User:Tkadm30/Notebook/Hypercomputation: Difference between revisions
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* Is pharmacological hypercomputation (PH) a dopamine-mediated synaptic function? (exocytosis) | * Is pharmacological hypercomputation (PH) a dopamine-mediated synaptic function? (exocytosis) | ||
* Cannabinoids may rewire the brain connectivity by enhancing functional | * Cannabinoids may rewire the brain connectivity by enhancing functional NMDA expression and [http://www.thenakedscientists.com/forum/index.php?topic=68779 cognitive intelligence]. | ||
=== Heteromeric transactivation of adenosine-CB1 receptors === | === Heteromeric transactivation of adenosine-CB1 receptors === |
Revision as of 04:05, 2 December 2016
Hypercomputation
Synaptic hypercomputation
The Synaptic Hypercomputation (SH) hypothesis states that the continuous phase transition of conscious states evolve via discrete computations mediated by neurexins and neuroligins proteins. This non-classical neurocomputational model is controlled by synaptic exocytosis, generating neural criticality in the CNS.
Pharmacological hypercomputation
- Is pharmacological hypercomputation (PH) a dopamine-mediated synaptic function? (exocytosis)
- Cannabinoids may rewire the brain connectivity by enhancing functional NMDA expression and cognitive intelligence.
Heteromeric transactivation of adenosine-CB1 receptors
How adenosine-CB1 heteromeric transactivation potentiate synaptic hypercomputation?
Neurexin-mediated trans-synaptic exocytosis
Could retrograde signaling promote synaptic proteins synthesis ? https://www.ncbi.nlm.nih.gov/pubmed/17035546