Recent research has been performed to understand how/if variations of metabolism may condition brain activity. Specifically, studies on hippocampus have gained relevance owing to its primary importance in cognitive processes. In this regard, in our laboratory, we found that feeding cycle influences the effect of insulin over the biophysics of certain voltage-activated potassium (K+) channels in acutely isolated rat hippocampal CA1 neurones (1). Other alterations of neuroactivity patterns have been detected during the feeding cycle, which suggest the involvement of other ion channels on these processes. Hence, here, it is intended to study mechanisms underlying the adaptation of intrinsic neuronal membrane properties during such metabolic conditions. In this work, electrophysiological techniques, namely whole-cell voltage clamp and excised inside-out patches, were used to study the biophysics of voltage-gated sodium (Na+) channels in acutely isolated CA1 hippocampal neurons, from Wistar rats (P21-29). These were decapitated after being subjected to overnight fasting and subsequently either fed for 45min (fed conditions) or not fed (Fasted conditions). Whole-cell Na+ currents, measured in fed and fasted condition, depicted the following values of current density: -1536 ± 120 pA/pF (n=21) and -995 ± 96 pA/pF (n=29), respectively. The average fitting parameters of steady-state of inactivation (-51.23 ± 1.4mV, fed conditions, n=24, and -58.41 ± 1,8mV, fasted conditions, n=27) clearly indicate that Na+ currents exhibited a significant depolarized voltage shift upon feeding. However, no differences were observed in time constant of inactivation (τh), neither in the rate of recovery from the inactivated state. In order to understand such differences obtained in the whole-cell currents, it was mandatory to survey the single Na+ activity. The Na+ currents recorded in excised inside-out configuration showed interesting differences in single channel conductance: 17.6 ± 0.96pS (fed, n=5) and 11.85 ± 1.01pS (fasted, n=8). Such differences corroborate the results of macroscopic recordings but do not exclude a change in the channel expression at the surface membrane. Thus, expression of Na+ channels on the plasma membrane of hippocampal neurons was also addressed by using an antibody that recognizes all voltage-gated Na+ channel (2). Results suggest a variation in the expression of these channels during feeding cycle. This work gives new insights into the comprehension of the influence of feeding on brain function. Namely, its effect on biophysics and molecular expression of voltage gated sodium channels present on the plasma membrane of the CA1 hippocampal neurons.