Signaling at nicotinic acetylcholine receptors (nAChRs) is vital for normal development of cerebral cortical circuits. These developing circuits are also shaped by fast-spiking (FS) inhibitory neurons in somatosensory cortex, an important model of development in rodents. Long-term deficits in sensory and cognitive processing can result from insults to either FS neurons or cholinergic function. Nicotine, the psychoactive component of tobacco, has been used extensively as an agonist to elucidate the functional properties of these receptors in the cholinergic system. Early exposure to nicotine during development results in long-term deficits in attention and sensory processing. While nicotinic dysfunction in FS neurons is implicated in a number of psychiatric and neurodevelopmental disorders, FS neurons have not been shown to have nicotinic responses in adults. Here, we establish the early timeline of how FS neurons respond to nicotine presynaptically and postsynaptically and test the prediction that nicotinic responses in FS neurons are developmentally regulated. We explored presynaptic effects from the early postnatal period through adolescence and found that nicotine drives early increases in frequency and amplitude of spontaneous synaptic currents. The increases in frequency persisted through development, but there were no amplitude changes after the second postnatal week, revealing an early window of nicotinic responses. The presynaptic effects we discovered demonstrate a potential weakness to nicotinic disruptions, including prenatal nicotine exposure and genetic mutations of nAChRs, specifically affecting FS neurons, which drive development of early cortical circuits. We also investigated somatodendritic effects of nicotine and found that FS neurons in primary somatosensory cortex (S1) lack these responses throughout development, as early as these neurons can be identified by their kinetic properties at P10. We ruled out desensitization as a mechanism for this finding, and RNAscope further revealed that FS neurons express abundant mRNA for multiple nAChR subunits beginning early in development. Finally, we found that Lynx1, a unique nicotinic modulator, is expressed in FS neurons in S1 from early in development and may act as a brake on nicotinic responses. The nicotinic mechanisms driving the development of FS neurons are understudied, despite the importance of both FS neurons and cholinergic signaling in cortical development. This work addresses this gap by examining nicotine's effects on FS neurons in the somatosensory cortex across different developmental stages, contributing to a better understanding of cholinergic regulation of these interneurons during cortical development.