TY - JOUR
T1 - Short-term depression at the reciprocal synapses between a retinal bipolar cell terminal and amacrine cells
AU - Li, Geng Lin
AU - Vigh, Jozsef
AU - Von Gersdorff, Henrique
PY - 2007/7/11
Y1 - 2007/7/11
N2 - Visual adaptation is thought to occur partly at retinal synapses that are subject to plastic changes. However, the locus and properties of this plasticity are not well known. Here, we studied short-term plasticity at the reciprocal synapse between bipolar cell terminals and amacrine cells in goldfish retinal slices. Depolarization of a single bipolar cell terminal for 100 ms triggers the release of glutamate onto amacrine cell processes, which in turn leads to GABAergic feedback from amacrine cells onto the same terminal. We find that this release of GABA undergoes paired-pulse depression (PPD) that recovers in <1 min (single exponential time constant, τ ≅ 12 s). This disynaptic PPD is independent of mGluR-mediated plasticity and depletion of glutamatergic synaptic vesicle pools, because exocytosis assayed via capacitance jumps (ΔCm) recovered completely after 10 s (τ ≅ 2 s). Fast application of GABA (10mΜ) onto outside-out patches excised from bipolar cell terminals showed that the recovery of GABAA receptors from desensitization depends on the duration of the application [fast recovery (<2 s) for short applications; slow (τ ≅ 12 s) for prolonged applications]. We thus blocked GABAA receptors and retested the GABAergic response mediated by nondesensitizing GABAC receptors to two rapid glutamate puffs onto the bipolar cell terminal. These responses consistently displayed PPD. Furthermore, blocking AMPA-receptor desensitization with cyclothiazide, or evoking GABA release with NMDA receptors, did not reduce PPD. We thus suggest that depletion of synaptic vesicle pools in GABAergic amacrine cells is a major contributor to PPD.
AB - Visual adaptation is thought to occur partly at retinal synapses that are subject to plastic changes. However, the locus and properties of this plasticity are not well known. Here, we studied short-term plasticity at the reciprocal synapse between bipolar cell terminals and amacrine cells in goldfish retinal slices. Depolarization of a single bipolar cell terminal for 100 ms triggers the release of glutamate onto amacrine cell processes, which in turn leads to GABAergic feedback from amacrine cells onto the same terminal. We find that this release of GABA undergoes paired-pulse depression (PPD) that recovers in <1 min (single exponential time constant, τ ≅ 12 s). This disynaptic PPD is independent of mGluR-mediated plasticity and depletion of glutamatergic synaptic vesicle pools, because exocytosis assayed via capacitance jumps (ΔCm) recovered completely after 10 s (τ ≅ 2 s). Fast application of GABA (10mΜ) onto outside-out patches excised from bipolar cell terminals showed that the recovery of GABAA receptors from desensitization depends on the duration of the application [fast recovery (<2 s) for short applications; slow (τ ≅ 12 s) for prolonged applications]. We thus blocked GABAA receptors and retested the GABAergic response mediated by nondesensitizing GABAC receptors to two rapid glutamate puffs onto the bipolar cell terminal. These responses consistently displayed PPD. Furthermore, blocking AMPA-receptor desensitization with cyclothiazide, or evoking GABA release with NMDA receptors, did not reduce PPD. We thus suggest that depletion of synaptic vesicle pools in GABAergic amacrine cells is a major contributor to PPD.
KW - Adaptation
KW - Amacrine cells
KW - Bipolar cell terminals
KW - Inner plexiform layer
KW - Membrane capacitance
KW - Microcircuits
KW - Paired-pulse depression
KW - Retina
KW - Short-term plasticity
UR - http://www.scopus.com/inward/record.url?scp=34447503746&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34447503746&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.0410-07.2007
DO - 10.1523/JNEUROSCI.0410-07.2007
M3 - Article
C2 - 17626198
AN - SCOPUS:34447503746
SN - 0270-6474
VL - 27
SP - 7377
EP - 7385
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 28
ER -