Pointing to a remembered visual target involves the transformation of binocular visual information into an appropriate motor output. Errors generated during pointing tasks may indicate the reference frames used by the CNS for the transformation and storage of the target position. Previous studies have proposed eye-, shoulder-, or hand-centered reference frames for various pointing tasks, depending on visual conditions. We asked subjects to perform pointing movements to remembered three-dimensional targets after a fixed memory delay. Pointing movements were executed under dim lighting conditions, allowing vision of the fingertip against a uniform black background. Subjects performed repeated movements to targets distributed uniformly within a small (radius 25 mm) workspace volume. In separate blocks of trials, subjects pointed to different workspace regions that varied in terms of distance and direction from the head and shoulder. Additional blocks were performed that differed in terms of starting position, effector hand, head rotation, and memory delay duration. Final pointing positions were quantified in terms of the constant and variable errors in three dimensions. The orientation of these errors was examined as a function of workspace location to identify the underlying reference frames. Subjects produced anisotropic patterns of variable error, with greater variability for endpoint distances from the body. The major axes of the variable-error tolerance ellipsoids pointed toward the eyes of the subject, independent of workspace region, effector hand (left or right), initial hand position, and head rotations. Constant errors were less consistent across subjects, but also tended to point toward the head and body. Both overshoots and undershoots of the target position were observed. Increasing the duration of the memory delay period increased the size but did not alter the orientation of the variable-error ellipsoids. Variability of the endpoint positions increased equally in all three Cartesian directions as the memory delay increased from 0.5 to 8.0 s. The anisotropy of variable errors indicates a viewer-centered reference frame for pointing to remembered visual targets with vision of the finger. The anisotropy of pointing variability stems from variability in egocentric binocular cues as opposed to reliance on allocentric visual references or to specific approximations in the sensorimotor transformation. Nevertheless, observed increases in variability with longer memory delays indicate that the short-term storage of the target position does not simply mirror the retinal and ocular sensory signals of the visually acquired target location. Thus spatial memory is carried out in an internal representation that is viewer-centered but that may be isotropic with respect to Cartesian space.
Pointing to a remembered visual target involves the transformation of visual information into an appropriate motor output, with a passage through short-term memory storage. In an attempt to identify the reference frames used to represent the target position during the memory period, we measured errors in pointing to remembered three-dimensional (3D) targets. Subjects pointed after a fixed delay to remembered targets distributed within a 22 mm radius volume. Conditions varied in terms of lighting (dim light or total darkness), delay duration (0.5, 5.0, and 8.0 sec), effector hand (left or right), and workspace location. Pointing errors were quantified by 3D constant and variable errors and by a novel measure of local distortion in the mapping from target to endpoint positions. The orientation of variable errors differed significantly between light and dark conditions. Increasing the memory delay in darkness evoked a reorientation of variable errors, whereas in the light, the viewer-centered variability changed only in magnitude. Local distortion measurements revealed an anisotropic contraction of endpoint positions toward an "average" response along an axis that points between the eyes and the effector arm. This local contraction was present in both lighting conditions. The magnitude of the contraction remained constant for the two memory delays in the light but increased significantly for the longer delays in darkness. These data argue for the separate storage of distance and direction information within short-term memory, in a reference frame tied to the eyes and the effector arm.
1 The effects of the dihydropyridine calcium channel antagonists, nifedipine and nimodipine (300 nM-30 pM) were tested in vitro on intracellularly recorded dopaminergic neurones in the rat ventral mesencephalon. 2 Bath applied nifedipine and nimodipine inhibited in a concentration-dependent manner the spontaneous firing discharge of the action potentials, whereas, the dihydropyridine calcium channel agonist, Bay K 8644 increased the firing rate. 3 Pacemaker oscillations and bursts of action potentials were produced by loading the cells with caesium. Nifedipine and nimodipine reduced the rate and the duration of the caesium-induced membrane oscillations and decreased the number of action potentials in a burst. During the blockade of potassium currents the dopaminergic neurones often developed a prolonged (100-800 ms) afterdepolarization that was also inhibited by dihydropyridines. 4 The spontaneous discharge of calcium spikes was also inhibited by both dihydropyridine calcium antagonists. The apparent input resistance and the level of membrane potential were not affected by the dihydropyridine calcium antagonists. 5 If the action potential duration was less than 150 ms the shape of the spike was not clearly influenced by both calcium antagonists. However, when the duration of the action potential was longer than 150-200 ms due to the intracellular injection of caesium ions plus the extracellular application of tetraethylammonium (10-50 mM), both nifedipine and nimodipine reversibly shortened the plateau potential. 6 It is suggested that nifedipine and nimodipine depress the rhythmic and bursting activity of the dopaminergic cells and shorten the calcium action potential by blocking dihydropyridine-sensitive high-threshold calcium currents.
1. Dopamine-containing neurons of the rat midbrain were recorded intracellularly in vitro. Anoxia (2-5 min) caused reversible membrane hyperpolarization (4-25 mV), which blocked spontaneous firing of action potentials. Under voltage clamp, anoxia produced an outward current (100-1,000 pA) associated with an increase in the apparent input conductance. 2. The mean reversal potential of the anoxia-induced response at 2.5 and 12.5 mM [K+] was -86 and -66 mV, respectively. 3. The effect of anoxia was not blocked by tetrodotoxin (TTX), saclofen, (-)sulpiride, or strychnine. Superfusate containing low calcium (0.5 mM CaCl2 and 10 mM MgCl2 or 0.5-1 mM CaCl2 and 1 mM CoCl2) or low sodium (25-40% of control) reduced the anoxia-induced outward current. 4. Extracellular barium (0.1-1 mM) blocked the anoxia-induced hyperpolarization/outward current. Other K+ channel blockers (tetraethylammonium, apamin, quinine, and glibenclamide) failed to reduce anoxia-induced current. 5. When the dopamine-containing neurons were loaded with cesium (1-2 mM), anoxia caused a reversible membrane depolarization and a block of the firing activity. This depolarization was voltage dependent; it was decreased or blocked by the hyperpolarization of the membrane. 6. Perfusion of the cells with 0.5-1 microM TTX did not affect the membrane depolarization/inward current caused by anoxia. These were also present when the cells were treated with the excitatory amino acid receptor antagonists D,L-2-amino-5-phosphonovalerate (APV) (30 microM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM). 7. The exposure of the neurons with low-sodium, low-calcium solutions reversibly reduced the depolarizing/inward effects of anoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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