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Neuropharmacology 101: Calm in Chaos: Exploring Anxiolytics


Diseases and disorders that affect the nervous system are becoming more prevalent. Due in part to ageing populations, the demand for effective treatments has never been more critical. Significant research has been devoted to the development of drugs to treat these conditions. However, the unique challenges posed by the nervous system make medication development a formidable task. One of the primary complexities in treating nervous system disorders is the Blood-Brain Barrier (BBB), a selective membrane that regulates the movement of molecules and ions between the blood and the brain. The BBB protects the brain from infection but makes it difficult for medications to reach their site of action in the nervous system. The first challenge to any neuropharmacology treatments, therefore, is finding drugs that can cross the BBB. This article series will detail the strategies used by different medications to cross this barrier and exert their effects on the nervous system.

Neuropharmacology emerged 50 years ago as a specialised branch of pharmacology that deals with drugs which influence the nervous system to treat or improve psychiatric and neurological diseases. The Neuropharmacology 101 series will explore six key categories of neuropharmacological drugs: antidepressants, anxiolytics, antipsychotics, antiepileptics, treatments for Parkinson’s and Alzheimer’s, and drugs of abuse. The Neuroscience 101 series aims to provide valuable insights into the intricacies of drug development for nervous system disorders, offering a comprehensive understanding of the challenges faced and the breakthroughs achieved. Reading this series will help readers to better understand the mechanisms, nuances, and prospects of treatments for psychiatric and neurological conditions.

This 101 series is divided into six articles including:

2. Neuropharmacology 101: Calm in Chaos: Exploring Anxiolytics

3. Neuropharmacology 101: Balancing the Mind with Antipsychotics

4. Neuropharmacology 101: Seizing Control: The Power of Antiepileptics

5. Neuropharmacology 101: Unravelling the Future of Parkinson’s and Alzheimer’s Treatments

6. Neuropharmacology 101: Beyond the High: The Complexities of Drugs of Abuse.

Neuropharmacology 101: Calm in Chaos: Exploring Anxiolytics

Anxiety is a normal emotion and can be helpful in moderation. Increased alertness, fear, and a rapid heart rate can alert us that we are in a risky situation and help us escape when necessary. However, excessive or constant feelings of anxiety can lead to anxiety disorders and have detrimental effects on our mental wellbeing, causing distress and even functional impairment. While anxiety is treatable, increasing rates of anxiety means that treatment options have been slow to keep up with demand. Nevertheless, as the understanding of the underlying neurobiological causes of anxiety increases, so may the development of new and more effective treatments. Anxiolytics are medications which are designed to alleviate anxiety symptoms. There are several types of anxiolytic drugs, including benzodiazepines and non-benzodiazepine alternatives such as buspirone. Early anxiety treatments, like barbiturates developed in 1903, were used to promote calming effects, reduce fear responses, decrease excessive anxiety and reduce the heart rate. More modern anxiolytics have been developed to target specific neurotransmitters in the brain for much more targeted anxiety treatments. While these medications can offer relief to those who suffer with anxiety, they also carry risks, including the potential for patients to become dependent on them (Sinclair & Nutt, 2007).



Although historically under-recognised and under-treated, anxiety disorders are among the most common psychiatric disorders and include panic disorder (PD), generalized anxiety disorder (GAD), social anxiety disorder (SAD), and specific phobias (SP). SAD and SP are the most prevalent types of anxiety. While each subtype of anxiety disorder has its own set of symptoms and challenges, they all share a common thread of excessive and persistent anxiety. Approximately 264 million people in the world suffer from one or more anxiety disorders, an increase of 15% in the last 20 years (Garakani et al., 2020).

There is a difference between anxiety and readiness. While readiness means that a person is ready for action and indicates an appropriate level of preparedness for certain situations to arise, anxiety, on the other hand, is excessive worry, usually prolonged and often disproportionate to the level of threat. While readiness and a certain level of worry can help us deal with stressful situations, anxiety disorders can have the opposite effect. They can be debilitating, and render a person who suffers from them less able to deal with stressful or unforeseen circumstances (Maximino, 2012).

Figure 1: Generalised Anxiety Disorder Symptoms (Unknown, 2020).

The Brain and Anxiety

Although anxiety is a normal emotional response, extreme or prolonged high levels of anxiety can cause lasting damage to the brain and cognitive function. Severe anxiety disorders can result in brain damage and loss of up to 8% of hippocampal volume (Lydiard, 2003). Anxiety can operate through several different circuits in the brain, depending on the type of anxiety a person is experiencing. Some key neuronal circuits involved in regulating the stress response are the HPA (hypothalamic-pituitary-adrenal) axis, autonomic nervous system. In times of acute anxiety, the neuropeptide CRF (corticotropin-releasing hormone) is released from the hypothalamus and stimulates the release of the stress hormone cortisol (Lydiard, 2003).

Certain brain structures, the basolateral amygdala (BLA) and the central nucleus of the amygdala (CeA) in particular, play key roles in anxiety. The BLA integrates sensory information and excites the CeA, causing the amygdala to trigger defensive responses in other brain regions, such as the hippocampus, periaqueductal gray and hypothalamus. While the role of the amygdala in fear conditioning is clear, it has been challenging to determine its involvement in sustained, chronic anxiety. Conversely, the bed nucleus of the stria terminalis (BNST), which is part of the extended amygdala and is closely linked to the CeA, seems to play a significant role in maintaining sustained anxiety through its GABAergic projections. Within the cerebral cortex, the medial prefrontal cortex (mPFC) and its subregions, such as the infralimbic (IL) and prelimbic (PL) cortex, are involved in threat response circuits by exciting (PL) or inhibiting (IL) the amygdala. Furthermore, a number of experiments in rodent models have shown that PL neurons transmit consistently during periods of sustained threat, implicating the PL in sustained anxiety. The hippocampus plays an important role in decision making and provides contextual information about environmental threats to the PL, while interoceptive signals from the anterior insula to the PL may contribute to maintaining high levels of anxiety. The prefrontal cortex contributes to anxiety through the dorsolateral prefrontal cortex (dlPFC), as seen in primate models of anxiety, where maternal separation activated the right dlPFC and deactivated the left dlPFC of young primates, and increased the risk of developing long-term anxiety traits. The role of the prefrontal cortex and dlPFC is evident, as primates with dlPFC dysfunction exhibit anxiety traits (Robinson et al., 2019).


Figure 2: Amygdala Neurocircuitry (Thompson and Neugebauer, 2017).

The Role of Neurotransmitters

Discerning the neurobiology of anxiety is complicated, as mood and anxiety can be influenced by a wide range of neuroendocrine, neurotransmitter, and neuroanatomical disruptions. Because these symptoms are interconnected, it has been a challenge for drug developers to determine which has the most functionally relevant effect, as it is helpful to know the cause of anxiety disorders in order to treat them. Several studies have suggested that anxiety disorders result from a dysfunction in the emotional response regulation system, which modulates brain circuits to regulate how a person responds emotionally to potentially threatening or fear-inducing stimuli. The emotional response regulation system involves neuronal circuits that include both bottom-up activity from the amygdala (signalling a potentially threatening stimulus) and top-down control mechanisms from the prefrontal cortex (which signal the emotional response) (Nuss, 2015).

Neurotransmitter imbalances, particularly in the emotional centres of the brain (known as the limbic system) as opposed to the cognitive centres, have been shown to disrupt signalling between neurons and lead to changes in mood (Martin et al., 2009). Although noradrenaline was once thought to mediate some forms of anxiety, it was later found to play only a minor role in the pathophysiology of anxiety. Similarly, neurotransmitters such as dopamine, histamine and acetylcholine seem to have little impact in this disorder and are not targets for current anxiolytic drugs. The most significant neurotransmitters in anxiety disorders appear to be GABA (gamma-aminobutyric acid) and serotonin (Hoehn‐Saric, 1982). The transmission of these neurotransmitters can significantly affect the level of anxiety a person experiences, as they are involved in regulating mood and anxiety levels. GABA is the main inhibitory neurotransmitter in the brain, meaning that it reduces or blocks chemical messages and counteracts the excitatory signals of glutamate. The balance of GABA and glutamate in the nervous system modulates neuronal excitability and emotional arousal. When these neurotransmitters are in balance, they prevent neuronal hyperexcitability, which has been implicated in anxiety disorders (Lydiard, 2003). Within the circuits of the amygdala, the inhibitory action of GABA plays an important role in modulating emotional responses and anxiety levels (Nuss, 2015).  Clinical evidence for the role of GABA in anxiety comes from patients in withdrawal states (e.g. from benzodiazepines) where GABAA receptor function is reduced (Sinclair & Nutt, 2007). The most predictable and reliable anxiolytic effects come from drugs that act on GABA transmission (Hoehn‐Saric, 1982).

Serotonin is associated with happiness and positive emotions, and helps regulate mood, sleep, and appetite. Because serotonin can be excitatory or inhibitory, depending on which receptor the molecule binds to and where the receptor is located in the brain, conflicting evidence has emerged on serotonin’s role in anxiety. In some cases, levels of this neurotransmitter are lower in those suffering from anxiety, while in others they are elevated. This controversy arose because some experimental evidence of conflict anxiety from rat models treated with drugs that act on serotonin indicated that serotonin increased anxiety, while in other experiments on rat models, showed that the subjects experienced anxiolytic effects from serotonin treatment, using electrical stimulation of the dorsal periaqueductal grey (dPAG) matter of the midbrain as an inducer. Eventually, it was determined that these responses were due to the fact that the rat models exhibited two different defensive responses because they were experiencing different emotions: anxiety and panic. They showed inhibitory avoidance in response to anxiety in the conflict tests and unidirectional escape in response to panic induced by electrical stimulation. The avoidance response is enhanced by serotonin released in forebrain structures such as the amygdala and prefrontal cortex, and by nerve fibres from the dorsal raphe nucleus (DRN), while the escape response is inhibited by serotonin from the dPAG through fibres also originating in the DRN. By understanding the nuances between anxiety and panic, researchers can conduct better experiments, leading to treatments tailored to relieve anxiety (Zangrossi & Graeff, 2014). The main pathways for serotoninergic projections to the forebrain are the medial raphe nucleus (MRN) and the dorsal raphe nucleus (DRN). The MRN modulates fear and anticipatory anxiety, while the DRN deals with cognitive processes that lead to anxiety. It has been suggested that high levels of serotonin in one of these pathways lead to anxiety, whereas high levels of serotonin in the other pathway reduce or prevent anxiety, as they will act on different serotonin receptors (Sinclair & Nutt, 2007). Although the exact role of serotonin in anxiety is not well understood, it is clear that serotonin plays a role in the pathophysiology of anxiety, as drugs such as selective serotonin reuptake inhibitors (SSRIs) that increase serotonin levels in the brain have been shown to be effective in treating certain anxiety disorders. Additionally, other non-benzodiazepine anxiolytics such as buspirone work by targeting serotonin receptors, particularly the 5-HT1A receptor subtype. Multiple types of serotonin receptors have been identified, and although they are not fully understood, full and partial agonists for 5-HT1A receptors have been used to treat some anxiety disorders, and 5-HT1C and 5-HT2 receptor antagonists may be indicated to treat GAD, further demonstrating the role of serotonin in anxiety. By modulating serotonin activity, SSRIs and other drugs can be used to alleviate anxiety symptoms (Baldwin & Rudge, 1995).


Figure 3: GABA in Anxiety Disorders (Lydiard, 2003).

While anxiety disorders have been shown to be rooted in neurotransmitter imbalances, the cause of these imbalances and signalling impairments could be due to environmental experiences, injury or genetic predisposition (Martin et al., 2009). While this further complicates our understanding of anxiety, it does open up new routes to develop psychological, behavioural, and pharmacological strategies that could help treat anxiety disorders (Nuss, 2015). 


Current treatments

Despite its prevalence, anxiety has received relatively little research and treatment development compared to other psychiatric disorders such as depression. This is probably due to the perception that anxiety can be adequately managed with current treatments. Current treatments include pharmacotherapies and drug interventions, as well as a range of non-drug treatments such as cognitive behavioural therapy and neurostimulation treatments, such as transcranial magnetic stimulation. However, only 60-85% of patients respond adequately to current treatments, and only 50% of patients recover from anxiety using such treatments. Several factors may contribute to these low outcomes, including poor adherence to treatment plans, substance use, comorbidities and misdiagnosis (Garakani et al., 2020). Some anxiolytics can be slow to take effect, usually two to four weeks, although an adjustment period of up to two months may be required for the patient to experience the full benefit of these medications. Although many drugs used to treat anxiety may also be deployed in depression treatments, lower doses are initially given to patients to treat anxiety, and the dose is slowly increased to a high level to achieve a significant response. Side effects of anxiolytics, such as sexual dysfunction and apathy syndrome (lack of emotion), can be dose-dependent, so careful monitoring of dosage is required to mitigate these side effects (Melaragno, 2021).



Some of the most commonly used anxiolytics are benzodiazepines, which include diazepam (first marketed as Valium), alprazolam (first marketed as Xanax), and lorazepam (first marketed as Ativan). These drugs have sedative, hypnotic (sleep-inducing), anticonvulsant, and muscle relaxant properties, and are classified as sedative-hypnotics and mild tranquillisers. The rapid onset and fast acting relief provided by benzodiazepines quickly made these drugs popular treatments for anxiety. Although benzodiazepines were the most commonly prescribed anxiolytics, concerns over effects such as dependence and severe withdrawal symptoms have reduced their use (Sinclair & Nutt, 2007). Benzodiazepines are among the most commonly used prescription drugs for recreational purposes. Abuse of these medications, usually in combination with opioids or alcohol, has reached epidemic proportions. Although most of the population is at low risk of abusing benzodiazepines, those with a history of substance abuse may be at high risk of abusing benzodiazepines (Schmitz, 2016). Since their development in 1960, eight benzodiazepines have been approved by the American Food and Drug Administration (FDA) for the treatment of anxiety and anxiety-related disorders. From the onset, these drugs were overprescribed and eventually their potential for abuse became evident (Argyropoulos & Nutt, 1999). Although they grew in popularity throughout the 1970s to become the most prescribed class of drugs, a worrying trend of benzodiazepine prescription abuse emerged in the 1980s (McGee et al., 2021).

Figure 4: Diazepam (Unknown, n.d).

The calming effects of benzodiazepines can lead to compulsive use and a cycle of dependency. Drug dependence is characterised by the patient experiencing negative symptoms, known as withdrawal, after stopping drug use. Symptoms of benzodiazepine withdrawal range from mild anxiety and insomnia to severe agitation and seizures. Patients are most at risk of developing dependence and withdrawal symptoms if they take benzodiazepines consistently and over a long period of time. If these drugs are used occasionally, for example to treat panic attacks, they can be used for longer periods with less risk of dependence. For patients who wish to stop taking benzodiazepines, gradually reducing the dose can reduce the withdrawal symptoms, although it may not prevent them altogether (Swaim, 2022). However, benzodiazepines are still used for patients that are not responding to other anti-anxiety medications (Melaragno, 2021).


While fears over patients becoming tolerant to and dependent on benzodiazepines may be somewhat justified, benzodiazepines can still be incredibly useful, and not taking advantage of all the treatment options available can be a great disservice to patients. Because the mechanisms of action of benzodiazepines are fairly well understood, their use can also help researchers in their continuing attempts to understand the neurobiological causes of anxiety and to develop new, safer treatments (Argyropoulos & Nutt, 1999). The mechanism of action of benzodiazepines focuses on promoting the inhibitory neurotransmitter GABA. Benzodiazepines reduce anxiety by increasing GABA activity by binding to the GABAA receptor, which allows negatively charged chloride ions to move into the neuron through ligand-gated chloride channels. As the neurons become more negatively charged, neuronal excitability is reduced and the neuron becomes less responsive to other, excitatory, neurotransmitters. This has an overall calming and even sedative effect on the patient (Benzo Info, 2022).

Much of the evidence for the ability of benzodiazepines to treat anxiety comes from the close correlation between the binding affinity of benzodiazepine at the GABAA receptor and the dose administered (Nuss, 2015). However, reducing the ability of excitatory neurotransmitters can impair other brain functions, including alertness, memory, emotional response, blood pressure and even muscle tone. Benzodiazepine receptors can also be found outside the nervous system, in the kidney, adrenal cortex, colon and blood cells. As a result, benzodiazepines can have system-wide side effects. Long term use of benzodiazepines can cause 'uncoupling' of the GABAA receptor, which could be due to changes in the gene expression of this receptor. This means that the benzodiazepines are less able to increase GABA transmission, and their effect is reduced, leading to tolerance and the need for higher doses and an increase in side effects. However, uncoupling can occur after just one week of benzodiazepine use, which is why some patients experience withdrawal symptoms after only a short period of benzodiazepine use (Benzo Info, 2022).

Figure 5: Symptoms of Benzodiazepine Withdrawal (Wilson, 2022).

Non-Benzodiazepine Alternatives

Due to the risks associated with benzodiazepines, non-benzodiazepine alternatives can offer a safer option for managing anxiety disorders without the potential for tolerance, dependence and addiction. These non-benzodiazepines are sometimes called 'Z drugs', as many of their names start with or include the letter Z, such as zopiclone, zaleplon and zolpidem (Benzo Info, 2022). When they were introduced in the 1990s, these drugs appeared to be the perfect replacement for the addictive benzodiazepines. Z drugs have short half-lives which reduces the likelihood of patients becoming tolerant and dependent on them, but there are still issues with the drugs. Like benzodiazepines, they still have the potential to be abused, and do have withdrawal symptoms. Additionally, Z drugs can cause parasomnias (a type of sleep disorder) and other potentially dangerous sleep-related behaviours (McGee et al., 2021).


The mechanism of action of Z drugs is very similar to that of benzodiazepines. Z drugs also act on the GABAA to promote the GABA neurotransmitter, but whereas benzodiazepines bind non-selectively to α-1, α-2, and α-3 GABAA receptors units, Z drugs act selectively on the α-1 GABAA subunit. Due to this selectivity, Z drugs can produce sedative-hypnotic effects similar to those of benzodiazepines without the dependence or system-wide effects of benzodiazepines. Unfortunately, this also means that while Z drugs are good at treating insomnia, they are not as effective as anxiolytics compared to benzodiazepines (McGee et al., 2021).


Another safer alternative to benzodiazepines could lie in selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs). Although developed as antidepressants, SSRIs and SNRIs have been shown to improve anxiety symptoms and are approved the treatment of anxiety disorders PD, GAD and SAD (Garakani et al., 2020). SSRIs have been shown to be effective in the treatment of GAD, with the SSRI escitalopram and the SNRI duloxetine having the largest effect sizes and therefore practical significance (He et al., 2019). Although these drugs increase serotonin, and the initial surge of this neurotransmitter can cause jitters or tremors, this can usually be reduced by adjusting the dose (Garakani et al., 2020). Additionally, it has been reported that SSRIs can initially increase anxiety symptoms, before their anxiolytic properties take effect (Sinclair & Nutt, 2007). Typical treatments with these medications last 3-6 months, but can last 1-2 years due to their relative safety. Unlike benzodiazepines, there is little evidence to suggest that long term use of SSRIs or SNRIs leads to adverse effects such as dependence (Garakani et al., 2020). SSRIs have become first-line treatments for anxiety due to their proven efficacy against a range of anxiety disorders, as well as few potential drug-drug interactions and adverse effects (Melaragno, 2021).


Figure 6: Action of SSRIs (Unknown, n.d).

Buspirone belongs to the azapirone class of drugs and was originally developed as an antipsychotic in 1968. Although it proved ineffective in this role, the anxiolytic properties of this drug were later discovered and this drug has since been approved for use as an anxiety treatment, both for the treatment of long-term anxiety disorders and for the relief of short-term anxiety symptoms. This drug is the second-line treatment for anxiety disorders after SSRIs or SNRIs, when these first-line drugs prove ineffective or their adverse effects have a severe impact on the patient (Wilson & Tripp, 2023). In cases where patients are concerned about the adverse sexual dysfunction symptoms of SSRIs, buspirone may be considered as a first-line treatment (Melaragno, 2021). Buspirone has become quite popular as it offers anxiolytic effects with fewer adverse side effects than many other anxiety treatments, and there are no reports of patients becoming physically dependent on the drug. There have also been no reports of overdose from taking buspirone alone (Wilson & Tripp, 2023). The drug starts working slowly and can take between 10 days and four weeks to take effect. Buspirone is usually well tolerated by patients and can be used as a monotherapy or alongside another drug or antidepressant to achieve higher efficacy results (Melaragno, 2021). This drug is often used in tandem with SSRIs or SNRIs for better responses and to reduce some of the sexual dysfunction side effects of SSRIs. However, buspirone has been shown to be less effective as an acute anxiolytic, as its effects can take a few weeks to materialise. There have also been some cases of movement disorders induced by buspirone (Garakani et al., 2020).

Buspirone is a is a partial agonist for the serotonin 5-HT1A receptor subtype. This drug also has a weak affinity for serotonin 5HT2 receptors and can act as a weak antagonist of dopamine D2 autoreceptors.  As buspirone has no effect on benzodiazepine GABA receptors, it is non-addictive. However, this means that it cannot be used to treat withdrawal symptoms from benzodiazepines or other addictive drugs such as barbiturates or alcohol. Additionally, patients who were previously treated with benzodiazepines have been shown to have a reduced response to subsequent buspirone treatment (Wilson & Tripp, 2023). The pharmacokinetics of buspirone have a major impact on the dosage requirements for this treatment. The drug is rapidly absorbed, reaching peak plasma levels in 40 to 90 minutes, and has a short half-life at approximately two to three hours. As a result of these fast pharmacokinetic properties, a dose of buspirone must be administered at least twice a day (either 7.5 mg twice a day or 5 mg three times a day). This can lead to problems with adherence and patients may find it difficult to follow their dosing schedule (Melaragno, 2021).


When prescribing anxiolytics, healthcare providers must weigh the potential benefits of symptom relief against the risks of medication dependency and adverse effects. For some individuals, particularly those with severe anxiety symptoms or panic disorder, the immediate relief provided by benzodiazepines may outweigh the risks associated with long-term use. However, for others, particularly those with a history of substance abuse or dependence, non-benzodiazepine alternatives such as buspirone may be a more appropriate choice. Regardless of the medication prescribed, it's essential for patients to be closely monitored by their healthcare providers to ensure safe and effective treatment. Regular assessments of symptom severity, medication efficacy, and any signs of dependency or adverse effects are essential to guide treatment decisions and adjust dosage regimens as needed (Edinoff et al., 2021).

Figure 7: Buspirone (Unknown, n.d).

Future Anxiolytics

New research into the treatment of anxiety has shifted the focus from targeting serotonin or GABA transmission to other neurotransmitters and pathways, including glutamate, neuropeptides, neurosteroids and cannabinoids. Cannabinoids target the cannabinoid type 1 (CB1), serotonergic type 1A (5HT1A) and the transient receptor potential vanilloid type 1 (TRPV1) receptors. Agonists for the CB1 receptor, such as the partial agonist Delta-9-tetrahydrocannabinol (THC), have biphasic effects, with low doses having anxiolytic properties and high doses having anxiogenic (anxiety-increasing) effects. Although it is widely believed that cannabis, cannabidiol (CBD) and other cannabinoids are safe, relaxing and can reduce anxiety, there is currently insufficient scientific evidence to suggest that cannabinoids are safe or significantly effective for patients with anxiety disorders. Some studies investigating CBD as an anxiolytic have shown promising signs that CBD may be effective against PD, GAD and SAD. However, the majority of trials investigated cannabinoids for the relief of chronic non-cancer pain, multiple sclerosis or fibromyalgia. Studies investigating the effect of these drugs specifically on anxiety would need to be conducted before such treatments could be used for anxiety disorders (Garakani et al., 2020).


Anxiety is a complex emotional state that serves a vital function in alerting us to potential threats. However, when anxiety becomes excessive or chronic, it can lead to debilitating anxiety disorders that significantly impair daily functioning and quality of life. While research and treatment development of anxiolytics has lagged, advancements in our understanding of the neurobiological underpinnings of anxiety have paved the way for the development of new and more effective treatments.

Anxiolytics, medications designed to alleviate anxiety symptoms, have evolved over time from early treatments such as barbiturates to more targeted options such as benzodiazepines and non-benzodiazepine alternatives like buspirone. Benzodiazepines, while effective in reducing anxiety symptoms, carry the risk of dependence and withdrawal symptoms, making them less favourable for long-term use. Non-benzodiazepine alternatives like buspirone offer a safer option with fewer side effects and no risk of physical dependence. Additionally, SSRIs and SNRIs have demonstrated efficacy in treating anxiety disorders with less risk of dependence. Understanding the neurobiological, psychological, and environmental factors that contribute to the basis of anxiety disorders has led to the development of pharmacological interventions that target these pathways. While challenges remain in optimizing treatment outcomes and minimizing side effects, continued research into the mechanisms of anxiety and the development of novel therapies offer hope for improved management of anxiety disorders in the future.

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Early treatments like barbiturates aimed to promote calmness and reduce fear responses. Modern anxiolytics target specific neurotransmitters, providing more precise treatments.

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