The mammalian retina encodes visual information in dim light using rod photoreceptors and a specialized circuit: rods→rod bipolar cells→AII amacrine cell. The AII amacrine cell uses sign-conserving electrical synapses to modulate ON cone bipolar cell terminals and sign-inverting chemical (glycinergic) synapses to modulate OFF cone cell bipolar terminals; these ON and OFF cone bipolar terminals then drive the output neurons, retinal ganglion cells (RGCs), following light increments and decrements, respectively. The AII amacrine cell also makes direct glycinergic synapses with certain RGCs, but it is not well established how many types receive this direct AII input.
View Article and Find Full Text PDFVisual neurons adapt to increases in stimulus contrast by reducing their response sensitivity and decreasing their integration time, a collective process known as 'contrast gain control.' In retinal ganglion cells, gain control arises at two stages: an intrinsic mechanism related to spike generation, and a synaptic mechanism in retinal pathways. Here, we tested whether gain control is expressed similarly by three synaptic pathways that converge on an OFF alpha/Y-type ganglion cell: excitatory inputs driven by OFF cone bipolar cells; inhibitory inputs driven by ON cone bipolar cells; and inhibitory inputs driven by rod bipolar cells.
View Article and Find Full Text PDFCone signals divide into parallel ON and OFF bipolar cell pathways, which respond to objects brighter or darker than the background and release glutamate onto the corresponding type of ganglion cell. It is assumed that ganglion cell excitatory responses are driven by these bipolar cell synapses. Here, we report an additional mechanism: OFF ganglion cells were driven in part by the removal of synaptic inhibition (disinhibition).
View Article and Find Full Text PDFRetinal ganglion cells fire spikes to an appropriate contrast presented over their receptive field center. These center responses undergo dynamic changes in sensitivity depending on the ongoing level of contrast, a process known as "contrast gain control." Extracellular recordings suggested that gain control is driven by a single wide-field mechanism, extending across the center and beyond, that depends on inhibitory interneurons: amacrine cells.
View Article and Find Full Text PDFPacing Clin Electrophysiol
May 2006
Background: Break excitation has been hypothesized as a mechanism for the initiation of reentry in cardiac tissue. One way break excitation can occur is by virtual electrodes formed due to a curving fiber geometry. In this article, we are concerned with the relationship between the peak gradient of fiber curvature and the threshold for break stimulation and the initiation of reentry.
View Article and Find Full Text PDFJ Cardiovasc Electrophysiol
July 2005
Unlabelled: Influences of spatial frequency of polarization.
Introduction: The mechanism by which an electric field induces a rotor during cross-field stimulation of cardiac tissue is not entirely known. Different heterogeneous aspects of cardiac tissue have been offered as possible theories, a prominent one being fiber curvature.
Objectives: Our goal is to determine if plunge electrodes change how the heart responds to electrical stimulation.
Background: Several experiments designed to study the induction of a rotor in cardiac tissue have used plunge electrodes to measure the transmural potential. It is our hypothesis that these electrodes may have affected the electrical response of the tissue to a shock.