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Concomitant consumption of ethanol and benzodiazepines (BZDs) play a significant role in the development of tolerance and physical dependence of BZDs. Adaptations within the glutamatergic system in response to prolonged ethanol exposure may in some respects, stimulate the physiological processes associated with experience-dependent synaptic plasticity. This study aims to investigate several changes that occur in central nervous system (CNS) receptors GABA, NMDA, 5-HT-3 (serotonin) and AMPA during concomitant consumption benzodiazepines and alcohol. Published literature provide an evidence of abuse potential of alcohol and its effect on GABAA receptor synaptic plasticity in neuronal disorders. These studies reveal that alterations in synaptic functions are believed to play a major role; although tolerance to alcohol intoxication probably occurs at multiple levels,. In particular, compensatory changes in excitatory NMDA and inhibitory GABA receptors probably contribute to the development of ethanol tolerance. These receptors are the sites of action of a number of drugs including barbiturates, benzodiazepines and anesthetics. The results also reveal contributions by other factors like decreased flux of chloride ion in the channels of chore at the GABAA and GABAB receptors, as well as the flux of calcium in NMDA responsible for neuronal and peripheral tissue disorders.