Sigmund Exner's (1887) einige beobachtungen über bewegungsnachbilder (some observations on movement aftereffects):an illustrated translation with commentary

In his original contribution, Exner’s principal concern was a comparison between the properties of different aftereffects, and particularly to determine whether aftereffects of motion were similar to those of color and whether they could be encompassed within a unified physiological framework. Despite the fact that he was unable to answer his main question, there are some excellent—so far unknown—contributions in Exner’s paper. For example, he describes observations that can be related to binocular interaction, not only in motion aftereffects but also in rivalry. To the best of our knowledge, Exner provides the first description of binocular rivalry induced by differently moving patterns in each eye, for motion as well as for their aftereffects. Moreover, apart from several known, but beautifully addressed, phenomena he makes a clear distinction between motion in depth based on stimulus properties and motion in depth based on the interpretation of motion. That is, the experience of movement, as distinct from the perception of movement. The experience, unlike the perception, did not result in a motion aftereffect in depth

Soluble substances released from postischemic reperfused rat hearts reduce calcium transient and contractility by blocking the L-type calcium channel

OBJECTIVES: This study was designed to investigate the effects of cardiodepressant substances released from postischemic myocardial tissue on myocardial calcium-regulating pathways. BACKGROUND: We have recently reported that new cardiodepressant substances are released from isolated hearts during reperfusion after myocardial ischemia. METHODS: After 10 min of global ischemia, isolated rat hearts were reperfused, and the coronary effluent was collected for 30 s. We tested the effects of the postischemic coronary effluent on cell contraction, Ca 2+ transients and Ca 2+ currents of isolated rat cardiomyocytes by applying fluorescence microscopy and the whole-cell, voltage-clamp technique. Changes in intracellular phosphorylation mechanisms were studied by measuring tissue concentrations of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), as well as activities of cAMP-dependent protein kinase (cAMP-dPK) and protein kinase C (PKC). RESULTS The postischemic coronary effluent, diluted with experimental buffer, caused a concentration-dependent reduction of cell shortening and Ca 2+ transient in the field-stimulated isolated cardiomyocytes of rats, as well as a reduction in peak L-type Ca 2+ current in voltage-clamped cardiomyocytes. The current reduction resulted from reduced maximal conductance - not from changes in voltage- and time-dependent gating of the L-type Ca 2+ channel. The postischemic coronary effluent modified neither the tissue concentrations of cAMP or cGMP nor the activities of cAMP-dPK and PKC. However, the effluent completely eliminated the activation of glycogen phosphorylase after beta-adrenergic stimulation. CONCLUSIONS Negative inotropic substances released from isolated postischemic hearts reduce Ca 2+ transient and cell contraction through cAMP-independent and cGMP-independent blockage of L-type Ca 2+ channels