What is Diazepam?

5 pages
1102 words
University of Richmond
Type of paper: 
This essay has been submitted by a student.
This is not an example of the work written by our professional essay writers.

Diazepam belongs to a class of drugs called benzodiazepines. Benzodiazepines are administered in the treatment of a variety of ailments including insomnia, muscle spasms, anxiety, and mental illness (Katzung et al, 2004, 91). Diazepam is the most common benzodiazepine, and it is included in the WHO list of essential medicines. Diazepam, like all other benzodiazepines has a benzene ring fused with a diazepine ring. This structural conformation is the basis of drug-receptor interaction that brings about the therapeutic effect of the drug. Since the drug is prescribed for more than one purpose, it interacts with different molecules in the body to result into the desired effect.

Trust banner

If this sample essay on"What is Diazepam?" doesn’t help,
our writers will!

The Role of the Target Molecule in Disease

Diazepam is used to treat sleep disturbances and muscular related disorders. In both of these cases, a molecule called gamma aminobutyric acid (GABA) works in conjunction with other organs and organ systems to cause alteration in sleep patterns and muscular activity. GABA binds to the GABA a receptors in the brain and somatic muscles to inhibit nerve condition across a cell membrane (Enna & Snyder, 1975, 82). In the brain, GABA inhibits the firing of neurons and thus down-regulates the brain activity. Down regulation of brain activity causes sleep, making GABA a major player in sedation. GABA receptors are also available in the muscles. GABA binds to its receptors to bring about muscle relaxation, sedation, and hypnosis. GABA receptors in the body are ion gated channels that open when GABA binds to allow the inflow of chloride ions into the cell and the efflux of potassium ions out of the cell. The rise in negative ion concentration hyperpolarizes the plasma membrane and increases the firing potential of nerve cells. Diazepam is a positive allosteric modulator and potentiates the binding ability of GABA receptors to GABA (Wang et al, 2015, 1).

As a muscle relaxer, diazepam can be used as an anti-seizure drug. GABA receptor conformation is altered in most genetically induced seizures. The change in the conformation of these receptors impairs the binding of the ligand to the receptor. Consequently, the activity of gamma aminobutyric acid is lowered. In turn, neurons in the brain fire spontaneously and excessively in response to a small stimulus (Galanopolou, 2008, 13).

In constant muscle contraction, for example in muscle spasms, post synaptic membrane depolarizes rapidly and takes a lot of time to polarize. As a result, the plasma membrane reaches the firing potential repetitively and the muscle remains in a contracted state (Treiman, 2001, 11). Gamma aminobutyric acid binds to its receptors, but its effects on membrane polarization are not sufficient to overcome the rapid depolarization of the membrane.

Anxiety is caused by regular and repeated firing of neurons in the prefrontal context of the brain. This repeated firing is attributable to the down regulation of receptors in the cortex (Sperk et al, 2004, 100). When the receptors in the brain are few, the available gamma butyric acid molecules are not able to reduce the transmission of nerve impulses. In such cases, a GABA agonist like diazepam is required to serve as an anxiolytic.

Mechanism of Action of Diazepam

Diazepam works diversely in different parts of the body. In the prefrontal context of the brain, diazepam modulates the activity of major inhibitory neurotransmitter called gamma aminobutryic acid (Nemeroff, 2002, 135). Gamma aminobutyric acid has two receptors in the brain. These receptors are named as gamma aminobutyric acid receptor a and gamma aminobutyric acid receptor b. These receptors are proteins belonging to the same family. The receptors are membrane proteins that traverse the cell membrane. Gamma aminobutyric acid receptor a is an ion gated channel whose conformation changes in response to binding of the neurotransmitter, while gamma aminobutyric acid b is a G protein coupled receptor (Christian et al, 2013, 1065). In the absence of diazepam, gamma aminobutyric acid binds to the ligand site of the transmembrane gamma aminobutyric acid a to cause the opening of the ion channel. As a result, chloride ions in the extracellular fluid enter the cell while potassium ions move out of the cell. The interior of the cell membrane becomes more negative and the membrane hyperpolarizes. Hyperpolarization of the plasma membrane inhibits the activity of the concerned cells or tissues. The binding of gamma aminobutyric acid in the G coupled receptor causes the activation of an inhibitory intracellular G-protein (Iismaa et al, 2013, 11). The activation of the inhibitory G protein in turn decreases the general activity of brain cells. As a positive allosteric modulator, diazepam binds on another site in the gamma aminobutyric acid receptor belonging to either class. This binding augments the allosteric conformation of the protein receptor. As a result, the respective effect of each receptor increases. For example, the binding of diazepam on ligand gated channels accentuates the influx of negatively charged chloride ions and the efflux of positively charged potassium ions. When diazepam binds to the G protein coupled receptor, a lot more of inhibitory G proteins are activated, and the inhibitory effects of GABA are potentiated. Research has also shown that diazepam inhibits the synthesis and release of acetylcholamine, a neurotransmitter that plays a key role in muscle contraction (Philis et al, 1980, 342).


Christian, C.A., Herbert, A.G., Holt, R.L., Peng, K., Sherwood, K.D., Pangratz-Fuehrer, S., Rudolph, U. and Huguenard, J.R., 2013. Endogenous positive allosteric modulation of GABA A receptors by diazepam binding inhibitor. Neuron, 78(6), pp.1063-1074.Enna, S.J. and Snyder, S.H., 1975. Properties of g-aminobutyric acid (GABA) receptor binding in rat brain synaptic membrane fractions. Brain Research, 100(1), pp.81-97.Galanopoulou, A.S., 2008. GABAA receptors in normal development and seizures: friends or foes?. Current neuropharmacology, 6(1), pp.1-20.Gallager, D.W., 1978. Benzodiazepines: potentiation of a GABA inhibitory response in the dorsal raphe nucleus. European journal of pharmacology, 49(2), pp.133-143. Iismaa, T.P., Biden, T.J. and Shine, J., 2013. G protein-coupled receptors. Springer Science & Business Media.Katzung, B.G., Masters, S.B. and Trevor, A.J. eds., 2004. Basic & clinical pharmacology (Vol. 8). New York, NY, USA:: Lange Medical Books/McGraw-Hill.

Nemeroff, C.B., 2002. The role of GABA in the pathophysiology and treatment of anxiety disorders. Psychopharmacology bulletin, 37(4), pp.133-146.

Phillis, J.W., Siemens, R.K. and Wu, P.H., 1980. Effects of diazepam on adenosine and acetylcholine release from rat cerebral cortex: further evidence for a purinergic mechanism in action of diazepam. British journal of pharmacology, 70(2), pp.341-348.Sperk, G., Furtinger, S., Schwarzer, C. and Pirker, S., 2004. GABA and its receptors in epilepsy. In Recent advances in epilepsy research (pp. 92-103). Springer US.Treiman, D.M., 2001. GABAergic mechanisms in epilepsy. Epilepsia, 42(s3), pp.8-12.Wang, C., Liu, J., Luo, F., Deng, Z. and Hu, Q.N., 2015. Predicting target-ligand interactions using protein ligand-binding site and ligand substructures. BMC systems biology, 9(1), p.1.

If you want discreet, top-grade help, order a custom paper from our experts.

If you are the original author of this essay and no longer wish to have it published on the SuperbGrade website, please click below to request its removal: