The motor systems of the mammalian brain are a remarkable product of many millions of years of evolution. It is the motor systems that make us and other mammals mobile, that guide our actions in response to sensory information and conversely modulate the very nature of the sensory input that our brain receives. The mystacial vibrissae or whiskers present on the face of mice are important sensors that provide high resolution tactile information to the brain. Whereas the pathways that are involved in signaling and processing sensory information from the whiskers have been the subject of intense investigation for many years, we know relatively little about how whisker movements are controlled by the brain. In the first part of the thesis, I present evidence for two parallel pathways originating from the neocortex that control antagonistic movements of the whiskers. I first describe whisker movements elicited upon Channelrhodopsin-2 (ChR2) stimulation of whisker somatosensory cortex (wS1) and whisker motor cortex (wM1). At short latencies, optogenetic stimulation of wS1 drove whisker retraction while optogenetic stimulation of wM1 drove rhythmic whisker protraction. Next, using recent developments in Rabies virus retrograde tracing, I mapped the location of the motor neurons in the facial nucleus, finding two distinct neuron pools for the extrinsic (retractor) muscle Nasolabialis and the intrinsic (protractor) follicular muscle. These distinct motor neuron populations received premotor input from different sources in the brainstem. While the premotor neurons of the extrinsic muscle were located more densely in the spinal trigeminal nucleus (Sp5), the premotor neurons of the intrinsic muscle were located more densely in the reticular formation (Rt). Anterograde tracing from wS1 and wM1 cortex revealed a complementary distribution of axons in the brainstem. Whereas wS1 strongly innervated Sp5, wM1 innervated the Rt. These data therefore begin to unravel the circuitry from the neocortex to the whisker motor neurons. In the second part of the thesis, I investigated the subthreshold and spiking correlates of whisker movements using whole-cell current clamp recordings of individual excitatory neurons in wM1. Brief 1 ms optogenetic stimulation of wS1 elicited rhythmic whisking after long latencies which was abolished upon pharmacological inactivation of wM1. Whole-cell recordings in wM1 during wS1 stimulation showed that the long-range synaptic input from wS1 to wM1 is encoded as a bi-phasic membrane potential response with an early depolarizing post-synaptic potential (Dep. PSP), followed by a hyperpolarizing post-synaptic potential (Hyp. PSP) in individual wM1 neurons. Approximately 150 ms after the wS1 stimulus, the Vm showed a rebound depolarization, which, on most trials, was followed by late rhythmic whisking. Whole-cell recordings during self-generated whisker movements showed that upon whisking, wM1 undergoes a profound cortical state change, where the mean Vm is more depolarized, slow fluctuations of the Vm are reduced and spike rates in layer 5 increase. Aligning the membrane potential trajectories to the onset of whisker movement epochs revealed that changes in Vm occurred almost 100 ms before movement onset. Finally, an examination of the Vm dynamics during rhythmic whisking showed that the Vm of individual wM1 neurons is modulated by the phase of the whisk cycle. This modulation is stronger in layer 2/3 compared to layer 5.