Certain pharmaceutical drugs induce sleep by modulating central nervous system neurotransmitters.
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Retrieved reference literature confirms that certain pharmaceutical drugs induce sleep and treat sleep disorders by modifying or enhancing central nervous system neurotransmission, such as benzodiazepines targeting GABA receptors.
also known as central nervous system depressants, or colloquially known as "downers", are a class of psychoactive drugs characterised by decreasing neurotransmission
Depressants, also known as central nervous system depressants, or colloquially known as "downers", are a class of psychoactive drugs characterised by decreasing neurotransmission levels, decreasing the electrical activity of brain cells, or reducing arousal or stimulation in various areas of the brain. Commonly used depressants include alcohol, opioids, and benzodiazepines. Some specific depressan
Benzodiazepines enhance the effect of the neurotransmitter gamma-Aminobutyric acid (GABA) at the GABAA receptor, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties. High doses of shorter-acting benzodiazepines induce anterograde amnesia, which may be helpful for surgical and procedural anesthesia to reduce patient recall. Midazolam is often used in anesthesiology. These properties make benzodiazepines useful in treating anxiety, insomnia, agitation, seizures, muscle spasms, alcohol withdrawal, and as a premedication for medical or dental procedures. Benzodiazepines are categorized as either short-, intermediate-, or long-acting. Short- and intermediate-acting benzodiazepines are preferred for the treatment of insomnia; longer-acting benzodiazepines are recommended for the treatment of anxiety.
In general, benzodiazepines are safe and effective in the short term, although cognitive impairments and paradoxical effects such as aggression or behavioral disinhibition occasionally occur. A minority of patients react to benzodiazepines with paradoxical agitation. Long-term use is controversial due to adverse psychological and cognitive effects, decreasing effectiveness, dependence, and benzodiazepine withdrawal syndrome, following withdrawal after long-term use. The elderly are at an increased risk of experiencing both short- and long-term adverse effects.
There is controversy concerning the safety of benzodiazepines in pregnancy. While they are not major teratogens, uncertainty remains as to whether they cause cleft palate in a small number of babies and whether neurobehavioral effects occur as a result of prenatal exposure; they are known to cause withdrawal symptoms in the newborn. Benzodiazepines can be overdosed and cause dangerous deep unconsciousness. However, they are much less toxic than their predecessors, barbiturates, and death rarely results when a benzodiazepine is the only drug taken; however, when combined with other central nervous system depressants such as alcohol and opioids, the potential for toxicity and fatal overdose increases. Benzodiazepines are commonly misused and…
cessive day-time sleepiness associated with the disorder. The level of arousal is controlled by an intricate interplay between distinct wakefulness- and sleep-promoting nuclei situated in the hypothalamus and brainstem and the interconnections between the nuclei and the neurotransmitters involved have been mapped. Wakefulness-promoting nuclei include the orexinergic lateral hypothalamic/perifornical area, the histaminergic tuberomammillary nucleus, the cholinergic pedunculopontine tegmental nucleus, the noradrenergic locus coeruleus, the 5-hydroxytryptaminergic raphe nuclei and possibly the dopaminergic ventral tegmental area. The major sleep-promoting nucleus is the GABAergic ventrolateral preoptic nucleus of the hypothalamus. Currently available and future drugs exert their therapeutic effects in the three major classes of sleep disorder (insomnia, hypersomnia, parasomnia) by modifying neurotransmission at distinct sites within the arousal-controlling neuronal network. This enables classification of therapeutic drugs for sleep disorders on the basis of their modes of action: drugs that interact with the GABAergic sleep-promoting system, drugs that interact with different wakefulness-promoting systems and drugs that modulate the level of arousal by mechanisms that do not initially involve the basic network (e.g. melatonin, adenosine). The development of novel therapeutic drugs for sleep disorders is based on the synthesis of molecular/cellular mechanisms and the sites of action within the arousal-controlling neuronal network.
Keywords: Sleep disorders, neural mechanisms, drug therapy, sleep-promoting system, wakefulness-promoting systems
According to a simple classification, sleep disorders can be divided into insomnia, hypersomnia (excessive daytime sleepiness, EDS), and parasomnia (behavioural disturbance related to sleep). These disorders can occur in isolation (primary sleep disorders) or in association with mental or physical illnesses (secondary sleep disorde
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