Posted by SLS on April 22, 2018, at 8:16:11
In reply to Re: TRIP8b inhibitors? Truly novel antidepressants., posted by linkadge on April 21, 2018, at 9:07:10
Hi, Linkadge.
> TRIP8b inhibitors apparently exert their effect through HCN1 channels (no expert here, just google searches).
>
> Ketamine inhibits HCN1. Zinc may also interact with both HCN channels and TRIP8b.Wow. Did you come across anything suggesting that there is a relationship between HCN channels and BDNF production?
> Keep in mind though, that this is the stress induced model of depression. While most people will experience some degree of depression if subjected to enough stress, not all depressive disorders are a result of external stress.
>
> Some researchers argue that focusing on the stress model of depression may be ignoring the underlying cause of a significant group of patients.I had an interesting thought, Linkadge. Regardless of psychosocial stress or biogenic etiologies, depression is itself a stress on the system. If the reaction to this stress is for the brain to increase TRIP8b activity and thus a worsening or persistence of depression, a positive feedback loop is created. Once created, the cycle must be hard to break. Persistent brain inflammation might follow a similar path. Just pondering.
- ScottSome see things as they are and ask why.
I dream of things that never were and ask why not.- George Bernard Shaw
poster:SLS
thread:1098278
URL: http://www.dr-bob.org/babble/20180331/msgs/1098303.html