Validity of the speed-accuracy tradeoff for prehension movements.

Subjects (n=12) grasped mirror-viewed visual targets with thumb and index finger, while prescribed movement time differed between blocks of trials. The variability of both final grip aperture (i.e. distance between thumb and index finger) and of final wrist position increased with decreasing movement time, indicating the existence of a speed-accuracy tradeoff both in the grasp and in the transport component of prehension. This tradeoff was limited to relatively short movement times (<400 ms) for the grasp component, but it extended to longer movement times for the transport component, which supports the view that the two components are controlled by separate mechanisms.

The coordination of hand transport and grasp formation during single- and double-perturbed human prehension movements.

We investigated the mechanisms underlying human prehension movements, by perturbing the size and position of virtual targets. Subjects grasped virtual target discs with thumb and index finger. In 25% of trials, target size or position (single perturbation), or both (double perturbation) were changed 300 ms after target appearance. The experiments were designed such that the kinematic profiles of grasp formation and hand transport had a similar shape, and were analysed by the same algorithm. We found that grasp kinematics were influenced by changes of target position, and transport kinematics by changes of target size; we also found that the kinematics of double-perturbation trials could not be explained as a linear combination of single-perturbation effects. These findings confirm and expand previous evidence against the view that grasp and transport are controlled by fully independent channels. Most importantly, we found that the time of correction onset was not the same for grasp and transport, neither in single- nor in double-perturbation trials. This outcome argues against a holistic (single-channel) model of prehension; instead, our data are consistent with the notion of two mutually coupled channels.

Speed-accuracy trade-off of grasping movements during microgravity.

BACKGROUND: Earthbound studies have shown that for pointing movements there is a specific relationship between movement speed, amplitude, and accuracy that is known as Fitts' law. We investigated the validity of Fitts' law for grasping movements in normal and microgravity. METHOD: Subjects performed grasping movements toward virtual targets under three different time constraint conditions before and during exposure to microgravity in parabolic flights. RESULTS: The "speed-accuracy trade-off" phenomenon was observed for the grasp component of prehension movements. The results were quantitatively similar in normal and microgravity such that increasing the speed resulted in a diminished accuracy. CONCLUSIONS: Fitts' law is partially valid for grasping movements toward virtual targets without visual feedback of the hand in normal gravity. In a microgravity environment, performance of grasping movements also follows some of the predictions of Fitts' law.

Reprogramming of grip aperture in a double-step virtual grasping paradigm.

The present study investigated the control of manual prehension movements in humans. Subjects grasped luminous virtual discs with the thumb and index finger, and we recorded the instantaneous grip aperture, defined as the 3-D distance between the thumb and index finger. Target size could remain constant (single-step trials) or unexpectedly change shortly after target appearance (double-step trials). In single-step responses, grip aperture varied throughout the movement in a consistent fashion. Double-step responses exhibited distinct corrective modifications, which followed the target change with a latency similar to the normal reaction time. This suggests that visual size information has a fast and continuous access to the processes involved in grip formation. The grip-aperture profiles of single-step responses had a different shape when the target called for an increase than when it called for a decrease in the initial finger distance. The same asymmetry was observed for aperture corrections in double-step trials. These findings indicate that increases and decreases of grip aperture are controlled through separate processes, engaged equally by the appearance and by the size change of a target. Corrections of grip aperture in double-step trials had a higher peak velocity and reached their maximum as well as their final value earlier than the aperture profiles of single-step trials. Nevertheless, the total duration of double-step trials was prolonged. These response characteristics did not fit with either of the three corrective strategies previously proposed for double-step pointing movements, which could indicate that grasping and pointing movements are controlled by different mechanisms. However, more data are needed to substantiate this view.

Identification of a functional cAMP response element in the secretogranin II gene.

Secretogranin II is an acidic secretory protein with a widespread distribution in secretory granules of neuronal and endocrine cells. The secretogranin II gene contains, like other members of the granin family, a cAMP response element (CRE) in its upstream region. To investigate the functional significance of this motif, intracellular cAMP levels were increased in a neuronal cell line derived from the septal region of the brain and the level of secretogranin II gene expression was analysed. It was found that increased cAMP levels did, in fact, induce secretogranin II gene expression. To analyse the cis-acting sequence responsible for this induction, a hybrid gene containing the upstream region of the mouse secretogranin II gene fused to beta-globin as a reporter was constructed. Transfection analysis revealed that cAMP-induced transcription of the secretogranin II promoter/beta-globin gene in septal and insulinoma cells. DNA-protein binding assays showed that recombinant CRE-binding protein (CREB), produced in bacteria or human cells, bound in a sequence-specific manner to the secretogranin II promoter CRE. Moreover, deletion mutagenesis revealed that the CRE motif is a bifunctional genetic regulatory element in that it mediates basal as well as cAMP-stimulated transcription. Interestingly, cAMP had no effect upon secretogranin II gene transcription in PC12 and neuroblastoma cells. An increase in the intracellular cAMP concentration activated a GAL4-CREB fusion protein upon transcription in neuroblastoma cells indicating the integrity of the cAMP signaling pathway to the nucleus. Basal as well as cAMP-stimulated transcription, directed from the secretogranin II promoter was, however, impaired in insulinoma cells by overexpression of CREB-2, a negative-acting CRE-binding protein. These results indicate that competitive effects are likely to occur between CRE-bound transcriptional activators and repressors. We conclude that cAMP-stimulated induction of secretogranin II gene transcription is mediated by the CRE motif in a cell-type-specific manner, and is likely to depend on the balance between positive and negative CRE-binding proteins in a particular cell type.

Immunological identification of candidate proteins involved in regulating active shape changes of outer hair cells.

By employing immunological methods, it has been demonstrated that myosin, myosin light chain (MLC) and myosin light chain kinase (MLCK) proteins in outer hair cells (OHC) are immunologically different from isoforms in platelets, smooth muscle and heart muscle, and are probably more related to isoforms found in red blood cells (RBC). Moreover, proteins related to band 3 protein (b3p) and protein 4.1 (p 4.1), ankyrin as well as fodrin and spectrin, but not glycophorin, have been identified in isolated OHCs. Both OHCs and RBC differ from other motile non-muscle cells in their lack of smooth muscle isoforms of actin, their common high levels of spectrin-, ankyrin- and band 3-like proteins, as well as the expression of the 80 kDa protein 4.1 isoform. The data support the notion that motility of OHC may be based upon regulation of the b3p/p 4.1/ankyrin complex, and thus may be reminiscent to the active shape changes in RBC.

Differential regulation of chromogranin B and synapsin I gene promoter activity by cAMP and cAMP-dependent protein kinase.

cAMP has neutrotrophic effects in the nervous system. We have investigated whether there is a correlation between cAMP-induced neurite outgrowth and induction of chromogranin B and synapsin I gene expression. These genes encode marker proteins of distinct populations of vesicles in neurons, neuroendocrine and endocrine cells, and in addition, they contain a cAMP response element (CRE) in their upstream regions, making it likely that cAMP-induced neuronal differentiation might be accompanied by increased transcription of these genes. We increased intracellular cAMP levels in neuronal and neuroendocrine cells and analyzed the levels of chromogranin B and synapsin I mRNA. Our data revealed that, while chromogranin B mRNA was in fact induced following cAMP stimulation, synapsin I mRNA was not affected. To analyze the cis-acting sequences, we constructed hybrid genes containing the upstream region of the mouse chromogranin B gene fused to a reporter gene. Similar plasmids containing the synapsin I or the glucagon promoter were constructed. Transfections of neuronal and endocrine cells, together with deletion mutagenesis, revealed that the CRE of the chromogranin B gene mediated the effect of cAMP upon transcription. This effect was mimicked by overexpression of the catalytic subunit of the cAMP-dependent protein kinase. In addition, overexpression of the negative-acting CRE-binding protein CREB-2 revealed that the chromogranin B CRE functions as a bifunctional genetic regulatory element in that it mediates basal as well as cAMP-stimulated transcription. Synapsin I gene expression, however, was not induced by either elevated intracellular cAMP concentration or by overexpression of protein kinase A, although a similar pattern of proteins, including CREB, bound to the synapsin I and chromogranin B CRE in vitro. Thus while the CRE element in the chromogranin B gene promoter is responsive to cAMP, the same element, when present in the synapsin I promoter, does not confer cAMP inducibility.

Cultivar-specific elicitation of barley defense reactions by the phytotoxic peptide NIP1 from Rhynchosporium secalis.

Resistance of barley to the phytopathogenic fungus, Rhynhosporium secalis race US238.1, was found to be controlled by resistance gene Rrs1, which segregated in a manner characteristics for a codominant gene. PRHv-1, a thaumatin-like pathogenesis-related protein, was shown to be encoded by a gene family on chromosome 1. As part of the barley defense response, significant accumulation of PRHv-1 and peroxidase transcripts was induced early during pathogenesis in two Rrs1 cultivars but not or to a lower level in a near-isogenic, susceptible rrs1 cultivar or a cultivar lacking known resistance genes. R. secalis secretes a small group of necrosis-inducing peptides. One of these, NIP1, which was detected in culture filtrates only of fungal race US238.1, was found to elicit the accumulation of PRHv-1 and peroxidase mRNAs in Rrs1 cultivars with a time course similar to that upon fungal infection. Therefore, NIP1 is a candidate for the product of fungal avirulence gene avrRrs1, which, together with barley resistance gene Rrs1, determines incompatibility of the interaction.