Selenium nanoparticle-loaded microneedle patches promote diabetic oral ulcer healing by regulating the inflammatory microenvironment through upregulation of SELENBP1-mediated mitophagy.
Authors: Wang X, Wan H, Cui X, Tan B, Wang H, He J, Yang Z, Han X, Xiao J, Tao G, He Y, Cai R
Journal: Journal of nanobiotechnology
eating disorders
mental health
open access
Abstract
There is much interest in the
use of psychedelic drugs to treat psychiatric disorders including
major depression and anxiety. Current investigations
of the mechanism of psychedelic drugs are focused on the role of the
5-HT receptor and its associated signaling pathways. There is general agreement that the hallucinogenic action of psychedelic
drugs is mediated by the 5-HT receptor. For example in
humans, the subjective effects of psilocybin (active molecule psilocin)
and lysergic acid diethylamide (LSD) were blocked by pretreatment
with the 5-HT receptor antagonist, ketanserin. Also, clinical studies using the PET 5-HT receptor
radioligand [C]Cimbi-36, report a correlation between
5-HT receptor occupancy and the intensity of psilocybin’s
subjective effects. In support of these
findings, there is a wealth of evidence from preclinical studies that
the head-twitch response to psychedelic drugs, a rodent proxy of the
human hallucinogenic effect, is 5-HT receptor-mediated. Much evidence also supports a key role
for the 5-HT receptor in psychedelic drug-induced neuroplastic
effects which
are widely considered central to the therapeutic effects of these
drugs. For example in preclinical studies, both
pharmacological blockade and genetic knockout (KO) of the 5-HT receptor were reported to prevent the increase in dendritogenesis
evoked by psychedelic drugs, both in primary cultured neurons and . Similar manipulations were also found to prevent psychedelic drug-induced
mRNA expression of plasticity-related genes such as , and , which each encode activity-dependent transcription factors or proteins
involved in various aspects of neuroplasticity such as regulation
of synaptic number and strength, spine density and morphology, memory
and LTP. There are, however, two studies finding that 5-HT receptor
antagonists did not block psychedelic drug-induced dendritogenesis, as well as evidence that this effect was mediated by a direct action
on TrkB. On the other hand, the adequacy
of antagonist dose in such studies has been questioned, and a recent study failed to confirm an action
of psychedelic drugs on TrkB.
use of psychedelic drugs to treat psychiatric disorders including
major depression and anxiety. Current investigations
of the mechanism of psychedelic drugs are focused on the role of the
5-HT receptor and its associated signaling pathways. There is general agreement that the hallucinogenic action of psychedelic
drugs is mediated by the 5-HT receptor. For example in
humans, the subjective effects of psilocybin (active molecule psilocin)
and lysergic acid diethylamide (LSD) were blocked by pretreatment
with the 5-HT receptor antagonist, ketanserin. Also, clinical studies using the PET 5-HT receptor
radioligand [C]Cimbi-36, report a correlation between
5-HT receptor occupancy and the intensity of psilocybin’s
subjective effects. In support of these
findings, there is a wealth of evidence from preclinical studies that
the head-twitch response to psychedelic drugs, a rodent proxy of the
human hallucinogenic effect, is 5-HT receptor-mediated. Much evidence also supports a key role
for the 5-HT receptor in psychedelic drug-induced neuroplastic
effects which
are widely considered central to the therapeutic effects of these
drugs. For example in preclinical studies, both
pharmacological blockade and genetic knockout (KO) of the 5-HT receptor were reported to prevent the increase in dendritogenesis
evoked by psychedelic drugs, both in primary cultured neurons and . Similar manipulations were also found to prevent psychedelic drug-induced
mRNA expression of plasticity-related genes such as , and , which each encode activity-dependent transcription factors or proteins
involved in various aspects of neuroplasticity such as regulation
of synaptic number and strength, spine density and morphology, memory
and LTP. There are, however, two studies finding that 5-HT receptor
antagonists did not block psychedelic drug-induced dendritogenesis, as well as evidence that this effect was mediated by a direct action
on TrkB. On the other hand, the adequacy
of antagonist dose in such studies has been questioned, and a recent study failed to confirm an action
of psychedelic drugs on TrkB.