The onset latencies of single-unit responses evoked by flashing visual stimuli were measured in the parvocellular (P) and magnocellular (M) layers of the dorsal lateral geniculate nucleus (LGNd) and in cortical visual areas V1, V2, V3, V4, middle temporal area (MT), medial superior temporal area (MST), and in the frontal eye field (FEF) in individual anesthetized monkeys. Identical procedures were carried out to assess latencies in each area, often in the same monkey, thereby permitting direct comparisons of timing across areas. This study presents the visual flash-evoked latencies for cells in areas where such data are common (V1 and V2), and are therefore a good standard, and also in areas where such data are sparse (LGNd M and P layers, MT, V4) or entirely lacking (V3, MST, and FEF in anesthetized preparation). Visual-evoked onset latencies were, on average, 17 ms shorter in the LGNd M layers than in the LGNd P layers. Visual responses occurred in V1 before any other cortical area. The next wave of activation occurred concurrently in areas V3, MT, MST, and FEF. Visual response latencies in areas V2 and V4 were progressively later and more broadly distributed. These differences in the time course of activation across the dorsal and ventral streams provide important temporal constraints on theories of visual processing.

Human visual function declines with age. Much of this decline is probably mediated by changes in the central visual pathways. We compared the stimulus selectivity of cells in primary visual cortex (striate cortex or V1) in young adult and very old macaque monkeys using single-neuron in vivo electrophysiology. Our results provide evidence for a significant degradation of orientation and direction selectivity in senescent animals. The decreased selectivity of cells in old animals was accompanied by increased responsiveness to all orientations and directions as well as an increase in spontaneous activity. The decreased selectivities and increased excitability of cells in old animals are consistent with an age-related degeneration of intracortical inhibition. The neural changes described here could underlie declines in visual function during senescence.

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Climbing fiber (CF) activation evokes a large all‐or‐nothing electrical response in Purkinje cells (PCs), the complex spike. It has been suggested that the role of CFs (and thus complex spikes) is that of a “teacher” in simple learning paradigms such as associative eyeblink conditioning. An alternative hypothesis describes the olivocerebellar system as part of a timing device and denies a role of the CF input in learning. To date, neither of these hypotheses nor others can definitively be verified or discounted. Similarly, the complex spike evades a clear understanding when it comes to the cellular events underlying complex spike generation. What is known, however, is that complex spikes are associated with large dendritic calcium signals that are required for the induction of long‐term depression (LTD) at the parallel fiber (PF)‐PC synapse. PF‐LTD is a form of long‐term synaptic plasticity that has been suggested to underlie certain forms of cerebellar motor learning. In contrast to the PF input, the CF input has been considered invariant. Our recent discovery of LTD at the CF input shows that complex spikes are less static than previously assumed. In addition to depression of CF‐evoked excitatory postsynaptic currents, long‐lasting, selective reduction of slow complex spike components could be observed after brief CF tetanization. To understand the functional implications of CF‐LTD, it is crucial to know the types of currents constituting the specific complex spike components. Here we review the “anatomy” of the complex spike as well as our observations of activity‐dependent complex spike waveform modifications. In addition, we discuss which properties CF‐LTD might add to the circuitry of the cerebellar cortex.