symptoms such as palpitation, anxiety, sweating, blood pressure alterations, and headache. Chronic stress has also been directly associated with the sustained release of norepinephrine in conditions characterized by the sustained release of norepinephrine. In children, social stressors that trigger the sustained release of norepinephrine are known to contribute significantly to suicidality, alter bodily homeostasis, hamper normal growth, negatively impact immunity, and damage many other normal functions. Norepinephrine is also studied in psychopharmacology; psychopharmacological insights on the relationship between the psycho-behavioral manifestation of neurological conditions and the direct influence of endocannabinoids. Early research in this regard suggests that alterations in the level of endocannabinoids induce specific psychotic symptoms. Also, exogenous cannabinoids appear to exacerbate pathological psychosis in patients suffering from psycho-behavioral anomalies (Garani et al., 2021). In the case of endocannabinoids, the duration of psychosis is comparatively longer, and endocannabinoids sometimes improve the symptomatic anomalies seen in neurodegenerative disease profiles. These observations have increased psychopharmacologists' interest in the therapeutic possibilities of exogenous cannabinoid administration for therapeutic purposes in neurological disorders. These interests prompted animal model research investigating the influence of exogenous cannabinoids in neurological conditions, with strict control on dose responses, symptom control, and side effects. Of all the compounds tested, anandamide produced impressive results. Anandamide is a neurotransmitter that exhibits structural similarity to tetrahydrocannabinol. Research has indicated that anandamide induces tetrahydrocannabinol-like effects because of this chemical mimicry. Tetrahydrocannabinol serves as the active principal ingredient of several exogenous cannabinoids. It aids in the regulation of appetite, memory, pain, depression, and fertility (Morales & Reggio, 2021). These exogenous molecules have been reported to bind specific receptor counterparts, resulting in appropriate homeostatic outcomes. Further research Early research into the pathology of depression identified possible drug targets to be explored in the development of an antidepressant treatment regimen. Iproniazid and other hydrazine derivatives earlier employed in the treatment of depression were found to elevate cerebral levels of serotonin and norepinephrine. These drugs also seem to act as monoamine oxidase inhibitors (MAOI), enhancing the life span of monoamine oxidase in the synaptic cleft. Later discoveries that imipramine and other tricyclic antidepressants inhibit the reuptake of monoamine from the synaptic cleft were also linked to the pharmacology of antidepressants. The inhibition of monoamine uptake in the synaptic cleft directly promotes the action of this moiety ad reportedly improves the symptomatology of depression (Foster et al., 2021). Judging from these early observations, antidepressants' common principle of action only affects the availability of endogenous neurotransmitters and monoamine oxidase. However, this simple explanation does not hold in many cases. In some, antidepressants fail to significantly elevate mood, and the treatment period before achieving improved symptomatology in some patients extended to about two weeks. Also, there have been multiple observations that antidepressant use in conditions with no direct link to monoamine or neurotransmitter levels seems to produce some clinical benefits. This has been reported largely in the context of antidepressant use as a therapy option in anxiety disorder, nervousness, obsessive-compulsive disorder (OCD), manic–
research suggests a link between dopamine, norepinephrine, and the pathophysiology of ADHD. The administration of norepinephrine-related drugs in combination with other therapy regimens for the management of ADHD has shown some improvements in symptomatic presentation (Van Stralen et al., 2021). There are multiple research submissions that also implicate the physiology of norepinephrine processing in the development of dementia and AD. has identified several endogenous molecules in humans such as enkephalins, which induce morphine-like effects in the brain. These molecules have a high solubility profile and can easily cross the blood–brain barrier to induce psychoactive actions in the central nervous system. Anandamide is abundant in the brain regions associated with memory and cognition, learning, and movement. Anandamide also seems to play a role in the embryonic development stage of pregnancy, as it has been identified as forming a chemical gateway between the mother and the fetus. Investigations exploring this gateway in pregnant individuals suggest that anandamide overdose is linked to severe side effects that resemble those recorded in cases of exogenous cannabinoid overdose. These side effects include effects such as lack of concentration and memory-related complications. To a significant extent, these overdose-related effects have been associated with alterations in the normal psycho-behavioral phenology in the offspring of rodents used in animal models of anandamide overdose. Beyond the pregnant individual– fetus connection and effects, the lack of anandamide has been linked to psycho-behavioral observations in the general population. The most studied effect in this regard is the development of chronic depression and anxiety in people with clinical presentation of anandamide insufficiency. As a therapy option, this compound has also shown some potential in psychopharmacology. Components that behave like synthetic anandamide have been demonstrated to help patients overcome the symptoms of chronic psycho-behavioral anomalies. depressive disorders, bedwetting in childhood, major depressive disorder, diabetic peripheral neuropathy pain, social fretfulness, and posttraumatic stress disorder. Today, alternative use of antidepressants has extended to cover conditions such as fibromyalgia, chronic hives (allergic reaction), hot flashes, drug-induced hyperhidrosis (sweating in excess), premenstrual symptoms, pruritus (itching), anorexia and bulimia nervosa, Tourette syndrome, and binge eating disorder. Given this, it became necessary to classify antidepressants based on their mechanism as reported by new clinical research. Today, antidepressants have been classified into five broad groups: • Tricyclic antidepressants (TCAs) • Selective serotonin-reuptake inhibitors (SSRIs) • Monoamine oxidase inhibitors (MAOIs) • Serotonin–norepinephrine reuptake inhibitor (SNRI) • Non-TCA antidepressants Tricyclic antidepressants actively block the reuptake of norepinephrine and serotonin in the central nervous system. As a direct effect of these actions, TCAs change the psycho- behavioral profile in many neurological conditions. Beyond their actions on norepinephrine and serotonin, TCAs have also been reported to block muscarinic receptors, histaminic receptors, and alpha-1 adrenergic receptors. Selective serotonin- reuptake inhibitors (SSRIs) are known to selectively block serotonin transport. The serotonin hypothesis of depression is supported by their negligible effect on the noradrenergic system; their high clinical efficacy; and the serotonin selectivity of reuptake inhibitors such as fluoxetine, sertraline, citalopram,
Endocannabinoids and Anandamide in Psycho-Behavioral Manifestations In the context of this course, there are interesting
Mechanism of Action of Neurotropic Drugs in the Biological Systems Antidepressants
Page 172
Book Code: PYFL4024
EliteLearning.com/Psychology
Powered by FlippingBook