Introduction: Fever and the use of drugs such as benzodiazepines (GABAA agonists) and ketamine (NMDA antagonist) occur relatively frequently in anesthesiology. Breathing is a pattern generated in the brain stem, product of a complex ponto-medullary networks, which control the respiratory motoneurons thanks to the interaction of the inspiratory neurons of the pre-Bötzinger complex and the espiratory ones of the Bötzinger complex. These neurons have membrane receptors of the GABAA and NMDA type, which show high thermo-dependence, however, the changes in the pattern of neuronal discharge induced by these drugs and changes in body temperature are unknown. Materials and methods: A validated model of pre-inspiratory neuron (pre-Bötzinger complex) was generated, increasing the synaptic GABAA weight equivalent to the effect of benzodiazepines or reducing the NMDA synaptic weight equivalent to the effect of ketamine in hypo- (35°C), normo- (37°C) or hyperthermia (40°C) quantifying the number and amplitude of neuronal discharges. Results: Increase in GABAA or reduction of NMDA synaptic weights at temperatures of 35°C, 37°C or 40°C proportionally reduced the number of spikes and the amplitude of the action potential of the Pre-I neuronal, showing dose-response 2nd order polynomial curves with increased slopes at 35°C and 40°C. Conclusion: benzodiazepines or ketamine through its receptors GABAA and NMDA modify in silico the discharge pattern of Pre-I neuron from Pre-Bötzinger nucleus, showing more gabaergic effect and higher thermo-dependence in the dose-response curves during hypo and hyperthermia which are relevant for clinical practice.