Prenatal nicotine exposure evokes changes in the incidence and degree of fetal electrocortical activation

The effects of acute and chronic nicotine (N) administration on fetal electrocorticogram (ECoG) were investigated with spectral analysis. Fetal lambs were instrumented surgically to permit unanesthetized ECoG monitoring and N administration. Acute exposure studies used 4-hr constant-rate infusions at 0.6, 3 or 10 mg/hr. Chronic exposure studies used continuous infusions at 1.2 mg/hr for 7 days. The fast Fourier transform and several derivative parameters were used to quantitate the fetal ECoG during both control records and N infusions. Four states were identified and quantitated in the control ECoG: high-voltage slow activity (State I); low-voltage, fast activity (State IV); and two transitional states of intermediate amplitude and frequency. Acute N infusions elicited changes in the incidence and degree of electrocortical activation that were biphasically dose-related. The 0.6-mg/hr infusion evoked electrocortical activation through an increase in the incidence of State IV. Higher infusion rates elicited progressively less electrocortical activation. The 3-mg/hr infusion affected marginal activation, through a reduction in the incidence of State I. The 10-mg/hr infusion elicited mixed activation and depression, as assessed by multiple parameter changes. Desensitization of several responses diminished the magnitude of depressive effect observed during the 3- and 10-mg/hr infusions. Chronic nicotine infusions elicited progressive augmentation of electrocortical activation, through increases in the incidence and frequencies of State IV. Tolerance to this activating response was not observed.