Long term potentiation, also known as LTP, is the strengthening of synapses based on specific patterns of brain activity. The brain is a network of billions of independent neurons connected to over thousands of others of neurons by synapses. These synapses communicate use acetylcholine to send signals. Some Nootropics form new synapses which open more bridges for communication, while others increase the levels of these neurotransmitters. With new neuron cells and the improved synaptic communication, it enhances the proliferation and growth of dendrites – the branched nerve cell extensions where neural impulses travel – boosting neural signaling. The brain activity increases which improves neural impulse transmission, enhances memory and thinking abilities, thus increasing neuroplasticity.
Where does Long term potentiation occur in the brain?
The brain controls just about everything a human does, for example, hearing, speech, smell, vision, etc, even while asleep. It has many parts which include the brainstem, cerebral cortex, cerebellum, corpus callosum, hippocampus, hypothalamus, pituitary gland, and thalamus. In this case, the part of the brain that plays a crucial role in the formation of memory and long term potentiation is the hippocampus. This was found out in 1957 when a bilateral hippocampal removal treatment was done on a patient suffering from epilepsy. It resulted in anterograde amnesia showing the importance of the role of the hippocampus in terms of memory. Therefore, any damages to the hippocampus will lead to the inability to form certain types of new memories.
Similarly, the frontal cortex is capable of supporting various sorts of memory, such as auditory sensory memory, tactile memory, and visual sensory memory, which are transient memories. However, a consolidation is required to enable the formation of long term memory.
The hippocampal-prefrontal cortical connection is routed through the subiculum. The subiculum processes and ingrates the information to other cortical areas. This means the connections subiculum receives are directional, contextual, positional, and sensory information. Specifically, the CA1 – the first region in the hippocampal circuit – pathways play a role in various forms of learning and memory.
Nootropics and Long term potentiation
Augmenting cAMP and PD4e Inhibition creates Long term potentiation. The synergistic effect of the two enhances cognitive function, specifically the retention of memory and new information. The ingredients that can either augment cAMP or cause PD4E inhibition are Artichoke Extract and Coleus Forskolin.
Artichoke Extract is the leaf of the Cynara Scolymus plant. It is one of the most effective and safest PD4E inhibitors. PD4E is an enzyme that breaks down cAMP molecules and blocks the breakdown of cAMP which increases the levels of cAMP in the brain. This can result in an overall increase in cognition, improved memory, and alertness. The leaves are also rich in luteolin flavonoids and caffeoylquinic acids are known to possess great amounts of antioxidant, lipid lowering properties, and hepatoprotective. In terms of Nootropics, the luteolin flavonoids from the artichoke extract show potent anti-inflammatory response by inhibiting NFkB signaling in the brain cells. This reduction of inflammation in the brain protects the brain from toxins, minimizes the effects of brain aging, and contributes to the stimulation of new neuron cells. The new neuron cells improve memory, increase neuroprotection, cognition, wakefulness and neuroplasticity.
Coleus Forskolin is from the root of the Coleus Forkohlii plant. It increases the cyclic adenosine monophosphate (cAMP) and cAMP-mediated functions through the activation of the enzyme adenylate cyclase. The cAMP is messenger systems that relay signals in the brain and the increase in cAMP improve cognitive function, restrain cell degranulation, lowers blood pressure, intraocular pressure, and stimulates lipolysis in fat cells. Additionally, due to the interference with platelet activation factor (PAF), Forskolin restrains the binding of PAF, independently of the cAMP formation.
The three characteristics researchers used to support the hypothesis that Long term potentiation may be a biological substrate for at least some forms of memory are associativity and specificity, cooperativity, and duration of Long term potentiation. Other pieces of evidence have consolidated this view include:
1) Several biochemical changes that occur after induction of LTP also occur during memory acquisition.
2) Inhibitors of hippocampal LTP also block hippocampal learning and retention of a task.
3) Rhythmic bursts of activity that induce LTP mimic naturally occurring theta rhythm recorded in the hippocampus during exploratory behavior.
4) LTP is most easily demonstrable in the hippocampus, an area of the brain known to be fundamentally important in memory acquisition.
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