Changes

==Mechanism of Action==

==Mechanism of Action==

Barbituates act by depressing the central nervous system (CNS) by acting at the ''Gamma Aminobutyric Acid A'' receptors (GABAa). They mimic and enhance GABA, which is the principle inhibitory neurotransmitter in the CNS. Once bound to the GABAa receptor they reduce the rate of GABA dissocation and thereby ''increase chloride conductance'' is maintained resulting in hyperpolarisation of the membrane and reduced neuronal excitability. However, as the concentration of barbituate increases, it starts to have a direct effect on the chloride conductance and it is this that is thought to bring about the anaesthetic effects, while the GABA related increases causes a sedative effect. They act to depress the motor centres allowing there use as an ''anticonvulsant'' agent, as well as depressing the sensory centres and inducing an anesthetised state.  

Barbituates act by depressing the central nervous system (CNS) by acting at the ''Gamma Aminobutyric Acid A'' receptors (GABAa). They mimic and enhance GABA, which is the principle inhibitory neurotransmitter in the CNS. Once bound to the GABAa receptor they reduce the rate of GABA dissocation and thereby ''increase chloride conductance'' is maintained resulting in hyperpolarisation of the membrane and reduced neuronal excitability. However, as the concentration of barbituate increases, it starts to have a direct effect on the chloride conductance and it is this that is thought to bring about the anaesthetic effects, while the GABA related increases causes a sedative effect. They act to depress the motor centres allowing their use as an ''anticonvulsant'' agent, as well as depressing the sensory centres and inducing an anesthetised state.

==Pharmacological Considerations==

==Pharmacological Considerations==