Moreover, 20 randomly selected rats possessing relatively high endogenous concentrations of d-Asp in the hippocampus were much faster in reaching the hidden platform, an event suggesting that their enhanced cognitive capability was functionally related to the high levels of d-Asp.
    Evidence for the involvement of D-aspartic acid ... [Amino Acids. 2010] - PubMed - NCBI

    Why do you think DAA or Sodium D-Aspartate compared to forskolin, is more effective at inducing LTP? Is it perhaps more selective than forskolin?

    Quote Originally Posted by mr.cooper69 View Post
    Also, there are much better PDE IV inhibitors than those listed (either do your own search or *possibly* wait a long time )
    Can you point me in the right direction for a better PDE4 inhibitor supplement? Luteolin?... also IN for a Coop Innovation? Perhaps a PES or AS product?!!

    Out of curiosity, whether this kind of supplementation works or not, I pulled the trigger and bought 2 bottles of Analyzed Supplements Forskolin-95 today. I've been wanting to use it for a few months now and just haven't gotten around to buying any

  5. Forskolin elevates cAMP by increasing the activity of adenyl cyclase. This is well down-stream of the first step in LTP: activation of the NMDA receptor. DAA is an NMDA agonist, so naturally, it will increase intracellular cAMP...and the entire cascade that follows.

    Luteolin has no bioavailability in humans. A coop's a maybe. It would definitely be a niche category, not sure how well it'd sell


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