本文提供了对达到血管载荷时CB1受体（CB1R）如何产生负面影响的解释。它描述了Anandamide和脂肪酸酰胺水解酶（FAAH）如何工作以影响整体情绪状态。当我们与外部刺激互动时，我们可以将这种互动感知为正，中性或负面。在存在消极或积极的事件的情况下，我们可以体验所谓的“amantatic load”。在某些情况下，当实现征静值负载时，CB1R可以脱敏。当遇到频繁响应时，CB1R变得漂亮化，响应不足或未能关闭对事件的响应。如果未实现amantatic载荷，则响应最终将在短期存储器中编码。如果实现了amantatic载荷，则事件可以存储在长期存储器中。各种精神状态可能是这种脱敏过程的结果。可以将Anandamide（CB1R激动剂）和FAAH（anondamide拮抗剂）的水平与阳性，中性和阴性事件进行比较。 These chemical releases could also lead to the overall emotional responses that we arrive at when facing a stimui. In conclusion, I find there to be a relationship between the CB1R, anandamide, FAAH and emotional expression. I hypothesize that the CB1R can become desensitized and can influence our overall emotional state.

CB1受体，脱敏，适应负荷，脂肪酸酰胺水解酶。

本文提供了对达到血管载荷时CB1受体（CB1R）如何产生负面影响的解释。它描述了Anandamide和脂肪酸酰胺水解酶（FAAH）如何工作以影响整体情绪状态。当我们与外部刺激互动时，我们可以将这种互动感知为正，中性或负面。在存在消极或积极的事件的情况下，我们可以体验所谓的“amantatic load”。在某些情况下，当实现征静值负载时，CB1R可以脱敏。当遇到频繁响应时，CB1R变得漂亮化，响应不足或未能关闭对事件的响应。如果未实现amantatic载荷，则响应最终将在短期存储器中编码。如果实现了amantatic载荷，则事件可以存储在长期存储器中。各种精神状态可能是这种脱敏过程的结果。可以将Anandamide（CB1R激动剂）和FAAH（anondamide拮抗剂）的水平与阳性，中性和阴性事件进行比较。 These chemical releases could also lead to the overall emotional responses that we arrive at when facing a stimui. In conclusion, I find there to be a relationship between the CB1R, anandamide, FAAH and emotional expression. I hypothesize that the CB1R can become desensitized and can influence our overall emotional state.

CB1受体，脱敏，适应负荷，脂肪酸酰胺水解酶。

一项关于“大麻二酚在精神疾病中的治疗作用的塑料和神经保护机制”的研究表明，CBD降低了四氢大麻酚的负面认知和精神影响，同时保留了它的有益行为。如果CBD降低了这种效果，那么它可能被证明是治疗心理障碍的可靠方法。有许多类型的大麻品系sativa, sativa hemp，和indica。其中，sativa有抗抑郁作用，indica有抑制作用，sativa hemp有中性作用。当它们结合在一起时，可以有效地治疗疼痛，产生欣快的效果。然而，这种关系需要进一步研究。

那么，如果那些菌株抓住钥匙来调节各种情绪状态怎么办？如果这些菌株对情感有不同的影响，怎么办？应解决这些问题。大麻素受体是ECS的一部分，主要位于大脑中，但也在肝脏，肾脏和肺部。这些是在缓冲休克期间受影响的相同器官。有两个已知的大麻素受体：CB1和CB2受体。CB1受体在脑和器官等地方发现。CB2受体在免疫系统和脊柱等地方发现。ECS旨在平衡和正常化受影响的区域，而最终试图保护它们免受损坏。它寻求在创伤期间正常化下丘脑 - 垂体 - 肾上腺轴（HPA）。 In a study titled: “The Role of the Endocannabinoid System in the Regulation of Hypothalamic Activity” [2] it was found that the ECS is known to regulate the HPA. This axis is responsible for neuroendocrine adaptation to stress responses. This adaptation leads to the release of adrenaline, cortisol and other chemical messengers. Anandamide is known to be released with cortisol. It is also known as the “feel-good” chemical experienced in a “runners’ high.” Anandamide is a natural cannabinoid produced in our body and is responsible for attaching to cannabinoid receptors. It is the agonist in this case. In response to shock, the HPA releases chemical messengers. These releases occur during hypovolemic shock, which is a condition that occurs when 20 percent or more of the body’s blood or fluid supply is lost and is considered life threatening. When sustaining hypovolemic shock, the body can lose too many fluids, and bodily organs can begin to fail. Organs that may be affected during hypovolemic shock include the brain, liver, kidneys and lungs. When experiencing shock, mechanisms in the body adapt to the stressor in an attempt to normalize functions. This attempt to normalize is known as “homeostasis.” In a study titled “Stress, Adaptation, and Disease: Allostasis and Allostatic Load” [3] stated that during shock, the Activation of Neural, Neuroendocrine and Neuroendocrine-immune mechanisms change when encountering potentially stressful events through the production of mediators such as adrenalin, cortisol and other chemical messengers. These changes are known as allostasis. The study continues, stating that allostasis is an essential component of regulating homeostasis and that it can become overactive. This is known as the allostatic load. Also, the study states that the “allostatic load” is reached when one of the following criteria are met: frequent activation of allostatic systems, failure to shut off allostatic activity after the stress, and inadequate response of allostatic systems, which leads to elevated activity of other normally counter-regulated allostatic systems after stress [3]. In hypovolemic shock, when the allostatic load has been reached, the chemical messengers released into the circulatory system would be hindered due to vascular resistance. Vascular resistance, in hypovolemic shock, is attributed to the loss of blood or fluid. The vessels constrict, thus inhibiting the bodies attempt to normalize function. When the fluid or blood loss is returned, vasodilation occurs. This allows the chemical messengers, such as the agonist anandamide to flow unrestricted again. However, at this point, the ECS has begun to normalize and may not need these chemical messengers anymore. One such chemical that may no longer be essential could be cortisol, and anandamide, as body functions stabilize. A study conducted on “Endocannabinoid Signaling and the Hypothalamic- Pituitary-Adrenal Axis” [2] stated that when activation of the CB1 receptor occurred, it promoted the return of the HPA axis to non-stressed levels. This would imply that if nonstressed levels where achieved, then activation would not be necessary. If activation is not necessary, then the CB1Rs would experience decreased responsiveness due to receptor overload, which would lead to receptor desensitization. They no longer need what they are receiving. The ECS is said to be the driving force behind homeostasis within the sympathetic and parasympathetic nervous systems. Both of these systems seek to normalize functioning while being monitored by the ECS. A study titled “Neuroendocrine System and the Autonomic Nervous System” [4] stated that both of these systems are the executing force controlled by the hypothalamus. In this study, it says that the autonomic nervous system is responsible for transmitting organ function back to the brain so that it can regulate these areas. If organ function is affected during hypovolemic shock, and the ECS is unable to maintain homeostasis, then the system could reach a state of allostatic load. The ECS is signaling for a hypothalamic-pituitary neurosecretion response, but it has the insufficient means to transport these secretions through the circulatory system as they occur. Many symptoms of shock show similarities in mental disorders such as PTSD, depression, anxiety disorder and bipolar disorder. These symptoms include: agitation, restlessness, anxiety, altered mental status, altered mental states, rapid or slowing heart rate, labored or irregular breathing, reduced body temperature, dilated pupils and falling blood pressure. It has been found that when the CB1R is given an antagonist, mental health problems can arise. In a study conducted on the “Efficacy and Safety of the Weight-Loss Drug Rimonabant” [5] randomized human trials found that the CB1R antagonist rimonabant had significant adverse psychiatric effects. In this study, it was found that patients experienced changes in thought patterns such as anxiety, depressed mood and even suicide. This would lead one to assume that if the CB1R is desensitized, then mental illness may arise. This would cause a decrease in the responsiveness of these receptors. When vasodilation occurs, the body is flooded with chemical messengers that are no longer needed. Since the ECS has regained balance, a system imbalance may occur because the overabundance of chemical messengers is no longer needed. This imbalance to the ECS could lead to the development of various mental disorders or altered mental states such as PTSD, depression, anxiety and bipolar disorder.

神经系统的研究”这个角色在内分泌功能的调节和控制人类能量平衡的”[6]指出,神经系统最近归因于作为一个重要的调节系统在大脑的操作在内分泌和免疫系统。该研究继续指出，它似乎在与生殖和应激反应有关的荷尔蒙的化学释放中起着非常重要的调节作用。这导致了我对非稳态负荷如何影响CB1R的解释，导致其损伤或脱敏。ECS负责在交感神经和副交感神经系统中创造稳态。ECS会在压力事件中激活，并保持活跃直到达到平衡。如果它不能保持这种微妙的平衡，它将成为一个不平衡的系统。这种不平衡被称为非稳态负荷。只要满足以下条件之一，CB1R的适应负荷就可以达到。ECS信号是由于创伤事件造成的内稳态经常接触一个有压力的事件反应不足一个压力的事件或关闭失败当压力事件发生时。可视参考图1A。我假设每种情况对CB1R有不同的影响，导致其脱敏。每个事件对CB1R的影响如下频繁的响应压力变化事件导致CB1R的脱敏，导致它变得过度活跃。对压力事件的反应不足导致CB1R脱敏，导致有效的CB1R。一个关闭失败，要么“洪水”,当压力事件导致CB1R脱敏时发生。这产生了不平衡，导致CB1R洪水，然后导致CB1R变得缺陷的恢复时间。当发生对压力事件的频繁反应时，经常访问下皮脑垂体 - 肾上腺轴（HPA）。它发生在暴露于多于一个压力事件期间HPA内的频繁化学释放，这导致过度刺激的CB1R并最终脱敏。

因此，可以通过补充这种过度刺激与苜蓿大麻和籼植物的中性的过度刺激来调节吗？通过这种组合，您可能会获得非综合性，抑郁症效果，这可能在补充过度刺激方面可以证明是可靠的。当血管收缩不允许HPA释放以通过循环系统移动时，发生不充分的响应的示例。这可能在缓慢休克期间经历。如果脱敏导致缺乏症，那么苜蓿大麻和苜蓿菌株将通过产生非精神活性的抗抑郁效果来平衡这种缺陷吗？由于ECSS无法恢复平衡，在从HPA泛滥时发生压力事件后，发生压力事件后发生故障。这可能是由于频繁的药物使用（洪水）或导致双相障碍（泛滥，缺乏）。苜蓿大麻厂是否可以是负责固定CB1R脱敏在这种情况下的中性植物？这可能需要进一步调查。提供了一个图表，用于可视化以下结论。 The above results are dependent on the state of allostatic load being met. The resulting mental state is depicted through the level of CB1R desensitization and what type of desensitization is sustained. PTSD and anxiety could arise from frequent exposure to a stressful stimuli or overstimulation of the CB1R. Depression could arise from an inadequate response to stressful stimuli resulting in a CB1R deficiency. Bipolar disorder could arise from the failure to shut off to a stressful event, resulting in an overstimulated CB1R followed by a deficiency. This needs to be investigated further, however.

在之前的假设的基础上，我形成了另一个关于anandamide和FAAH之间的关系以及这些水平如何影响我们的情绪状态的假设。这一假设涉及到在积极、消极和中性外部刺激存在时的情绪调节，从而导致情绪反应。我们如何调节情绪反应是神经科学中一个尚未回答的问题。当我们与外界刺激互动时，就会产生行为反应。[7]在“外部刺激对下丘脑内卡巴醇注射引起的情绪厌恶反应的影响”一项研究中观察到，猫对积极和中性刺激的反应产生了截然相反的情绪反应。该研究测试了威胁性刺激(看到一只吠叫的狗)和中性刺激(闪光和音调)对情绪厌恶反应的影响，当注射卡巴醇时。所有的威胁刺激都导致猫的发声能力显著增加。相比之下，同等强度的中性刺激没有产生反应。当我们受到外部刺激时，ECS通过HPA控制我们体内anandamide和FAAH的释放。这就是为什么理解这个系统功能的重要性是很重要的，这就是内稳态。 In a study on the “Modulation of Anxiety through a Blockade of Anandamide Hydrolysis” [8] when tetrahydrocannabinol was administered to humans it produced subjective responses that were controlled by the CB1Rs. This indicated that they might contribute to emotional control. If cannabis has been found to produce the responses indicated above, then the various strains of cannabis may hold the keys to providing a safe means to regulate mood disorders.

在另一项关于“CB1R缺乏如何减少轮跑活动:对情绪行为和海马神经发生的影响”的研究中，研究人员称，在过度刺激的小鼠中央CB1R中，观察到慢性自愿轮跑活动;而且，药理学结果表明，CB1R可能参与了轮跑行为和跑步诱导的海马神经发生。内源性大麻素系统负责维持交感神经和副交感神经系统的稳态。海马体将编码的传入情绪反应传递给控制CB1受体(CB1R)的交感神经系统。CB1Rs负责这些编码的情绪反应的表达。在研究小说的潜在治疗价值FAAH抑制剂用于治疗焦虑”[10]发现当新enol-carbamate ST4070药物抑制FAAH体内,观察到它增强的神经信号的大脑区域参与情绪控制。因此，这是否表明anandamide通过与CB1Rs的相互作用影响编码情绪的表达，导致由于FAAH不活跃而增加的刺激?如果是这样，那么不同水平的anandamide和FAAH会导致不同的行为反应。这可能会导致不可接受的行为，导致许多认知障碍。认知障碍基本上是频繁的异常行为的表现。 Anandamide is known as the “feel good” chemical and agonist that binds to the CB1R. The fatty acid amide hydrolase (FAAH) is an antagonist of anandamide. A study conducted on the “Interactions Between Anandamide and Corticotropin-Releasing Factor Signaling Modulate Human Amygdala Function and Risk for Anxiety Disorders: An Imaging Genetics Strategy for Modeling Molecular Interactions” [11] suggested that interactions between the anandamide and corticotropin-releasing factor (CRF1) receptor extinction showed a reduction in both anandamide and FAAH. If anandamide is released with CRF1 and binds to the CB1R to signal homeostasis in the amygdala, then the desensitization of the CB1R could produce a constant state of stress and hinder anandamides ability to signal the down regulation of the amygdala. CB1R desensitization could explain the occurrence of adrenal fatigue syndrome. It could also explain the similarities that exist in disorders like anxiety, ptsd, bipolar and schizophrenia. Given the above argument, I hypothesize that increases and/or decreases in anandamide and FAAH expression, directly influence which emotional states are created through their interaction with each other, and that they work to influence the CB1R. Also, the type of stimuli being faced, whether positive, negative or neutral, would influence the levels of anandamide and FAAH being expressed. The previous model for allostatic load can be used in relation to this hypothesis. In this instance, the following analogy was made:

总之，我已经解释了我的两个假设，并列出了可能发生在ECS中的类似物，CB1Rs, anandamide (CB1R激动剂)和FAAH (anandamide拮抗剂)。我描述了当面对单一或反复发生的压力事件时，适应负荷如何使CB1Rs脱敏。我提供了一个图表供参考，可以发现各种改变的心理状态都很适合这个模型。我已经介绍了各种大麻品系的功能及其相应的效果和可能的治疗价值。解释了ECS是如何通过化学信使影响情绪状态的。我还提出了两种不同但相互关联的假设，它们分别受到anandamide和FAAH水平的影响。虽然这些都是假设的价值，但系统会寻求平衡;当我们谈论ECS, CB1Rs, anandamide, FAAH，内稳态和情绪时，平衡可能是相关的，因为我们通过这个系统寻求它。然而，进一步的分析是必要的。