This thesis aims to understand cellular mechanisms that underlie ensemble activity in the primary visual cortex (V1). First, I asked, when V1 is activated by sensory stimulation, what is the temporal correlation between the synaptic inputs to nearby neurons? This question underlies the origin of correlated activity, the mechanism of how visually evoked activity emerges and propagates in cortical circuits, and the relationship between spontaneous and evoked activity. I have recorded membrane potential (V_m) from pairs of V1 complex cells in anesthetized cats and found that visual stimulation suppressed low-frequency membrane potential synchrony (0-10 Hz), and often increased synchrony at high frequencies (20-80 Hz). The increase in high-frequency synchrony occurred for neurons with similar orientation preferences and for neurons with different orientation preferences and occurred for a wide range of stimulus orientations. Thus, while only a subset of neurons spike in response to visual stimulation, a far larger proportion of the circuit is correlated with spiking activity through subthreshold, high-frequency synchronous activity that crosses functional domains. Next, to examine how the feedforward inputs contribute to the visually evoked V_m fluctuations, I combined whole-cell recordings of L2/3 complex cells with extracellular recordings of L4 simple cells. I found that spikes of simple cells were coupled to the trough phase of V _m fluctuations in complex cells. The data are reminiscent of the asymmetrical spike cross-correlation between simple and complex cells reported previously. Could these V_m STA waveforms indicate monosynaptic connectivity between recorded cells, or rather reflect more complex interactions in the circuits? I then applied juxtacellular stimulation to drive simple cell and examined the postsynaptic effect. The V_m STAs calculated with visually driven spikes and juxtacellularly induced spikes were very different. The data suggest that cells showing asymmetrical V_m STA waveforms were not necessarily connected. Finally, we found that the synaptic inputs that were arriving at simple and complex cells were offset in time. The results bear on the interpretation of spike cross-correlograms, challenge the relationship between neural activity and connectivity and provide insight into the feedforward modulation of complex-cell activity by inputs from simple cells.