Nociception can trigger an increase in the expression of different genes and their product that can mediate or modulate nociception related changes in the brain. There are a number of experimental model of inflammatory pain provide evidence that nociception results in increased expression of early immediate genes, c-fos that are associated with a hyper neuronal activity. It has also been proven that ɣ-Aminobutyric Acid (GABA), an amino acid neurotransmitter, can involve in inhibitory control of nociception and mediate sensory inputs at the spinal cord level. GABA itself has an effect on the expression of certain genes including c-fos in different disease conditions such as seizures. The present study was designed to investigate the effect of Gabapentin, an analogue of GABA, on the expression of c-fos in carrageenan induced-acute inflammation. Our results have been shown that in the animal receiving the only carrageenan, there was a marked increase in the expression of the c-fos gene in different brain areas with different intensity. Results show that Gabapentin treatment has a potency to inhibit the expression of the c-fos gene, which the hallmark of neuronal hyperactivity during inflammatory pain. Gabapentin also prevented the development of other pain-related behaviours, such as paw withdrawal latency responses; we observed that pain scores were not statistically different from baseline. This study suggests that modulating the neurotransmission of nociception can suppress effectively the level of nociception associated with acute inflammation with reducing side effect associated with the extended use of conventional anti-inflammatory drugs.