alywest
Member
- Joined
- Apr 19, 2017
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I'm sure that anyone on this forum who has struggled with depression has at least heard about ketamine treatments. However, their high cost and unlikelihood (re: not gonna happen in this lifetime) of insurance covering ketamine treatments makes it prohibitive for most people. Not to mention that it's a bit weird...horse tranquilizer? I had a friend who became addicted to ketamine and always seemed spaced out and not himself. Could agmatine possibly be the answer to MDD?
Single administration of agmatine reverses the depressive-like behavior induced by corticosterone in mice: Comparison with ketamine and fluoxetine. - PubMed - NCBI
Single administration of agmatine reverses the depressive-like behavior induced by corticosterone in mice: Comparison with ketamine and fluoxetine.
Agmatine is a neuromodulator that has been proposed as a therapeutic strategy for the treatment of major depressive disorder (MDD). A previous study reported that agmatine caused a fast-acting effect in mice subjected to chronic mild stress without causing changes in the levels of synaptic proteins in the prefrontal cortex. We examined whether a single administration of agmatine is able to counteract the depressive-like behavior induced by chronic administration of corticosterone, a pharmacological model of stress, paralleled with the modulation of synaptic protein levels in the prefrontal cortex and hippocampus. Female mice received corticosterone (20 mg/kg, p.o.) for 21 days and, in the last day of treatment, were administered with a single dose of agmatine (0.1 mg/kg, p.o.), fluoxetine (10 mg/kg, p.o.; control for a conventional antidepressant) or ketamine (1 mg/kg, i.p.; control for a fast-acting antidepressant). Agmatine, similar to ketamine, reversed the depressive-like behavior induced by corticosterone in the tail suspension test (TST), an effect that was not observed in mice treated with fluoxetine. The immunocontent of GluA1 was increased by all the treatments in the hippocampus of control mice, whereas PSD95 was not significantly altered by treatments in any brain structure. Although the levels of synaptic proteins do not seem to account for the behavioral findings reported here, the present study provides clear evidence for the fast-acting antidepressant profile of agmatine in the TST, similar to ketamine.
Also interesting:
Jansen, K. L. R. (1996)
Using ketamine to induce the near -death experience: mechanism of action and therapeutic potential.
Yearbook for Ethnomedicine and the Study of Consciousness (Jahrbuch furr Ethnomedizin und Bewubtseinsforschung) Issue 4, 1995 (Ed.s C. Ratsch; J. R. Baker); VWB, Berlin, pp55-81.
"Near-death experiences (NDE's) can be induced using the dissociative drug ketamine. Advances in neuroscience have recently provided us with new insights as to the mechanisms involved at the mind -brain interface. On the 'brain' side, it is now clear that these NDE's are due to blockade of brain receptors (drug binding sites) for the neurotransmitter glutamate. These binding sites are called the N-methyl-D-aspartate (NMDA) receptors. Conditions which precipitate NDE's (low oxygen, low blood flow, low blood sugar, temporal lobe epilepsy etc.) have been shown to release a flood of glutamate, over-activating NMDA receptors. This overactivation can kill brain cells ('excito' toxicity). Ketamine prevents excitotoxicity. Conditions which trigger a glutamate flood may also trigger a flood of ketamine-like brain chemicals which bind to NMDA receptors to protect cells, leading to an altered state of consciousness like that produced by ketamine."
From:
Agmatine and Near-Death Experiences
Single administration of agmatine reverses the depressive-like behavior induced by corticosterone in mice: Comparison with ketamine and fluoxetine. - PubMed - NCBI
Single administration of agmatine reverses the depressive-like behavior induced by corticosterone in mice: Comparison with ketamine and fluoxetine.
Agmatine is a neuromodulator that has been proposed as a therapeutic strategy for the treatment of major depressive disorder (MDD). A previous study reported that agmatine caused a fast-acting effect in mice subjected to chronic mild stress without causing changes in the levels of synaptic proteins in the prefrontal cortex. We examined whether a single administration of agmatine is able to counteract the depressive-like behavior induced by chronic administration of corticosterone, a pharmacological model of stress, paralleled with the modulation of synaptic protein levels in the prefrontal cortex and hippocampus. Female mice received corticosterone (20 mg/kg, p.o.) for 21 days and, in the last day of treatment, were administered with a single dose of agmatine (0.1 mg/kg, p.o.), fluoxetine (10 mg/kg, p.o.; control for a conventional antidepressant) or ketamine (1 mg/kg, i.p.; control for a fast-acting antidepressant). Agmatine, similar to ketamine, reversed the depressive-like behavior induced by corticosterone in the tail suspension test (TST), an effect that was not observed in mice treated with fluoxetine. The immunocontent of GluA1 was increased by all the treatments in the hippocampus of control mice, whereas PSD95 was not significantly altered by treatments in any brain structure. Although the levels of synaptic proteins do not seem to account for the behavioral findings reported here, the present study provides clear evidence for the fast-acting antidepressant profile of agmatine in the TST, similar to ketamine.
Also interesting:
Jansen, K. L. R. (1996)
Using ketamine to induce the near -death experience: mechanism of action and therapeutic potential.
Yearbook for Ethnomedicine and the Study of Consciousness (Jahrbuch furr Ethnomedizin und Bewubtseinsforschung) Issue 4, 1995 (Ed.s C. Ratsch; J. R. Baker); VWB, Berlin, pp55-81.
"Near-death experiences (NDE's) can be induced using the dissociative drug ketamine. Advances in neuroscience have recently provided us with new insights as to the mechanisms involved at the mind -brain interface. On the 'brain' side, it is now clear that these NDE's are due to blockade of brain receptors (drug binding sites) for the neurotransmitter glutamate. These binding sites are called the N-methyl-D-aspartate (NMDA) receptors. Conditions which precipitate NDE's (low oxygen, low blood flow, low blood sugar, temporal lobe epilepsy etc.) have been shown to release a flood of glutamate, over-activating NMDA receptors. This overactivation can kill brain cells ('excito' toxicity). Ketamine prevents excitotoxicity. Conditions which trigger a glutamate flood may also trigger a flood of ketamine-like brain chemicals which bind to NMDA receptors to protect cells, leading to an altered state of consciousness like that produced by ketamine."
From:
Agmatine and Near-Death Experiences
