Ca2+-transmitter release coupling was examined using bipolar cells with large presynaptic terminals dissociated from the goldfish retina. Presynaptic Ca2+ current (I(Ca)) was recorded under the whole-cell voltage clamp. Release of excitatory amino acid transmitter was simultaneously monitored as the current through N-methyl-D-asperate (NMDA) receptors of reporter cells or as the membrane capacitance (C(m)) change associated with exocytosis. When I(Ca) was activated by a long depolarizing pulse, a double-peaked transmitter-induced current (I(tr)) was elicited in reporter cells. The rapid component of I(tr) was evoked immediately after the onset of depolarization, and was affected only slightly by intracellularly applied Ca2+ chelators. The delayed slow component of I(tr) was elicited during depolarization once a fixed amount of Ca2+ was accumulated in presynaptic terminals, and its appearance was suppressed or retarded by Ca2+ chelators. Two components of transmitter release were also recognized by monitoring C(m) changes elicited by the activation of I(Ca). These results suggest that bipolar cells have at least two pools of synaptic vesicles; a small, immediately releasable pool and a large releasable pool. The rapid and the delayed slow components of transmitter release may reflect exocytosis and mobilization of synaptic vesicles, respectively.
"However, a small, fast component of refilling with a time constant of a few hundred milliseconds has been noted when examining recovery of the releasable pool; this component has been attributed to the refilling of the rapid pool when calcium channels are open (Mennerick & Matthews, 1996). Consistent with a calcium-dependent mechanism, this component is inhibited by intracellular addition of the calcium buffer EGTA (Gomis et al., 1999; see also Sakaba et al., 1997). Together, these observations support that in the Mb1 bipolar cell, as has been described for other neurons and secretory cells, there is calcium-accelerated refilling pool of the rapidly-releasing pool (von Ruden & Neher, 1993; Dittman & Regehr, 1998; Stevens & Wesseling, 1998; Wang & Kaczmarek, 1998; Gomis et al., 1999; Sakaba & Neher. "
[Show abstract][Hide abstract] ABSTRACT: Bipolar cells play a vital role in the transfer of visual information across the vertebrate retina. The synaptic output of these neurons is regulated by factors that are extrinsic and intrinsic. Relatively little is known about the intrinsic factors that regulate neurotransmitter exocytosis. Much of what we know about intrinsic presynaptic mechanisms that regulate glutamate release has come from the study of the unusually large and accessible synaptic terminal of the goldfish rod-dominant bipolar cell, the Mb1 bipolar cell. However, over the past several years, examination of presynaptic mechanisms governing neurotransmitter release has been extended to the mammalian rod bipolar cell. In this review, we discuss the recent advances in our understanding of synaptic vesicle dynamics and neurotransmitter release in rodent rod bipolar cells and consider how these properties help to shape the synaptic output of the mammalian retina.
"These phases are believed to correspond with the release of synaptic vesicles docked at the base of ribbons (the rapidly releasable pool, RRP) and those tethered higher up the ribbon (the reserve pool), respectively (von Gersdorff et al. 1996). Two components of exocytosis are also observed in responses evoked by glutamate release from isolated BCTs, using horizontal cells as a reporter system (Sakaba et al. 1997; von Gersdorff et al. 1998). The amacrine/ganglion cell response to the transient and sustained phases of BC exocytosis will depend on the subtypes and activation properties of postsynaptic glutamate receptors. "
[Show abstract][Hide abstract] ABSTRACT: Direct recordings from the large axon terminals of goldfish retinal bipolar cells (BCs) have revealed detailed information about the properties and regulation of exocytosis at this ribbon-type synapse. However, the relationship between BC exocytosis and evoked postsynaptic responses in amacrine and ganglion cells is not known. To address this, I have made paired recordings from BC terminals (BCTs) and neurons in the ganglion cell layer (GCL) in goldfish retinal slices. BCT depolarisation evoked short-latency, AMPA/kainate receptor-mediated EPSCs in connected GCL neurons. NMDA receptors contributed to the response at +40 mV but not at 60 mV. Evoked EPSCs contained multiple temporal components that differed in their relative amplitudes between pairs. Changing the duration or amplitude of the presynaptic stimulus affected the size and kinetics of the EPSC, with weaker stimuli slowing the EPSC activation rate. Paired-pulse stimulation caused greater depression of fast than slow EPSC components. A linear relationship was found between the amount of BCT exocytosis, measured via changes in membrane capacitance, and the charge of evoked EPSCs, whether they were mediated by AMPA/kainate receptors alone or in combination with NMDA receptors. In addition, analysis of miniature EPSCs in GCL neurons provided estimates of the quantal content of evoked EPSCs. The results demonstrate the feasibility of using this paired recording system to study synaptic transfer at ribbon synapses, and indicate that both the rapid and sustained phases of BC exocytosis are encoded in the postsynaptic response.
The Journal of Physiology 03/2010; 588(Pt 9):1489-98. DOI:10.1113/jphysiol.2009.185850 · 5.04 Impact Factor
"Under some conditions, the response may even become regenerative (Protti et al., 2000). In response to a sustained depolarization, there is an initial burst of release from the Mb1 bipolar cell that is followed by a prominent, longer-lived secondary component of release (Sakaba et al., 1997; von Gersdorff et al., 1998). Both sustained and transient components of light-evoked release are also observed in neurons postsynaptic to the mammalian rod bipolar cell (Nelson, 1982; Kolb & Nelson, 1983; Dacheux & Raviola, 1986; Bloomfield & Xin, 2000; Pang et al., 2004). "
[Show abstract][Hide abstract] ABSTRACT: To better understand synaptic signaling at the mammalian rod bipolar cell terminal and pave the way for applying genetic approaches to the study of visual information processing in the mammalian retina, synaptic vesicle dynamics and intraterminal calcium were monitored in terminals of acutely isolated mouse rod bipolar cells and the number of ribbon-style active zones quantified. We identified a releasable pool, corresponding to a maximum of 7 s. The presence of a smaller, rapidly releasing pool and a small, fast component of refilling was also suggested. Following calcium channel closure, membrane surface area was restored to baseline with a time constant that ranged from 2 to 21 s depending on the magnitude of the preceding Ca2+ transient. In addition, a brief, calcium-dependent delay often preceded the start of onset of membrane recovery. Thus, several aspects of synaptic vesicle dynamics appear to be conserved between rod-dominant bipolar cells of fish and mammalian rod bipolar cells. A major difference is that the number of vesicles available for release is significantly smaller in the mouse rod bipolar cell, both as a function of the total number per neuron and on a per active zone basis.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.