PubMed · 5308085
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G A Todor. 1968. [Objective adaptometry in expert practice].. https://pubmed.ncbi.nlm.nih.gov/5308085/
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1. Nitric oxide (NO) production in the nervous system has been implicated in cellular mechanisms of learning and memory. Our study investigates an in vivo sensorimotor model of learning. It demonstrates that a localized vestibulocerebellar injection of the NO synthase inhibitor, L-NG-monomethyl-arginine (L-NMMA), which specifically blocks NO production, inhibited the acquisition of adaptive vestibulo-ocular reflex (VOR) gain increases but not gain decreases in the goldfish. 2. Restoration of NO production by concomitant administration of L-arginine (the substrate for NO synthase) and L-NMMA suppressed the inhibitory effect of L-NMMA on adaptive gain increases. 3. This effect of L-NMMA was stereospecific because injection of D-NMMA did not suppress adaptive VOR gain increases. 4. Injection of L-NMMA after VOR adaptation had no effect on retention, failing to alter the postadaptive recovery after a VOR gain increase. 5. In conclusion, acquisition of adaptive VOR gain increases are affected by cerebellar NO inhibition. However, because gain decreases are not, they may involve either non-NO cerebellar or extracerebellar mechanisms. In addition, different processes for acquisition and retention of gain increases may be operating, because inhibition of cerebellar NO affects the acquisition but not the retention phase.
Teleost rod photoreceptors elongate in the light and shorten in darkness. We are investigating the role of cAMP-dependent protein kinase (PKA), phosphatases and target phosphoproteins in the regulation of photoreceptor cell shape. Preparations of rod fragments, consisting of the motile inner segment with attached photosensory outer segment (RIS-ROS), undergo light-stimulated elongation in culture. The PKA-selective inhibitor, H89, enhanced RIS-ROS elongation in both light and darkness, suggesting that elongation is associated with dephosphorylation of PKA substrates. Okadaic acid and calyculin A, inhibitors of type 1 and 2A phosphatases, blocked light-dependent and light-independent elongation with relative potencies suggesting that elongation requires dephosphorylation by type 1 phosphatase in light and type 2A phosphatase in darkness. To identify targets of PKA and phosphatases, RIS-ROS were isolated from retinas prelabeled with 32P-orthophosphate, and then incubated in the presence of kinase inhibitors or phosphatase inhibitors. Two phosphoproteins, PP33 and PP35, were phosphorylated by PKA and dephosphorylated by type 1 or 2A phosphatases in light- and dark-cultured RIS-ROS. PP35 (but not PP33) was immunoprecipitated by an antibody to phosducin, a PKA-regulated modulator of phototransduction (Lee et al., 1992); PP35 was also phosphorylated in vitro by a Ca2+ calmodulin-activated kinase. PP33 further differed from PP35 in its phosphopeptide maps and phosphorylation by PKC. We conclude that RIS-ROS elongation is correlated with the dephosphorylation of PKA substrates by type 1 or 2A phosphatases. Candidate mediator proteins include PP35, a fish phosducin homolog, and PP33, a newly described photoreceptor phosphoprotein.
Prolonged adaptation to motion in a given direction produces distinctly different visual motion aftereffects (MAEs) when viewing static vs. dynamic test displays. The dynamic MAE can be exactly simulated by real motion, whereas the static MAE cannot. In addition, the magnitude of the dynamic MAE depends on the bandwidth of motion directions experienced during adaptation, whereas the static MAE does not. Evidently a stationary pattern does not directly activate the neural mechanisms affected during motion adaptation, whereas a dynamic visual display does. These results imply that the traditional explanation of the MAE needs modification.