IPUB/BRANMA
Indian pathway to universal bliss/
brahmAnandamArga 2.0
Blockage of mTOR signaling blocks ketamine induced synaptogenesis and ketamine’s antidepressant like effects.[
MTor and rapamycin
In summary preclinical and clinical data suggest that low doses of ketamine initiate brain plasticity processes and increases prefrontal connectivity, thus reversing the potential effects of chronic stress and depression. These antidepressant effects are likely mediated by a glutamate search in the PFC, increased AMPA receptor activation, and increased Apple cycling; the latter of which is itself mediated by Nero classes it he related signaling pathways, particularly BDNF and TORC1. That I have also shown that ketamine's express blockage of NMDA receptors, presumably extra synaptic may facilitate synaptogenesis.
So in theory ketamine administration along with rapamycin may have a synergistic effect on synaptogenesis.
There is growing evidence for ketamine’s efficacy for a variety of other psychiatric conditions, including: bipolar disorder,[87] posttraumatic stress disorder,[88; 89] obsessive compulsive disorder,[90; 91] and substance abuse/dependence.[92] Ketamine has also been shown to rapidly reduce acute suicidality.[19; 93] Controlled research is needed to determine if ketamine’s clinical effects are reliable for these other conditions.
It is likely that the glutamate surge, prefrontal synaptogenesis, and prefrontal connectivity are implicated in ketamine’s psychiatric effects for non-depressive disorders, but these ideas are largely hypothetical at present.
Investigations of ketamine’s antidepressant mechanism of action have aided in the development of alternative models of depression and paved the way for the development of novel pharmacological antidepressant agents. Drugs that target neuroplasticity-related signaling pathways and synaptogenesis hold particular promise for MDD and other psychiatric disorders associated with chronic stress.
Indian pathway to universal bliss/
brahmAnandamArga 2.0
Blockage of mTOR signaling blocks ketamine induced synaptogenesis and ketamine’s antidepressant like effects.[
MTor and rapamycin
In summary preclinical and clinical data suggest that low doses of ketamine initiate brain plasticity processes and increases prefrontal connectivity, thus reversing the potential effects of chronic stress and depression. These antidepressant effects are likely mediated by a glutamate search in the PFC, increased AMPA receptor activation, and increased Apple cycling; the latter of which is itself mediated by Nero classes it he related signaling pathways, particularly BDNF and TORC1. That I have also shown that ketamine's express blockage of NMDA receptors, presumably extra synaptic may facilitate synaptogenesis.
So in theory ketamine administration along with rapamycin may have a synergistic effect on synaptogenesis.
There is growing evidence for ketamine’s efficacy for a variety of other psychiatric conditions, including: bipolar disorder,[87] posttraumatic stress disorder,[88; 89] obsessive compulsive disorder,[90; 91] and substance abuse/dependence.[92] Ketamine has also been shown to rapidly reduce acute suicidality.[19; 93] Controlled research is needed to determine if ketamine’s clinical effects are reliable for these other conditions.
It is likely that the glutamate surge, prefrontal synaptogenesis, and prefrontal connectivity are implicated in ketamine’s psychiatric effects for non-depressive disorders, but these ideas are largely hypothetical at present.
Investigations of ketamine’s antidepressant mechanism of action have aided in the development of alternative models of depression and paved the way for the development of novel pharmacological antidepressant agents. Drugs that target neuroplasticity-related signaling pathways and synaptogenesis hold particular promise for MDD and other psychiatric disorders associated with chronic stress.
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