This study investigates the neurophysiological basis of aperiodic EEG and the background spectral trend. Using biophysical modeling, the researchers show that aperiodic neural activity can generate detectable scalp potentials and shape broadband EEG features, but these aperiodic signals do not significantly affect brain rhythm quantification. They also demonstrate that rhythmic EEG signals are corrupted by shifts in synapse properties. The study uses EEG recordings from human subjects under propofol administration, a GABA receptor agonist, to show that propofol causes broadband EEG changes that match its known effects on GABA receptors. The researchers then use their model to correct for these confounding broadband changes, revealing that delta power increases within seconds of individuals losing consciousness. The study highlights how EEG signals are shaped by neurophysiological factors beyond brain rhythms and how these signals can mislead traditional EEG interpretation. The research also shows that the EEG spectral trend is influenced by synaptic kinetics, excitatory-inhibitory ratios, and aperiodic network dynamics. The study concludes that spectral detrending is necessary to accurately interpret EEG data, especially when analyzing the effects of pharmacological interventions. The findings suggest that changes in synaptic current properties necessitate detrending to accurately interpret spectral changes as variations in neural activity. The study also emphasizes the importance of considering the physiological and biophysical justification for spectral detrending.This study investigates the neurophysiological basis of aperiodic EEG and the background spectral trend. Using biophysical modeling, the researchers show that aperiodic neural activity can generate detectable scalp potentials and shape broadband EEG features, but these aperiodic signals do not significantly affect brain rhythm quantification. They also demonstrate that rhythmic EEG signals are corrupted by shifts in synapse properties. The study uses EEG recordings from human subjects under propofol administration, a GABA receptor agonist, to show that propofol causes broadband EEG changes that match its known effects on GABA receptors. The researchers then use their model to correct for these confounding broadband changes, revealing that delta power increases within seconds of individuals losing consciousness. The study highlights how EEG signals are shaped by neurophysiological factors beyond brain rhythms and how these signals can mislead traditional EEG interpretation. The research also shows that the EEG spectral trend is influenced by synaptic kinetics, excitatory-inhibitory ratios, and aperiodic network dynamics. The study concludes that spectral detrending is necessary to accurately interpret EEG data, especially when analyzing the effects of pharmacological interventions. The findings suggest that changes in synaptic current properties necessitate detrending to accurately interpret spectral changes as variations in neural activity. The study also emphasizes the importance of considering the physiological and biophysical justification for spectral detrending.