Mecamylamine attenuates dexamethasone-induced anxiety-like behavior in association with brain derived neurotrophic factor upregulation in rat brains

The postnatal origin of adult neural stem cells and the effects of glucocorticoids on their genesis

“…For example, changes in glucocorticoid receptors in the brain during neonatal development can lead to a number of hormonal and behavioral impairments in adult rats [44], and prenatal DEX treatment elicits long-term behavioral alterations related to anxiety and auditory processing [45]. In fact, DEX has been used as a model of anxiety [46] even though the effects of DEX are known to depend on the time when it was administered [47]. Thus, DEX treatment provokes slight delays in some parameters of neurodevelopment and physical maturation at P7 and P14, but not P20.…”

Kinetic modeling of one-pot myrtenol amination over Au/ZrO2 catalyst

“…On the other hand, terpenes, extracted from biomass, are inexpensive renewable raw materials that have biological activity and are widely used in the development of new medicines. In particular complicated terpene amines, synthesized from renewable raw materials, were recently shown to exhibit specific physiological properties and can be used as intermediates of potential drugs for neurological diseases [1][2][3][4]. At the same time, application of gold catalysts for fine chemical synthesis is a promising direction due to its outstanding activity and/or selectivity in various reactions [5][6][7][8][9].…”

The influence of glucocorticoids on neuronal survival and synaptic function

“…The attenuation of BDNF transcription seems to be most obvious 4 h after corticosterone administration (72) . Recently, Park et al discovered DEX-induced anxiety-like behavior followed by benefi cial recovery effects by mecamylamine, an antagonist of nicotinic acetylcholine receptors (11) . They clearly showed that rats injected with DEX exhibit increased anxiety-like behavior and decreased levels of BDNF signaling, including phosphorylated extracellular signal-regulated protein kinase (pERK) and pCREB in cerebral cortex, which was ameliorated by mecamylamine administration (11) .…”

“…Recently, Park et al discovered DEX-induced anxiety-like behavior followed by benefi cial recovery effects by mecamylamine, an antagonist of nicotinic acetylcholine receptors (11) . They clearly showed that rats injected with DEX exhibit increased anxiety-like behavior and decreased levels of BDNF signaling, including phosphorylated extracellular signal-regulated protein kinase (pERK) and pCREB in cerebral cortex, which was ameliorated by mecamylamine administration (11) . Using cultured cortical neurons, we recently reported that pretreatment with glucocorticoids inhibits neurotransmitter release and upregulation of synaptic proteins stimulated by BDNF (13,73) .…”

“…Furthermore, recent studies including ours, suggest a possible interaction between growth factors and glucocorticoids. In rat cerebral cortex, mecamylamine, an acetylcholine receptor antagonist, reversed glucocorticoidstimulated downregulation of brain-derived neurotrophic factor (BDNF), a critical neurotrophin (11) . In cultured neurons, acute application of glucocorticoids induced activation of TrkB, a critical BDNF receptor (12) , whereas long-term pretreatment with glucocorticoids decreased BDNF-mediated synaptic function (13) .…”