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.

The zones of the flocculus have been mapped in many species with a noticeable exception, the mouse. Here, the functional map of the mouse was constructed via extracellular recordings followed by tracer injections of biotinylated-dextran-amine and immunohistochemistry for heat-shock protein-25. Zones were identified based on the Purkinje cell complex spike modulation occurring in response to optokinetic stimulation. In zones 1 and 3 Purkinje cells responded best to rotation about a horizontal axis oriented at 135 degrees ipsilateral azimuth, whereas in zones 2 and 4 they responded best to rotation about the vertical axis. The tracing experiments showed that Purkinje cells of zone 1 projected to the parvicellular part of lateral cerebellar nucleus and superior vestibular nucleus, while Purkinje cells of zone 3 projected to group Y and the superior vestibular nucleus. Purkinje cells of zones 2 and 4 projected to the magnocellular and parvicellular parts of the medial vestibular nucleus, while some also innervated the lateral vestibular nucleus or nucleus prepositus hypoglossi. The climbing fiber inputs to Purkinje cells in zones 1 and 3 were derived from neurons in the ventrolateral outgrowth of the contralateral inferior olive, whereas those in zones 2 and 4 were derived from the contralateral caudal dorsal cap. Purkinje cells in zones 1 and 2, but not in zones 3 and 4, were positively labeled for heat-shock protein-25. The present study illustrates that Purkinje cells in the murine flocculus are organized in discrete zones with specific functions, specific input - output relations, and a specific histochemical signature.

The responses of neurons in areas V1 (17) and V2 (18) of anesthetized and paralyzed rhesus monkeys and cats were recorded while presenting a set of computer-generated visual stimuli that varied in pattern, texture, luminance, and contrast. We find that a class of extrastriate cortical cells in cats and monkeys can signal the presence of boundaries regardless of the cue or cues that define the boundaries. These cue-invariant (CI) cells were rare in area V1 but easily found in V2. CI cortical cells responded more strongly to more salient boundaries regardless of the cue defining the boundaries. Many CI cortical cells responded to illusory contours and exhibited the same degree of orientation and direction selectivity when tested with boundaries defined by different cues. These cells have significant computational power inherent in their receptive fields since they were able to generalize across stimuli and integrate multiple cues simultaneously in order to signal boundaries. Cells in higher order cortical areas such as MT (Albright, 1992), MST (Geesaman & Anderson, 1996), and IT (Sary et al., 1993) have previously been reported to respond in a cue invariant fashion. The present results suggest that the ability to respond to boundaries in a cue-invariant manner originates at relatively early stages of cortical processing.

The climbing fibre (CF) input controls cerebellar Purkinje cell (PC) activity as well as synaptic plasticity at parallel fibre (PF)-PC synapses. Under high activity conditions, CFs release not only glutamate, but also the neuropeptide corticotropin-releasing factor (CRF). Brief periods of such high CF activity can lead to the induction of long-term depression (LTD) at CF-PC synapses. Thus, we have examined for the first time the role of CRF in regulating excitatory postsynaptic currents (EPSCs) and long-term plasticity at this synapse. Exogenous application of CRF alone transiently mimicked three aspects of CF-LTD, causing reductions in the CF-evoked excitatory postsynaptic current, complex spike second component and complex spike afterhyperpolarization. The complex spike first component is unaffected by CF-LTD induction and was similarly unaffected by CRF. Application of a CRF receptor antagonist reduced the expression amplitude and induction probability of CF-LTD monitored at the EPSC level. Collectively, these results suggest that under particular sensorimotor conditions, co-release of CRF from climbing fibres could down-regulate excitatory transmission and facilitate LTD induction at CF-PC synapses. Inhibition of either protein kinase C (PKC) or protein kinase A (PKA) attenuated the effects of CRF upon CF-EPSCs. We have previously shown that CF-LTD induction is PKC-dependent, and here demonstrate PKA-dependence as well. These results suggest that both the acute effects of CRF on CF-EPSCs as well as the facilitating effect of CRF on CF-LTD induction can be explained by a CRF-mediated recruitment of PKC and PKA.

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