Neurons in the cerebral cortex are organized into anatomical columns, with ensembles of cells arranged from the surface to the white matter. Within a column, neurons often share functional properties, such as selectivity for stimulus orientation; columns with distinct properties, such as different preferred orientations, tile the cortical surface in orderly patterns. This functional architecture was discovered with the relatively sparse sampling of microelectrode recordings. Optical imaging of membrane voltage or metabolic activity elucidated the overall geometry of functional maps, but is averaged over many cells (resolution >100 microm). Consequently, the purity of functional domains and the precision of the borders between them could not be resolved. Here, we labelled thousands of neurons of the visual cortex with a calcium-sensitive indicator in vivo. We then imaged the activity of neuronal populations at single-cell resolution with two-photon microscopy up to a depth of 400 microm. In rat primary visual cortex, neurons had robust orientation selectivity but there was no discernible local structure; neighbouring neurons often responded to different orientations. In area 18 of cat visual cortex, functional maps were organized at a fine scale. Neurons with opposite preferences for stimulus direction were segregated with extraordinary spatial precision in three dimensions, with columnar borders one to two cells wide. These results indicate that cortical maps can be built with single-cell precision.

The role of divalent transition metal ions in neural function is poorly understood. In excess, these ions are associated with neurological disorders such as Wilson's disease, Pick's disease and epileptic seizures. We suggest that zinc ions, which are contained in nerve terminals, are extruded into the extracellular space during neuronal activity. Excessive levels of zinc may be released during intense neuronal activation, and contribute to the paroxysm and toxic damage observed. Zinc ions are contained in high concentrations in mossy fibres of the hippocampal formation, and it is the postsynaptic neurones of these fibres which are most susceptible to the toxic effects of kainic acid, a potent convulsant, or to chronic exposure to organometallic compounds. Here we demonstrate for the first time that Zn2+ is released into the extracellular space during excitation of hippocampal slices.

In vivo whole-cell recordings revealed that during repeated stimulation, synaptic responses to deflection of facial whiskers rapidly adapt. Extracellular recordings in the somatosensory thalamus revealed that part of the adaptation occurs subcortically, but because cortical adaptation is stronger and recovers more slowly, cortical mechanisms must also contribute. Trains of sensory stimuli that produce profound sensory adaptation did not alter intrinsic membrane properties, including resting membrane potential, input resistance, and current-evoked firing. Synaptic input evoked via intracortical stimulation was also unchanged; however, synaptic input from the somatosensory thalamus was depressed by sensory stimulation, and this depression recovered with a time course matching that of the recovery of sensory responsiveness. These data strongly suggest that synaptic depression of thalamic input to the cortex contributes to the dynamic regulation of neuronal sensitivity during rapid changes in sensory input.

Pigeons were trained to peck either of two response keys for food reinforcement on equated aperiodic schedules. The distribution of responding at the two keys was studied as reinforcement was delayed for various durations. The relative frequency of responding at each key was shown to match the relative immediacy of reinforcement, immediacy defined as the reciprocal of the delay of reinforcement.The present experiment extends the investigation of reinforcement delay described by Chung (1965 auditory feedback to the pigeon. The chamber was illuminated by a white bulb, and, except when the magazine was operated, each response key was transilluminated by a 7-w red bulb. A continuous white masking noise was delivered during sessions. ProcedurePecks on either of the two response keys were, at first, reinforced on a variable-interval schedule with an average interval of 1 min. Two independent programmers arranged reinforcements for responses on the two response keys, with the restriction that a switch from one response key to the other prevented reinforcement for 1 sec (changeover delay or COD l-sec). When the rate of pecking on the two keys became stable and approximately equal, delays of reinforcement were initiated. For subjects 237, 236, 415, and 416, responses on the left key were reinforced after an 8-sec delay (standard key). Reinforcements for responses on the right key were delayed for various durations ranging from 1 to 30 sec (experimental key). The intervals of delay imposed on the experimental key, in-irregular order, were: 1, 2, 4, 6, 8, 12, 16, 20, 24, and Between the response-to-be-reinforced and delivery of the reinforcement, the chamber 67 1967, 10,[67][68][69][70][71][72][73][74] NUMBER I (JANUARY)