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Unformatted text preview: BIPN 140: Cellular Neurobiology LECTURE #7: Synaptic Transmission I
[Website: http://www.biology.ucsd.edu/classes/bipn140.FA10] INSTRUCTORS Nicholas C. Spitzer (email@example.com) Darwin K. Berg (firstname.lastname@example.org) ANNOUNCEMENTS 1st Midterm Exam: Oct 19, 5 pm, here (Solis 107). Review Session: Oct 18, 5-7 pm, Center 109. Old problem set Q&A & Exam Keys will be available on website. Podcast now available for lecture material. Fig 5.1 Electrical & chemical synapses differ in transmission mechanisms Fig 5.2a Structure & function of gap junctions at electrical synapses Figure 5.2b Structure & function of gap junctions at electrical synapses Fig 5.2c Structure & function of gap junctions at electrical synapses Fig 5.3 Sequence of events involved in transmission at a typical chemical synapse Fig 5.5 Metabolism of small-molecule & peptide transmitters Fig 5.6a/b Synaptic transmission at the neuromuscular junction Fig 5.6c/d Synaptic transmission at the neuromuscular junction
(in low [Ca++]) Fig 5.7 Quantized distribution of EPP amplitudes evoked in a low Ca2+ solution Fig 5.8a,c Relationship of SV exocytosis and quantal transmitter release Fig 5.13a Presynaptic proteins & their roles in synaptic vesicle cycling Fig 5.13b Presynaptic proteins & their roles in synaptic vesicle cycling Fig 5.14a Molecular mechanisms of exocytosis during neurotransmitter release Fig 5.14b Molecular mechanisms of exocytosis during neurotransmitter release Fig 5.15 Molecular mechanisms of endocytosis following neurotransmitter release Science 289:953-957 (2000) Calcium Sensitivity of Glutamate Release in a Calyx-Type Terminal
by Johann H. Bollmann,1* Bert Sakmann,1 J. Gerard G. Borst1,2 BACKGROUND Calcium influx into the presynaptic terminal is needed to trigger SV exocytosis and NT release. Previously thought that high calcium concentrations were needed, i.e. [Ca2+]i > 100 µM, in the terminal. EXPERIMENT Chose a large synapse where the presynaptic terminal formed a large caylx around the postsynaptic cell body. Loaded the calyx with a “caged compound” containing calcium that could be released locally by photoactivation. Quantified the release with a calcium fluorescent sensor. Simultaneously measured responses in the postsynaptic cell with a second patch-clamp electrode. Fig. 2. Relation between [Ca21]i and the rate of exocytosis in the calyx of Held. [A] ( Top) Photodiode traces of [Ca]i jumps. (Bottom) Corresponding EPSCs [B] A uniform increase of the [Ca]i in the terminal to <1.5 µM (top) causes increase in small EPSC frequency (bottom traces). (Asterisks mark putative quantal release events.) [C] Summary of relation between peak release rates and [Ca]i, displayed on log-log coordinates. [D] [Ca]i dependence of the delays between the [Ca]i jump and the onset of release. RESULTS Small amounts of calcium, e.g. 1 µM, are sufficient to trigger release. Even smaller amounts, e.g. 0.3 µM, can rapidly deplete the releasible SV pool, e.g. in < 0.5 ms. An increase to 10 µM for the duration of a presynaptic AP would be sufficient to elicit a full PSP. TAKEHOME: A brief, localized, increase in calcium is sufficient to trigger NT release. ...
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