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GABA (γ-aminobutyric acid) is a significant neurotransmitter that is involved in anxiety and in the anxiolytic action of numerous medications that are prescribed to treat the full range of anxiety disorders; additionally, GABA, is the primary inhibitory neurotransmitter in the brain and generally serves a critical role in the regulation of reducing the activity of many other neurons (Stahl & Muntner, 2019, p. 397). GABAergic neurons have a ubiquitous presence throughout the central nervous system (CNS) and almost non-existent outside of the spinal cord and brain (Nutt & Malizia, 2001). GABA determines the state of excitability in all the areas of the brain and neuronal activity is controlled by the balance between excitatory inputs, primarily in the form of glutamatergic, and inhibitory GABAergic activity (Nutt & Malizia, 2001).

GABA is created from the amino acid glutamate, also known as glutamic acid, through the actions of the enzyme glutamic acid decarboxylase, also known as GAD, and when formed in the presynaptic neurons, GABA is carried by vesicular inhibitory amino acid transporters into synaptic vesicles (Stahl & Muntner, 2019, p. 397). GABA is stored in the synaptic vesicles until it is released into the synapse during inhibitory neurotransmission (Stahl & Muntner, 2019, p. 397). Neurotransmitters are endogenic and permit neurons to communicate with each other throughout the body and GABA accounts for approximately 40% of the inhibitory processing in the brain (Sheffler et al., 2020).

Three primary types of GABA receptors and multiple subtypes exist in the body and the major types are known as GABAA, GABAB, and GABAC receptors; however, it has been shown that GABAA are the primary receptor targets of benzodiazepines, sedative hypnotics, alcohol, and barbiturates (Stahl & Muntner, 2019, p. 397). It is by binding to the benzodiazepine sensitive subtypes of GABAA receptors that causes the sedative and motoric effect of the medication (Duke et al., 2018). However, not all GABAA subtype receptors are sensitive to benzodiazepine and the subtype receptors that have a sensitivity to benzodiazepine enhance the phasic postsynaptic inhibition, which results in the anxiolytic effect of the medication (Stahl & Muntner, 2019, p. 402).

The classification of anxiety disorders is dynamic and everchanging; however, benzodiazepines are believed to have anxiolytic effects on all of them to varying degrees (Griebel & Holmes, 2013). Benzodiazepines do not target specific GABAA receptor subtypes and the neural circuitry involved in anxiety has not been well defined and is not entirely understood (Griebel & Holmes, 2013). Despite this, benzodiazepines for the treatment of anxiety have been well established in extensive clinical trails in the 1960s through the 1990s, and in 1977 were the most prescribed medications in the world (Balon et al., 2020).

Partly due to its popularity, its relative safety compared to sedative-hypnotics, its many uses, and its addictive properties, benzodiazepines have a high incidence of overdose and use disorder (Kang et al, 2020). Benzodiazepines generally provide quick relief from anxiety and anxiety related disorders, and when used in anxiety disorders have a better side effect profile than antidepressants (Balon et al., 2020). The anxiolytic, anticonvulsive, muscle-relaxing, and hypnotic properties of benzodiazepines make them a popularly prescribed medication; however, these same properties often lead to physical dependence and addiction for some patients (Park, 2020). Addiction symptoms often mimic undertreated insomnia and anxiety and may lead to higher doses or longer durations, which, along with lower level of education, are risk factors for developing an addiction disorder (Park, 2020). Benzodiazepine disorder is associated with increased insomnia severity, alcohol dependence, and antidepressant use and use disorder (Park, 2020). The chronic use of benzodiazepines can cause physical dependence, evidenced by withdrawal syndrome, addiction, intoxication, and overdose (Park, 2020).

A diagnosis of benzodiazepine use disorder is evidenced by at least two of the following, occurring within a one-year period:

1. Sedatives, hypnotics, or anxiolytics are often taken in larger amounts or over a longer period than was intended.

2. A persistent desire or unsuccessful efforts to cut down or control sedative, hypnotic, or anxiolytic use.

3. A great deal of time is spent in activities necessary to obtain the sedative, hypnotic, or anxiolytic; use the sedative, hypnotic, or anxiolytic; or recover from its effects.

4. Craving, or a strong desire or urge to use the sedative, hypnotic, or anxiolytic.

5. Recurrent sedative, hypnotic, or anxiolytic use resulting in a failure to fulfill major role obligations at work, school, or home.

6. Continued sedative, hypnotic, or anxiolytic use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of sedatives, hypnotics, or anxiolytics.

7. Important social, occupational, or recreational activities are given up or reduced because of sedative, hypnotic, or anxiolytic use.

8. Recurrent sedative, hypnotic, or anxiolytic use in situations in which it is physically hazardous.

9. Continued sedative, hypnotic, or anxiolytic use despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the sedative, hypnotic, or anxiolytic.

10. Tolerance.

11. Withdrawal (Park, 2020).

The withdrawal of benzodiazepine often begins with autonomic hyperactivity and will often include insomnia, nausea or vomiting, hand tremors, psychomotor agitation, anxiety, hallucination or illusions, and grand mal seizures (Park, 2020). Despite the possibility of abuse, addiction, and overdoses with the use of benzodiazepines, Balon et al., believe that “we should not deprive our patients of efficacious and well tolerated medications because of historical mishaps, personal and specialty biases, and negative marketing propaganda” (2020).

Making the health care system available to rural and underserved areas as been a challenge for policymakers and the health care system. General disparities between rural and urban workforce capacities are well documented (Hough, Willging, Altshul, & Adelsheim, 2019). The disparities people in rural and underserved areas face are not only in terms of location and access but also in terms of health, which is health disparity. Andrew and Boyle (2018) define health disparity as population-specified differences in the presence of disease, health outcomes, or access to health care.

One important way that we, as advanced practice nurses, can help to eliminate disparities in rural and underserved areas is by autonomous practice. Ortiz and colleagues (2018) confirm, one study of persons residing in full-practice states, 62% had higher geographic accessibility to primary care clinicians (including ARNPs), compared to 35% in restricted states. Advanced practice nurses are able and willing to fill in the gap created by physician shortages in rural and underserved areas. ARNPs functioning at the level for which they are prepared could help to improve health care access disparities in areas with severe physicians shortages such as rural areas where shortages have persisted and are anticipated for the foreseeable future, Ortiz and colleagues conclude.