In this lecture we’ll cover the pharmacology of the anxiolytic and Hypnotic Medicines So let’s get it right is the anxiolytic’s primary use Hypnotic medications are used to treat anxiety and anxiety insomnia is generally defined An emotional state characterized by excessive feelings of fear and fear Nervousness while insomnia is generally defined as the inability to start Maintain or achieve restful sleep now in order to have a better understanding How do anxiolytics and hypnotics work First we need to discuss a role GABA in the central nervous system, so gamma-aminobutyric acid or GABA’s The short is a major inhibitor of the neurotransmitter what that means When GABA reaches and binds to a particular receptor on nerve cells, it reduces The level of activity of that neuron makes it less likely to release its potential Now GABA is recognized by both ligand-gated and G-Protein Associated with GABA Receptors In this lecture we are going To focus on, GABA ligates a faster receptor called GABA-A because that is it The main goal of many anxiolytic and hypnotic agents now is the GABA-A receptor Up of five subunit proteins arranged to form a central pore these subunit have They are labeled with Greek letters such as alpha beta gamma and delta monocytes The formation of GABA-A receptors in the brain most often consists of two Alpha groups two beta units and one gamma or delta subunit moreover Each subunit and many other subtypes exist and function of each GABA-A receptor It is based on the subunit that the example GABA-A receptor contains The alpha-1 subunit appears to be involved in sleep while the alpha-2 subunit appears Or alpha-3 seems to be involved in anxiety now when GABA molecules bind To the GABA-A receptor is the cause of the formative changes that Results in opening the central pores that allow negatively charged chloride Ions to rush into the cell and this in turn increases the negative charge inside Postsynaptic cell that makes it more difficult to excite The input to cause the action potential is now the GABA-A receptor is in height Focus in the limbic system One part of the limbic system is The amygdala that contains many neurons that use the GABA neurotransmitter to Control of feelings of fear and anxiety in times of nervous tension in nerve cells The amygdala quickly flames sending exciting signals to other areas of the brain it It is this type of shooting that leads to a feeling of panic or fear of inhibiting Interneurons in the amygdala regulate these emotions via the release of GABA The release of GABA and binding to postsynaptic receptors such as GABA-A It blocks the extraordinary signals that result in feelings of anxiety and fear GABA thus has a calming effect on our emotions and prevents us from getting sick Becoming mired in stressful situations is now a plus The neurotransmitter binding site GABA also contains the GABA-A receptor In which anxiolytic and soft drugs bind these drugs can be divided into Three groups are benzodiazepines, barbiturates, and non-benzodiazepine hypnotics Let us now discuss these one by one Details ranging from benzodiazepines that benzodiazepines get their name from Its chemical structure includes the benzene ring fused to the diazepine ring Their binding site appears to be the region between alpha and gamma The subunit on the GABA-A receptor it’s so important to remember Benzodiazepines do not bind to GABA cross-recognition site The alpha and beta subunits thus do not stimulate the opening of the channel Directly as GABA instead of binding from a benzodiazepine to its receptor site This leads to GABA affinity for GABA binding site Increase the channel frequency open and turn increase flow The chloride ions are in the postsynaptic cell which ultimately makes it difficult Exciting input to potential action effect even when excited Signals caused by fear or stress are dampened in this way and the result is Reduce anxiety and feel more calm in addition to benzodiazepines They can also produce mild muscle relaxation as a result of their action on GABA Receptors in the spinal cord and brain stem are examples Benzodiazepines are Alprazolam, chlordiazepoxide, and clonazepam diazepam Lorazepam and temazepam when it comes to the side effects of the most benzodiazepines They are related to common anesthesia and muscle relaxation action Decreased drowsiness include dizziness, alertness and concentration as well Impaired motor coordination Now let’s move on to the next group Barbiturates Therefore barbiturates bind to the GABA-A receptor The alpha or beta subunit that is different from the GABA and the binding site Also different from the now just like benzodiazepine binding site Benzodiazepines and barbiturates enhance the effect of GABA at the GABA-A receptor But instead of the ions increasing the channel’s opening frequency, they increase The duration of the ion channel opening is in other words unlike benzodiazepines Barbiturates hold the ion channel open continuously for long periods of time in Additionally, barbiturates can reduce excitatory activity Neurotransmitters such as acetylcholine and glutamate, in higher doses they can Also mimic GABA and directly activate GABA receptors thus lead to deep Central nervous system depression that’s why barbiturates have so much less A therapeutic indication of benzodiazepines which means that the toxic dose is not significant Higher than dose therapeutic examples of barbiturates include Pentobarbital Phenobarbital and Cyobarbital when it comes to the side The effects of barbiturates most often cause dizziness, vertigo, anesthesia As well as poor memory and attention moreover due to its narrowness A therapeutic indication is important to remember that it is even a small barbiturate An overdose can lead to coma or death due to a respiratory depression.

Now let’s act On our last group of drugs this is a non-hypnotic benzodiazepine as I am Mentioned at the beginning of this lecture GABA-A receptors in different regions of the central nervous system From different groups of subunits the specific subunit appears Mediated anesthesia is alpha-1 isoform as its name implies Non-hypnotic benzodiazepine is structurally different from Benzodiazepines as you may already have guessed they selectively bind to Alpha-1 subunit of the GABA-A receptor leading to the opening of the chloride channel With the resulting hyperpolarization membrane due to alpha-1 They contain high GABA-A receptors expressed following enhanced zones Brain differential correlation for benzodiazepine non-spermatogenic to these A receptor that produces sleepiness but no anti-anxiety effect is an example The non-hypnotic benzodiazepines are Zolpidem Zaleplon and Eszopiclone When It relates to the side effects that non-benzodiazepine hypnotics can cause Cognitive impairment, including memory, loss of daytime sedation and impairment From the motor post however I wanted to thank you for watching I hope you Enjoy this video and stay tuned for more as usual

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