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Peter D Lukasiewicz - One of the best experts on this subject based on the ideXlab platform.

  • Distinct Ionotropic GABA Receptors Mediate Presynaptic and Postsynaptic Inhibition in Retinal Bipolar Cells
    2013
    Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D Lukasiewicz
    Abstract:

    Ionotropic GABA receptors can mediate presynaptic and postsynaptic inhibition. We assessed the contributions of GABA A and GABA C receptors to inhibition at the dendrites and axon terminals of ferret Retinal bipolar cells by recording currents evoked by focal application of GABA in the Retinal Slice. Currents elicited at the dendrites were mediated predominantly by GABA A receptors, whereas responses evoked at the terminals had GABA A and GABA C components. The ratio of GABA C to GABA A (GABA C: GABA A) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABA C:GABA A could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABA C:GABA A was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studie

  • Glutamate Uptake Limits Synaptic Excitation of Retinal
    2013
    Co-Authors: Ganglion Cells, Matthew H. Higgs, Peter D Lukasiewicz
    Abstract:

    EPSCs of Retinal ganglion cells decay more slowly than do those of most other CNS neurons, in part because of the long time course of glutamate release from bipolar cells. Here we investigated how glutamate clearance and AMPA receptor desensitization affect ganglion cell EPSCs in the salamander Retinal Slice preparation. Inhibition of glutamate uptake greatly prolonged ganglion cell EPSCs evoked by light or monosynaptic electrical stimuli but had little effect on spontaneous miniature EPSCs (mEPSCs). This suggests that single quanta of glutamate are cleared rapidly by diffusion but multiple quanta can interact to lengthen the postsynaptic response. Some interaction between quanta is likely to occur even when glutamate uptake is not inhibited. This seems to depend on quantal content, because reducing glutamate release with low Ca 2 �, paired-pulse depression, or weak stimuli shortened the EPS

  • distinct ionotropic gaba receptors mediate presynaptic and postsynaptic inhibition in Retinal bipolar cells
    The Journal of Neuroscience, 2000
    Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D Lukasiewicz
    Abstract:

    Ionotropic GABA receptors can mediate presynaptic and postsynaptic inhibition. We assessed the contributions of GABAA and GABAC receptors to inhibition at the dendrites and axon terminals of ferret Retinal bipolar cells by recording currents evoked by focal application of GABA in the Retinal Slice. Currents elicited at the dendrites were mediated predominantly by GABAA receptors, whereas responses evoked at the terminals had GABAA and GABAC components. The ratio of GABAC to GABAA(GABAC:GABAA) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABAC:GABAA could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABAC:GABAA was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABAA β2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABAC ρ subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABAA receptors mediate GABAergic inhibition on bipolar cell dendrites in the OPL, that GABAA and GABACreceptors mediate inhibition on axon terminals in the IPL, and that the GABAC:GABAA on the terminals may tune the response characteristics of the bipolar cell.

  • Distinct Ionotropic GABA Receptors Mediate Presynaptic and Postsynaptic Inhibition in Retinal Bipolar Cells
    The Journal of Neuroscience, 2000
    Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D Lukasiewicz
    Abstract:

    Ionotropic GABA receptors can mediate presynaptic and postsynaptic inhibition. We assessed the contributions of GABA(A) and GABA(C) receptors to inhibition at the dendrites and axon terminals of ferret Retinal bipolar cells by recording currents evoked by focal application of GABA in the Retinal Slice. Currents elicited at the dendrites were mediated predominantly by GABA(A) receptors, whereas responses evoked at the terminals had GABA(A) and GABA(C) components. The ratio of GABA(C) to GABA(A) (GABA(C):GABA(A)) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABA(C):GABA(A) could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABA(C):GABA(A) was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABA(A) beta2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABA(C) rho subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABA(A) receptors mediate GABAergic inhibition on bipolar cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate inhibition on axon terminals in the IPL, and that the GABA(C):GABA(A) on the terminals may tune the response characteristics of the bipolar cell.

  • nbsp;GABA(C) receptors control adaptive changes in a glycinergic inhibitory pathway in salamander retina
    2000
    Co-Authors: Paul B. Cook, Peter D Lukasiewicz, John S. Mcreynolds
    Abstract:

    We studied the role of GABA in adaptive changes in a lateral inhibitory system in the tiger salamander retina. In dark-adapted Retinal Slice preparations picrotoxin caused a slow enhancement of glycine-mediated IPSCs in ganglion cells. The enhancement of glycinergic IPSCs developed slowly over the course of 5–20 min, even though picrotoxin blocked both GABAA and GABAC receptors within a few seconds. The slow enhancement of glycinergic IPSCs by picrotoxin was much weaker in light-adapted preparations. The slow enhancement of glycinergic inhibitory inputs was not produced by bicuculline, indicating that it involved GABAC receptors. The responses of ganglion cells to direct application of glycine were not en-hanced by picrotoxin, indicating that the enhancement was not caused by an action on glycine receptors. In dark-adapted eyecup preparations picrotoxin caused a slow enhancement o

Colleen R Shields - One of the best experts on this subject based on the ideXlab platform.

  • Distinct Ionotropic GABA Receptors Mediate Presynaptic and Postsynaptic Inhibition in Retinal Bipolar Cells
    2013
    Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D Lukasiewicz
    Abstract:

    Ionotropic GABA receptors can mediate presynaptic and postsynaptic inhibition. We assessed the contributions of GABA A and GABA C receptors to inhibition at the dendrites and axon terminals of ferret Retinal bipolar cells by recording currents evoked by focal application of GABA in the Retinal Slice. Currents elicited at the dendrites were mediated predominantly by GABA A receptors, whereas responses evoked at the terminals had GABA A and GABA C components. The ratio of GABA C to GABA A (GABA C: GABA A) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABA C:GABA A could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABA C:GABA A was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studie

  • distinct ionotropic gaba receptors mediate presynaptic and postsynaptic inhibition in Retinal bipolar cells
    The Journal of Neuroscience, 2000
    Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D Lukasiewicz
    Abstract:

    Ionotropic GABA receptors can mediate presynaptic and postsynaptic inhibition. We assessed the contributions of GABAA and GABAC receptors to inhibition at the dendrites and axon terminals of ferret Retinal bipolar cells by recording currents evoked by focal application of GABA in the Retinal Slice. Currents elicited at the dendrites were mediated predominantly by GABAA receptors, whereas responses evoked at the terminals had GABAA and GABAC components. The ratio of GABAC to GABAA(GABAC:GABAA) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABAC:GABAA could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABAC:GABAA was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABAA β2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABAC ρ subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABAA receptors mediate GABAergic inhibition on bipolar cell dendrites in the OPL, that GABAA and GABACreceptors mediate inhibition on axon terminals in the IPL, and that the GABAC:GABAA on the terminals may tune the response characteristics of the bipolar cell.

  • Distinct Ionotropic GABA Receptors Mediate Presynaptic and Postsynaptic Inhibition in Retinal Bipolar Cells
    The Journal of Neuroscience, 2000
    Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D Lukasiewicz
    Abstract:

    Ionotropic GABA receptors can mediate presynaptic and postsynaptic inhibition. We assessed the contributions of GABA(A) and GABA(C) receptors to inhibition at the dendrites and axon terminals of ferret Retinal bipolar cells by recording currents evoked by focal application of GABA in the Retinal Slice. Currents elicited at the dendrites were mediated predominantly by GABA(A) receptors, whereas responses evoked at the terminals had GABA(A) and GABA(C) components. The ratio of GABA(C) to GABA(A) (GABA(C):GABA(A)) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABA(C):GABA(A) could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABA(C):GABA(A) was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABA(A) beta2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABA(C) rho subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABA(A) receptors mediate GABAergic inhibition on bipolar cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate inhibition on axon terminals in the IPL, and that the GABA(C):GABA(A) on the terminals may tune the response characteristics of the bipolar cell.

Heinz Wässle - One of the best experts on this subject based on the ideXlab platform.

  • Glycinergic amacrine cells of the rat retina
    The Journal of comparative neurology, 1998
    Co-Authors: Nicole Menger, David V. Pow, Heinz Wässle
    Abstract:

    Physiological studies of neurons of the inner retina, e.g., of amacrine cells, are now possible in a mammalian Retinal Slice preparation. The present anatomical study characterizes glycinergic amacrine cells of the rat retina and thus lays the ground for such future physiological and pharmacological experiments. Rat retinae were immunolabeled with antibodies against glycine and the glycine transporter-1 (GLYT-1), respectively. Glycine immunoreactivity was found in approximately 50% of the amacrine and 25% of the bipolar cells. GLYT-1 immunoreactivity was restricted to glycinergic amacrine cells. They were morphologically characterized by the intracellular injection of Lucifer Yellow followed by GLYT-1 immunolabeling. Eight different types of glycinergic amacrine cells could be distinguished. They were all small-field amacrine cells with bushy dendritic trees terminating at different levels within the inner plexiform layer. The well-known AII amacrine cell was encountered most frequently. From our measurements of the dendritic field sizes and the density of glycinergic cells, we estimate that there are enough glycinergic amacrine cells available to make sure that all eight types and possibly more tile the retina regularly with their dendritic fields.

  • Different Contributions of GABAA and GABAC Receptors to Rod and Cone Bipolar Cells in a Rat Retinal Slice Preparation
    Journal of neurophysiology, 1998
    Co-Authors: Thomas Euler, Heinz Wässle
    Abstract:

    Euler, Thomas and Heinz Wassle. Different contributions ofGABAA and GABAC receptors to rod and cone bipolar cells in a rat Retinal Slice preparation. J. Neurophysiol. 79: 1384–1395, 1998. Whole cel...

Frank S Werblin - One of the best experts on this subject based on the ideXlab platform.

  • amacrine to amacrine cell inhibition in the rabbit retina
    Journal of Neurophysiology, 2008
    Co-Authors: Hainann Hsueh, Alyosha Molnar, Frank S Werblin
    Abstract:

    We studied the interactions between excitation and inhibition in morphologically identified amacrine cells in the light-adapted rabbit Retinal Slice under patch clamp. The majority of on amacrine c...

  • dopamine modulates gabac receptors mediating inhibition of calcium entry into and transmitter release from bipolar cell terminals in tiger salamander retina
    The Journal of Neuroscience, 1995
    Co-Authors: D P Wellis, Frank S Werblin
    Abstract:

    Using optical recording techniques, we directly monitored pre- and postsynaptic calcium dynamics at bipolar cell terminals while inhibiting synaptic release with applied GABA and modulating inhibition with dopamine. To monitor pre-synaptic activity, individual bipolar cells in the Retinal Slice were filled with either fura-2 or fluo-3 through a patch electrode. Calcium entry into bipolar terminals, elicited by depolarization from -60 mV to 0 mV, was reduced to 36% of control in the presence of 200 microM bath-applied GABA. Further addition of 100 microM dopamine to the bath relieved the GABAergic inhibition and nearly doubled the calcium entry. Yet dopamine alone had no apparent direct effect upon calcium entry. The relief from GABAergic inhibition could be reproduced with SKF-38393, a dopamine D1 receptor agonist, and with forskolin, an adenylyl cyclase activator, suggesting that dopamine acts through a cAMP second-messenger pathway. To monitor transmitter release from bipolar cells, Slices were loaded with fura- 2AM, a membrane permeable form of the dye. Puffs of 110 mM KCl at bipolar dendrites depolarized bipolar cells and elicited calcium signals that could be monitored both at bipolar terminals and in postsynaptic cells. Consistent with the results above, GABA inhibited calcium entry at bipolar terminals and also reduced transmitter release, measured as a decrease in calcium entry in amacrine and ganglion cells. The addition of dopamine relieved this inhibition and increased transmitter release. Our results show the spatiotemporal correlation between the GABAergic inhibition of calcium entry at bipolar terminals, the resulting reduction in postsynaptic activity, and the relief of this inhibition with dopamine.

  • a novel gaba receptor on bipolar cell terminals in the tiger salamander retina
    The Journal of Neuroscience, 1994
    Co-Authors: Peter D Lukasiewicz, Bruce R. Maple, Frank S Werblin
    Abstract:

    We studied the pharmacology of the GABA receptors on bipolar cell terminals in the Retinal Slice preparation. Whole-cell patch-clamp recordings were made from the somas of bipolar cells and GABA was puffed near their terminals, after synaptic transmission was blocked. GABA puffs evoked a large chloride current that was reduced by picrotoxin, but in many cells this current was insensitive to blockade by the competitive GABAA receptor antagonists bicuculline and SR95531. Pentobarbital, an enhancer of GABAA receptor-mediated responses, did not significantly increase the magnitude of the current responses to GABA puffed at the bipolar cell terminals. To confirm the effectiveness of GABAA antagonists and pentobarbital in the Slice preparation, we measured GABA currents in ganglion cells. In contrast to bipolar cells, the ganglion cell GABA responses were strongly reduced by both bicuculline and SR95531. In addition, pentobarbital strongly enhanced the action of GABA at the ganglion cells. The isomeric GABA agonists cis- and transaminocrotonic acid (CACA and TACA), elicited picrotoxin- sensitive currents in both bipolar and ganglion cells. TACA was more effective than CACA at both cell types. In bipolar cells, TACA and CACA currents were relatively resistant to bicuculline blockade, but in ganglion cells both currents were reduced by bicuculline. GABA receptors on bipolar terminals appear to be pharmacologically different from the GABA receptors found on ganglion cell dendrites. The bipolar cell terminal GABA receptor pharmacology is similar to the pharmacology reported for the rho 1 GABA receptor subunit that was isolated from retina and expressed in Xenopus oocytes (Cutting et al., 1991; Polenzani et al., 1991; Shimada et al., 1992). This receptor, which is both bicuculline and pentobarbital insensitive, has been called the GABAC receptor (Johnston, 1986; Shimada et al., 1992). However, some bipolar cells were somewhat sensitive to blockade by bicuculline, suggesting that these cells had both GABAA and GABAC receptors on their bipolar terminals.

  • characterization of the glutamate transporter in Retinal cones of the tiger salamander
    The Journal of Neuroscience, 1993
    Co-Authors: Scott Eliasof, Frank S Werblin
    Abstract:

    L-Glutamate elicits an inwardly rectifying current at hyperpolarized potentials in isolated Retinal cones of the tiger salamander, as measured under whole-cell patch clamp. Evidence presented in this article supports the notion that cones possess a high-affinity glutamate transporter. This glutamate-elicited current shows no desensitization over a period of several minutes, and has an affinity (Km) of 10 microM. The inward current is mimicked by the amino acids L-aspartate, D-aspartate, L-cysteate, and to a lesser extent D-glutamate. It is neither blocked by the glutamate receptor antagonists kynurenic acid (1 mM), 6-cyano-7-nitroquinoxaline-2,3-dione (100 microM), or 2-amino-5-phosphonovalerate (100 microM), nor elicited by the glutamate receptor agonists (100 microM each) kainate, quisqualate, NMDA, or 2-amino-4-phosphonobutyrate. The glutamate-elicited current was reduced by the glutamate transport blockers dihydrokainate (DHKA), DL-threo-beta-hydroxyaspartate (beta HA), and L-trans-pyrrolidine-2,4-dicarboxylic acid. When glutamate was present on both sides of the membrane, the blockers reduced both uptake and release; the blocker-sensitive current as a function of membrane potential represents the transport current-voltage relation (I-V), and the reversal potential of the I-V represents the transporter equilibrium potential. This potential was a function of the equilibrium potential for glutamate. DHKA and beta HA depolarized horizontal cells in a Retinal Slice, and abolished their light responses, suggesting that in the absence of glutamate transport, glutamate concentrations in the cleft rise to a level that saturates the postsynaptic receptors. The high capacity of the cone glutamate transporter is well suited for the rapid removal of glutamate from the synaptic cleft required for the signaling of a light onset to postsynaptic cells.

  • amacrine cells in the tiger salamander retina morphology physiology and neurotransmitter identification
    The Journal of Comparative Neurology, 1991
    Co-Authors: Chenyu Yang, Frank S Werblin, Peter Lukasiewicz, Greg Maguire, Stephen Yazulla
    Abstract:

    Amacrine cells of the vertebrate retina comprise multiple neurochemical types. Yet details of their electrophysiological and morphology properties as they relate to neurotransmitter content are limited. This issue of relating light responsiveness, dendritic projection, and neurotransmitter content has been addressed in the Retinal Slice preparation of the tiger salamander. Amacrine cells were whole-cell clamped and stained with Lucifer yellow (LY), then processed to determine their immunoreactivity (IR) to GABA, glycine, dopamine or tyrosine hydroxylase (TOH), and glucagon antisera. Widefield, ON-OFF amacrine cells were glycine-IR. The processes of these cells extended laterally in the inner plexiform layer (IPL) from 250–600 μm. They were either multistratified in the IPL or monostratified near the IPL midline. Three multistratified ON-OFF narrowfield glycine-IR cells also were found. Four types of ON amacrine cells were found to be GABA-IR; all types had their processes concentrated in the proximal IPL (sublamina b). Type I cells were narrowfield (∼ 100 μm) with a compact projection. Type II cells were widefield (220–300 μm) with a sparse projection. Type III cells had an asymmetrical projection and varicose processes. Type IV cells were pyriform and monostratified in sublamina b. One narrowfield ON-OFF amacrine cell, with processes broadly distributed in the middle of the IPL, was GABA-IR. This cell appeared similar to an ON-OFF cell that was glycine-IR and may comprise a type in which GABA and glycine colocalize. Another class of amacrine cell, with processes forming a major plexus along the distal border of the IPL and a lesser plexus in the proximal IPL, produced slow responses at light ON and OFF; these cells were dopamine/TOH-IR. A narrowfield class of transient ON-OFF amacrine cell, with processes ramifying throughout both sublaminae a and b of the IPL, were glucagon-IR; these cells appeared to be dye-coupled at the soma. We have shown that, with respect to GABA, glycine, dopamine, and glucagon, salamander amacrine cells fall into rather discrete groups on the basis of ramification patterns in the IPL and responses to photic stimulation. The physiological, structural, and neurochemical diversity of amacrine cells is indicative of multiple and complex roles in Retinal processing.

Greg Maguire - One of the best experts on this subject based on the ideXlab platform.

  • differential expression of voltage gated k and ca2 currents in bipolar cells in the zebrafish Retinal Slice
    European Journal of Neuroscience, 1998
    Co-Authors: Victoria P Connaughton, Greg Maguire
    Abstract:

    Whole-cell voltage-gated currents were recorded from bipolar cells in the zebrafish Retinal Slice. Two physiological populations of bipolar cells were identified. In the first, depolarizing voltage steps elicited a rapidly activating A-current that reached peak amplitude or = 10 ms after step onset and did not inactivate. IK was antagonized by internal caesium and external tetraethylammonium. Bipolar cells expressing IK also expressed a time-dependent h-current at membrane potentials -50 mV activated ICa, which reached peak amplitude between -20 and -10 mV. ICa was eliminated in Ca+2-free Ringer and blocked by cadmium and cobalt, but not tetrodotoxin. In most cells, Ica was transient, activating rapidly at -50 mV. This current was antagonized by nickel. The remaining bipolar cells expressed a nifedipine-sensitive sustained current that activated between -40 and -30 mV, with both slower kinetics and smaller amplitude than transient ICa. IK(Ca) was elicited by membrane depolarizations > -20 mV. Bipolar cells in the zebrafish Retinal Slice preparation express an array of voltage-gated currents which contribute to non-linear I-V characteristics. The zebrafish Retinal Slice preparation is well-suited to patch clamp analyses of membrane mechanisms and provides a suitable model for studying genetic defects in visual system development.

  • dopamine enhances a glutamate gated ionic current in off bipolar cells of the tiger salamander retina
    The Journal of Neuroscience, 1994
    Co-Authors: Greg Maguire, F Werblin
    Abstract:

    The transmitter glutamate is thought to be used by all vertebrate photoreceptors to drive the second-order neurons of the retina, horizontal and bipolar neurons. Dopamine, an endogenous Retinal neurotransmitter localized to amacrine and interplexiform cells, has previously been shown to enhance glutamate-gated currents in Retinal horizontal cells. In the present study we demonstrate that bipolar cells, like horizontal cells, possess glutamate receptors that are modulated by dopamine. We then identify some components of the pathway through which dopamine acts. We used whole-cell patch recording to measure how bath-applied dopamine modulated the currents elicited by puffs of transmitter solutions at bipolar cell dendrites. Excitatory amino acid-gated currents were evoked by pressure ejecting 1 mM glutamate or 10 microM kainate for 40 msec through a micropipette positioned at the dendrites of bipolar cells. Bath-applied dopamine (20 microM) enhanced the response to glutamate in OFF bipolar cells in the Retinal Slice by 40% and in isolated OFF bipolar cells by 65%. We also explored the components of the intracellular pathway mediating this modulation. Response enhancement was blocked by the D1 receptor antagonist SCH23390, but not by the D2 receptor antagonist spiperone, suggesting that the enhancement by dopamine is mediated by a D1 receptor. GDP-beta-S, a G-protein inactivator, blocked the enhancing action of dopamine, suggesting that the D1 receptor activated a G-protein to enhance the glutamate-gated current. Both 8-(4-chlorophenylthio)adenosine, a cAMP analog, and the addition of the catalytic subunit of protein kinase A (PKA) to the recording pipette enhanced glutamate-gated currents, while H-7, a PK inactivator, and PKI20amide, a PKA-specific inhibitor, blocked the enhancing action of dopamine. These data suggest that dopamine acts at D1 receptors in the dendrites of bipolar cells to activate adenyl cyclase, which through cAMP enhances a glutamate-gated current in bipolar cell dendrites. Thus, dopamine may modulate synaptic transmission from photoreceptors to OFF bipolar cells.

  • amacrine cells in the tiger salamander retina morphology physiology and neurotransmitter identification
    The Journal of Comparative Neurology, 1991
    Co-Authors: Chenyu Yang, Frank S Werblin, Peter Lukasiewicz, Greg Maguire, Stephen Yazulla
    Abstract:

    Amacrine cells of the vertebrate retina comprise multiple neurochemical types. Yet details of their electrophysiological and morphology properties as they relate to neurotransmitter content are limited. This issue of relating light responsiveness, dendritic projection, and neurotransmitter content has been addressed in the Retinal Slice preparation of the tiger salamander. Amacrine cells were whole-cell clamped and stained with Lucifer yellow (LY), then processed to determine their immunoreactivity (IR) to GABA, glycine, dopamine or tyrosine hydroxylase (TOH), and glucagon antisera. Widefield, ON-OFF amacrine cells were glycine-IR. The processes of these cells extended laterally in the inner plexiform layer (IPL) from 250–600 μm. They were either multistratified in the IPL or monostratified near the IPL midline. Three multistratified ON-OFF narrowfield glycine-IR cells also were found. Four types of ON amacrine cells were found to be GABA-IR; all types had their processes concentrated in the proximal IPL (sublamina b). Type I cells were narrowfield (∼ 100 μm) with a compact projection. Type II cells were widefield (220–300 μm) with a sparse projection. Type III cells had an asymmetrical projection and varicose processes. Type IV cells were pyriform and monostratified in sublamina b. One narrowfield ON-OFF amacrine cell, with processes broadly distributed in the middle of the IPL, was GABA-IR. This cell appeared similar to an ON-OFF cell that was glycine-IR and may comprise a type in which GABA and glycine colocalize. Another class of amacrine cell, with processes forming a major plexus along the distal border of the IPL and a lesser plexus in the proximal IPL, produced slow responses at light ON and OFF; these cells were dopamine/TOH-IR. A narrowfield class of transient ON-OFF amacrine cell, with processes ramifying throughout both sublaminae a and b of the IPL, were glucagon-IR; these cells appeared to be dye-coupled at the soma. We have shown that, with respect to GABA, glycine, dopamine, and glucagon, salamander amacrine cells fall into rather discrete groups on the basis of ramification patterns in the IPL and responses to photic stimulation. The physiological, structural, and neurochemical diversity of amacrine cells is indicative of multiple and complex roles in Retinal processing.