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![Figure 2.](/view/journals/anpr/54/3/inline-i0003-3006-54-3-118-f02.gif)
Dose-response curve for benzodiazepines.
![Figure 3.](/view/journals/anpr/59/1/inline-i0003-3006-59-1-28-f03.png)
Biotransformation of various benzodiazepines. Parent drugs and their active metabolites vary in their elimination half-lives: L, >24 hours; I, 6–24 hours; and S, <6 hours (derived from Mihic and Harris7).
![<bold>Figure 1. </bold>](/view/journals/anpr/69/1/inline-i0003-3006-69-1-49-f01.png)
Schematic of GABAA receptor depicting competitive antagonism between flumazenil and midazolam at the benzodiazepine (BZD) binding site. Flumazenil acts as a negative allosteric modulator of GABA by facilitating closure of the chloride ion (Cl−) channel and preventing the influx of Cl− ions.
![Figure 2.](/view/journals/anpr/59/1/inline-i0003-3006-59-1-28-f02.png)
The GABAA receptor complex. The GABAA receptor complex consists of several protein subunits, with each comprised further of subunit families. These subunits provide myriad sites or receptors at which drugs may bind. While GABA and its precise receptor is the normal “commander” of the chloride channel, benzodiazepines can potentiate its influence. Additional drugs such as propofol and barbiturates not only potentiate the influence of GABA but are able to open the channel directly.
![Figure 3.](/view/journals/anpr/54/1/inline-i0003-3006-54-1-9-f03.gif)
Mechanism of N2O-induced anxiolysis. N2O is thought to cause activation of the benzodiazepine (BZ) binding site as its effects are blocked by flumazenil. This action facilitates γ-aminobutyric acid (GABA) activation of its binding site, resulting in chloride ion influx. The increased chloride ion concentration in the neuron might cause activation of calmodulin (CaM), which then activates the enzyme nitric oxide synthase (NOS). NOS converts the amino acid L-arginine (L-Arg) to L-citrulline (L-Cit) and NO, which stimulates the enzyme soluble guanylyl cyclase producing the second messenger cyclic guanosine monophosphate (cyclic GMP). The cyclic GMP, in turn, stimulates a cyclic GMP-dependent protein kinase (PKG) that leads to the anxiolytic drug effect.