Short-term saccadic adaptation in the macaque monkey: a binocular mechanism.

Saccadic eye movements are rapid transfers of gaze between objects of interest. Their duration is too short for the visual system to be able to follow their progress in time. Adaptive mechanisms constantly recalibrate the saccadic responses by detecting how close the landings are to the selected targets. The double-step saccadic paradigm is a common method to simulate alterations in saccadic gain. While the subject is responding to a first target shift, a second shift is introduced in the middle of this movement, which masks it from visual detection. The error in landing introduced by the second shift is interpreted by the brain as an error in the programming of the initial response, with gradual gain changes aimed at compensating the apparent sensorimotor mismatch. A second shift applied dichoptically to only one eye introduces disconjugate landing errors between the two eyes. A monocular adaptive system would independently modify only the gain of the eye exposed to the second shift in order to reestablish binocular alignment. Our results support a binocular mechanism. A version-based saccadic adaptive process detects postsaccadic version errors and generates compensatory conjugate gain alterations. A vergence-based saccadic adaptive process detects postsaccadic disparity errors and generates corrective nonvisual disparity signals that are sent to the vergence system to regain binocularity. This results in striking dynamical similarities between visually driven combined saccade-vergence gaze transfers, where the disparity is given by the visual targets, and the double-step adaptive disconjugate responses, where an adaptive disparity signal is generated internally by the saccadic system.

Macaque pontine omnipause neurons play no direct role in the generation of eye blinks.

We recorded the activity of pontine omnipause neurons (OPNs) in two macaques during saccadic eye movements and blinks. As previously reported, we found that OPNs fire tonically during fixation and pause about 15 ms before a saccadic eye movement. In contrast, for blinks elicited by air puffs, the OPNs paused <2 ms before the onset of the blink. Thus the burst in the agonist orbicularis oculi motoneurons (OOMNs) and the pause in the antagonist levator palpabrae superioris motoneurons (LPSMNs) necessarily precede the OPN pause. For spontaneous blinks there was no correlation between blink and pause onsets. In addition, the OPN pause continued for 40-60 ms after the time of the maximum downward closing of the eyelids, which occurs around the end of the OOMN burst of firing. LPSMN activity is not responsible for terminating the OPN pause because OPN resumption was very rapid, whereas the resumption of LPSMN firing during the reopening phase is gradual. OPN pause onset does not directly control blink onset, nor does pause offset control or encode the transition between the end of the OOMN firing and the resumption of the LPSMNs. The onset of the blink-related eye transients preceded both blink and OPN pause onsets. Therefore they initiated while the saccadic short-lead burst neurons were still fully inhibited by the OPNs and cannot be saccadic in origin. The abrupt dynamic change of the vertical eye transients from an oscillatory behavior to a single time constant exponential drift predicted the resumption of the OPNs.

Localization of electrogenic Na/bicarbonate cotransporter NBCe1 variants in rat brain.

The activity of HCO(3)(-) transporters contributes to the acid-base environment of the nervous system. In the present study, we used in situ hybridization, immunoblotting, immunohistochemistry, and immunogold electron microscopy to localize electrogenic Na/bicarbonate cotransporter NBCe1 splice variants (-A, -B, and -C) in rat brain. The in situ hybridization data are consistent with NBCe1-B and -C, but not -A, being the predominant NBCe1 variants in brain, particularly in the cerebellum, hippocampus, piriform cortex, and olfactory bulb. An antisense probe to the B and C variants strongly labeled granule neurons in the dentate gyrus of the hippocampus, and cells in the granule layer and Purkinje layer (e.g. Bergmann glia) of the cerebellum. Weaker labeling was observed in the pyramidal layer of the hippocampus and in astrocytes throughout the brain. Similar, but weaker labeling was obtained with an antisense probe to the A and B variants. In immunoblot studies, antibodies to the A and B variants (alphaA/B) and C variant (alphaC) labeled approximately 130-kDa proteins in various brain regions. From immunohistochemistry data, both alphaA/B and alphaC exhibited diffuse labeling throughout brain, but alphaA/B labeling was more intracellular and punctate. Based on co-localization studies with antibodies to neuronal or astrocytic markers, alphaA/B labeled neurons in the pyramidal layer and dentate gyrus of the hippocampus, as well as cortex. alphaC labeled glia surrounding neurons (and possibly neurons) in the neuropil of the Purkinje cell layer of the cerebellum, the pyramidal cell layer and dentate gyrus of the hippocampus, and the cortex. According to electron microscopy data from the cerebellum, alphaA/B primarily labeled neurons intracellularly and alphaC labeled astrocytes at the plasma membrane. In summary, the B and C variants are the predominant NBCe1 variants in rat brain and exhibit different localization profiles.