Benzodiazepines nervous system

Various 1.4-benzodiazepines with a five-membered heteroaromatic ring fused to the 1,2-bond, such as 17, where A represents a heteroaromatic ring, have been prepared by such methods and tested for activity on the central nervous system, as cholecystokinin antagonists and as antagonists of platelet activating factors.245... 

The most common side effects associated with benzodiazepine therapy include central nervous system (CNS) depressive effects (e.g., drowsiness, sedation, psychomotor... 

Benzodiazepines reduce fibrinogen binding and platelet aggregation Central Nervous System Acts as sedative-hypnotic, opens ion channel, chloride ion... 

Substance-Induced Anxiety Disorder. Numerous medicines and drugs of abuse can produce panic attacks. Panic attacks can be triggered by central nervous system stimulants such as cocaine, methamphetamine, caffeine, over-the-counter herbal stimulants such as ephedra, or any of the medications commonly used to treat narcolepsy and ADHD, including psychostimulants and modafinil. Thyroid supplementation with thyroxine (Synthroid) or triiodothyronine (Cytomel) can rarely produce panic attacks. Abrupt withdrawal from central nervous system depressants such as alcohol, barbiturates, and benzodiazepines can cause panic attacks as well. This can be especially problematic with short-acting benzodiazepines such as alprazolam (Xanax), which is an effective treatment for panic disorder but which has been associated with between dose withdrawal symptoms. 

Substances with a neuromodulatory effect on brain neurotransmitters by direct actions of specific receptors that modify the actions of the transmitters listed include prostaglandins, adenosine, enkephalins, substance P, cholecystokinin, endorphins, endogenous benzodiazepine receptor ligands, and possibly histamine. CNS, central nervous system. NMDA, N-methyl-D-aspartate. Strych, strychnine. 

The benzodiazepines such as diazepam, oxazepam, and temazepam are common causes of acute poisoning, but rarely cause serious toxicity by themselves, even in enormous doses. They can potentiate central nervous system depression from other drugs, including alcohol. 

Mohler H, Benke D, Fritschy JM, Benson J (2000) The benzodiazepine site of GABAa receptors. In Martin DL, Olsen RW (eds) GABA in the nervous system the view at fifty years. Lippincott, Philadelphia, pp 97-112... 

Buspirone is as effective as the benzodiazepines in the treatment of general anxiety. However, the full anxiolytic effect of buspirone takes several weeks to develop, whereas the anxiolytic effect of the benzodiazepines is maximal after a few days of therapy. In therapeutic doses, buspirone has little or no sedative effect and lacks the muscle relaxant and anticonvulsant properties of the benzodiazepines. In addition, buspirone does not potentiate the central nervous system depression caused by sedative-hypnotic drugs or by alcohol, and it does not prevent the symptoms associated with benzodiazepine withdrawal. 

The benzodiazepines bind with high affinity to specific macromolecules within the central nervous system. These benzodiazepine-binding sites (receptors) are closely associated with the receptors for j-aminobutyric... 

The distribution of the benzodiazepines from blood to tissues and back again is a dynamic process with considerable influence on the onset and duration of the therapeutic effects produced by these compounds. Those having greater lipid solubility tend to enter the central nervous system more rapidly and thus tend to produce their effects more quickly. Several of the benzodiazepines have therapeutic effects that are much shorter in duration than would be predicted based on their rates of metabolism and excretion redistribution away from the central nervous system is of primary importance in terminating their therapeutic effects. 

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