Your welcome. One strategy that usually works is to "copy" six to ten word from the original quote and paste them directly into the search bar. Google usually finds the source relatively efficiently. (The "sigma" symbol complicated this particular case however)
I always enjoy your analysis of the science here although unfortunately I only feel confident in understanding about 70% of the science :-)
Another DD technique I have found to be useful (for me anyway) is to look for "comparator" drugs that companies use in their research.
What follows are two links. The Wayne State A2-73 study and a paper about the "comparator" drug that was used.
"ANAVEX2-73 inhibits OL cell death induced by staurosporine (apoptosis), excitotoxicity (glutamate via ionotropic receptors), ROS (induced by H2O2) and a mediator of inflammation (QA) but not nitric oxide or KA. For OPCs, of the toxic agents assessed so far, ANAVEX2-73 also protects from the same agents as found for OL. This pattern of in vitro protection for OL and OPC is the same as we reported for DM (Lisak 2014 et al.), chemically unrelated, but sharing both s-1R agonist and NMDA antagonist functions with ANAVEX 2-73. DM is a non-competitive agonist and ANAVEX2-73 a competitive agonist for s-1R. ANAVEX2-73 is also an agonist for muscarinic receptors and affects Na+ channel site 2. The relative roles of these molecules at s-1 and NMDA receptors and the role of muscarinic receptors and Na+ channel site 2 activity for ANAVEX2-73 in relation to OL and OPC protection is not as yet clear and will require further study. DM, ANAVEX2-73 and future s-1R agonists might have a protective role in treatment of patients with MS.
"Previous reports implicate s1 receptors as protein targets for existing and novel antidepressant drugs [10]. Currently marketed antidepressant drugs, such as tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors (SSRIs), and newer generations of antidepressant drugs, bind to these receptors [10]. Earlier studies also demonstrate that s1 receptor agonists can modulate the activities of neurotransmitter systems, signaling pathways and brain regions implicated in the pathophysiology of depression [10] and that s1 receptor knockout mice exhibit a depressive-like phenotype [16]. The potential clinical relevance of these observations is further supported by reports that s1 receptor agonists produce antidepressant effects in experimental animals and humans [17], [18], [19], [20], [21], [22]. Notably, the s1 receptor agonist igmesine hydrochloride proved to be as effective an antidepressant as the well-established SSRI fluoxetine in some clinical trials, though not in all cases [10], [22]. Compared to existing medications, s1 receptor agonists may facilitate a more rapid onset of antidepressant efficacy [23]. Consistent with this, s1 receptor agonists such as (+)-pentazocine and SA 4503 can enhance serotonergic neuronal firing in the dorsal raphe nucleus after only two days of treatment, compared to the two weeks of treatment that is typically required of conventional antidepressant drugs [24], [25].
What strikes me, is just how ubiquitous sigma1 agonists seem to be. Perhaps rather than focusing solely on sigma1's role it needs to be made more clear why A2-73 is more effective than the multiple of other drugs which appear to effect the same Sigma1 receptors?
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