Your competent? doctor started using this for your depression years ago, right? And with your risk of PTSD and needing neurogenesis, what's not to like?
Since there is a 23% chance of stroke survivors getting PTSD what is your doctor's prevention plan?
New Depression Treatment So Obvious You Won’t Believe It’s NEVER Been Tried Before - nitrous oxide(laughing gas) February 2017
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?
The latest here:
Nitrous oxide promotes exploratory activity and stimulates neurogenesis in a male rat model of post-traumatic stress disorder
Introduction
In light of recent global stressful events, such as the COVID 19 pandemic, earthquakes, and ongoing conflicts, post-traumatic stress disorder (PTSD) has emerged as a serious mental health concern (Chamaa et al., 2021, Mann et al., 2024). The prevalence of PTSD cases resulting from either a single or multiple traumatic events has markedly increased in recent years (Zhai and Du, 2024). The psychological burden of these traumatic events is profound and warrants greater emphasis on prioritizing mental health (Hoppen et al., 2021). PTSD symptoms include hyperarousal, an overgeneralized threat response to safe environments, and involuntary reliving of traumatic events through flashbacks or distressing thoughts (Hammell et al., 2020).
PTSD is particularly debilitating as it is characterized by a pathological endurance of memories, manifesting as either vivid involuntary flashbacks or disorganized voluntary recollections of the traumatic event (Brewin, 2011). This is attributed to dysfunction in mechanisms that regulate memory storage and expression (Pitts et al., 2022). Given the pivotal role the hippocampus has in memory formation and storage and mediating responses to stress and fear, it has an established direct pathophysiological involvement in PTSD (Zilcha-Mano et al., 2023). Studies have shown that PTSD patients exhibit reduced hippocampal volume, with smaller volumes correlating with more severe symptoms (Hinojosa, 2022, O'Doherty et al., 2015). Additionally, spatial working memory, a hippocampal related function, has been linked to re-experiencing of symptoms in PTSD (Mathew et al., 2022).
The dentate gyrus (DG) of the hippocampus harbors one of the two neurogenic niches in the adult brain (Kempermann et al., 2015). Within this region, the process of neurogenesis is highly sensitive and can be influenced by a variety of intrinsic and extrinsic factors that may either promote or inhibit the generation of new neurons. Factors such as stress, infections, and inflammation can lead to suppression of neurogenesis (Darwish et al., 2019, Darwish et al., 2022), with chronic stress particularly affecting the proliferation of neural progenitor cells in the DG (Gould and Tanapat, 1999). This decline in neurogenesis linked to chronic stress is suspected to be primarily due to elevated glucocorticoid levels, which interfere with the survival and proliferation of neural stem cells (Shin et al., 2024). Additionally, this phenomenon may involve other mechanisms, including increased apoptosis, oxidative stress, inflammation, and autophagy (Kohda et al., 2007, Liu et al., 2016). In contrast, several antidepressants have been shown to enhance hippocampal neurogenesis, highlighting their therapeutic potential in the treatment of stress-related disorders (Santarelli et al., 2003). Furthermore, invasive approaches such as deep brain stimulation and kainic acid stimulation, have also been reported to boost hippocampal neurogenesis (Chamaa et al., 2022, Chamaa et al., 2016, Zhang et al., 2014). However, the clinical applicability of these methods is limited due to their invasive nature.
Nonetheless, enhancing neurogenesis has been associated with improved stress coping, enhanced fear extinction, reduced anxiety-like behavior, and behavioral recovery in animal models of stress and trauma-related disorders (Schoenfeld et al., 2019). Such findings suggest that stimulating hippocampal neurogenesis may represent a promising avenue for mitigating PTSD-related symptoms. Till now, a substantial number of PTSD patients do not respond to cognitive behavioral therapy nor pharmacological treatments such as SSRIs (selective serotonin re-uptake inhibitors) or tetracyclic antidepressants (Burback et al., 2024, Williams et al., 2022). Therefore, there is an urgent need for innovative and fast-acting therapeutic interventions, as the incidence of diagnosed and undiagnosed PTSD continues to rise. Boosting hippocampal neurogenesis might stand as a potential therapeutic option. We have previously shown that exposure to nitrous oxide (N2O), an NMDA receptor antagonist, can significantly enhance the proliferation of hippocampal neural stem cells (NSCs) (Chamaa et al., 2018). NMDA receptor antagonists, such as ketamine, have gained attention as rapid-acting antidepressants, with evidence suggesting they can boost hippocampal neurogenesis through mechanisms that enhance synaptic plasticity and neurotrophic signaling (Yamada and Jinno, 2019, Zanos and Gould, 2018). Nitrous oxide has been explored as a treatment for PTSD in war veterans, yielding promising results (Varias et al., 2020). It has also demonstrated efficacy and safety for treatment-resistant depression in randomized controlled trials. Given the modulatory effect of nitrous oxide on hippocampal NSCs proliferation and the pivotal role of the hippocampus in PTSD, we propose that 70 % nitrous oxide can reverse the suppressed neurogenesis observed in the single prolonged stress (SPS) model of PTSD-like in rats. Therefore, in this study, we will investigate the mechanisms and effects of nitrous oxide exposure in treating memory and anxiety-related PTSD-like symptoms in the SPS rat model, suggesting nitrous oxide as a promising therapeutic approach to improve PTSD-like symptoms.
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