and paroxetine. The action of drugs in this classification results in an abrupt increase in serotonin in the somatodendritic area of serotonergic neurons, which causes desensitization of the somatodendritic serotonin-1A autoreceptors. As a result, the neuronal impulse flow is positively influenced by an increased release of serotonin from the axon terminal and subsequent desensitization of postsynaptic serotonin receptors. Clinical research and animal models of antidepressant treatments suggest that the desensitization of these receptors may contribute to the therapeutic actions of SSRIs, or it could account for the development of tolerance to acute side effects of SSRIs. Analysis of the SSRIs also suggests that these drugs may cause a slow wave of disinhibition of serotonin receptors in the central nervous system. In this case, the actions of antidepressants are mediated by a pathway from the midbrain raphe to the prefrontal cortex (Orth et al., 2022). The side effects generated by SSRIs include anxiety, sleep disturbances, sexual dysfunction (decreased libido, reduced pleasurability, and reduction in arousal), and gastrointestinal disturbances. Preliminary examinations exploring the pharmacology of these side effects have implicated the possible toxicity effects of these drugs on certain serotonin pathways. The most studied side effect of SSRIs is their interaction with sexual functioning. Studies in this regard have indicate a contradictory reciprocal relationship between dopamine and serotonin, with dopamine tending to enhance sexual functioning and serotonin tending to inhibit it. The serotonin pathway descending from the brainstem down the spinal cord to spinal neurons that mediate various spinal reflexes is significantly implicated in sexual dysfunction effects in the form of ejaculation and orgasm problems. Enhanced serotonergic flow through this pathway reportedly inhibits sexual functioning, and these inhibitory effects are mediated through the serotonin receptors. The mechanism of action of drugs classified as serotonin– norepinephrine reuptake inhibitors (SNRIs) appears to be dose dependent. These drugs, including venlafaxine, tend to mediate the action of different antidepressants, receptor Anxiolytics Anxiety disorders are considered to be one of the most common psychiatric conditions globally. In the U.S. alone, the lifetime prevalence of anxiety is pegged at 32%, with the most commonly diagnosed anxiety disorders being social anxiety disorder and specific phobia. According to World Health Organization estimates, anxiety cases increased by 15% from 2015 to 2020, with about 264 million people suffering from anxiety disorders globally. The burden of anxiety diagnoses on the economy also appears to be significant, with work and school absences directly linked to decreased economic productivity. Research on the development of standard regimens for the treatment of anxiety disorders has received significant interest since the early 2000s. Studies have also focused on understanding the pathology of anxiety disorders in a bid to design better drug candidates for therapy. Anxiolytics seem to exert multiple effects on the central nervous system to improve the symptomatology of anxiety disorders. Since their introduction about 60 years ago, benzodiazepines have shown impressive results in the clinical management of anxiety disorders. Chlordiazepoxide and diazepine were the first members of this class to be clinically approved as anxiolytics in humans. Since their introduction, more drugs have been developed with different mechanisms of action and pharmacokinetics. In psychopharmacology, the development of anxiolytics was relatively slow compared to other classes of psychotropic drugs. The mechanism of the anxiolytic action of benzodiazepines was first described in 1977, when researchers identified high-affinity binding sites for benzodiazepines in the brain (Rodríguez-Landa et al., 2022). Subsequent research explained how benzodiazepine modulates the function of γ -aminobutyric acid (GABA) by increasing the inhibitory actions of GABA at the GABA receptors. This inhibitory action is also
interaction, and side effect mediation when administered in different doses. At low doses, these drugs typically act as an antidepressant. At medium to high doses, the SNRIs have additional significant effects in the reuptake of norepinephrine. They are also considered safe for long-term clinical use. Unlike SSRIs, SNRIs block the 5-HT2 receptor and produce fewer side effects than SSRIs do. However, this advantage does not guarantee a superior antidepressant action in many patients, and the selection of antidepressants largely depends on different specifics (Ghossoub et al., 2021). Mirtazapin, a noradrenergic and specific serotonergic antidepressant, has both pro-adrenergic and proserotonergic actions. A few drugs with mirtazapine-like effects have been described in different research submissions over the years. The pro-adrenergic and proserotonergic actions of these new drugs seem to be mediated by their alpha2-antagonist properties. They affect the disinhibition of both serotonin and norepinephrine neurotransmission in multiple animal models of depression. Mirtazapine and some drugs in this class also appear to not exert any toxicity effects due to 5-HT2 stimulation. As a direct result of its strong antihistaminic properties, Mirtazapine has been profiled to cause few side effects such as weight gain and sedation (Jilani et al., 2022). A new class of antidepressants with similar effects is the new serotonin reuptake enhancer. Tianeptine, a tricyclic compound of dibenzothiazepine type reportedly increases the presynaptic uptake of serotonin after single as well as repeated administration. However, on further investigation, researchers concluded that the antidepressant actions of tianeptine are not linked to any form of interaction with the 5-HT postsynaptic systems. It has no affinity for alfa1 adrenergic receptors, H1 antihistaminic receptors, or the muscarinic receptors. It just seems to enhance serotonin reuptake. The exact mechanism of these actions is still under scrutiny. Tianeptine also reportedly has a few side effects, including gastralgia, abdominal pain, dry mouth, anorexia, nausea, vomiting, flatulence, insomnia, drowsiness, nightmares, asthenia, and tachycardia. linked to the enhanced influx of chloride ions through the chloride channels to potentiate GABA receptors' action. This complex mechanism was further complicated by the discovery of more than 16 different subunits of the GABA-A receptors and the observation that benzodiazepines do not bind to all combinations of these different subunits. In animal models of anxiety exploring the clinical effects of benzodiazepines, researchers confirmed that benzodiazepines bind at the interface between the alpha and gamma subunits, with less action on the beta subunit. To be sensitive to benzodiazepines, it appears a GABA-A receptor requires the presence of a gamma subunit and an adjacent alpha 1, 2, 3, or 5 subunit. GABA-A receptors containing the alpha 4 and 5 subunits appear to be insensitive to benzodiazepine action due to a slight modification in a single amino acid positioning. The complexities in the interactions between benzodiazepines and the GABA receptors are extensively explored in psychopharmacology for therapeutic purposes. This has positioned benzodiazepines as a versatile option with therapeutic benefits beyond the clinical treatment of anxiety disorder. This class of drugs is also widely prescribed for the management of a range of neurological conditions such as alcohol withdrawal, mania, insomnia, muscle spasms, epilepsy, movement disorders, agitation, catatonia, and REM sleep disorders (Balon & Starcevic, 2020). It is important to note that certain psychotropic drugs have been identified as exerting anxiolytic actions in the central nervous despite not being expressly classified as anxiolytics. In psychopharmacology guidelines, these drugs are predominantly used as an alternative therapeutic for anxiety disorders. For instance, anticonvulsant medications such as pregabalin, gabapentin, tiagabine, topiramate, and lamotrigine have been
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