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FIGURE 4–5. Modes of interneuronal communication.Panel A. Different connection patterns dictate how information flows between neurons. In synaptic divergence, one neuron (a) may disseminate information to several postsynaptic cells (b–f) simultaneously (information flow is shown by arrows). Alternatively, in the case of synaptic convergence, a single neuron (d) may receive input from an array of presynaptic neurons (a–c). In presynaptic inhibition, one neuron (b) can modulate information flowing between two other neurons (from a to c) by influencing neurotransmitter release from the presynaptic neuron's terminals; this can be inhibitory (as shown) or facilitatory. Panel B. Neurons may modulate their own actions. In feedforward inhibition, the presynaptic cell (a) may directly activate a postsynaptic cell (b) and at the same time modulate its effects via activation of an inhibitory cell (c), which in turn inhibits the cell (b). In recurrent inhibition, a presynaptic cell (a) activates an inhibitory cell (b) that synapses back onto the presynaptic cell (a), limiting the duration of its activity. ap = action potential; li = lateral inhibition; ri = recurrent inhibition.Source. Adapted from Shepherd GM, Koch C: "Introduction to Synaptic Circuits," in The Synaptic Organization of the Brain, 3rd Edition. Edited by Shepherd GM. New York, Oxford University Press, 1990, pp. 3–31.

FIGURE 4–6. Synaptic ultrastructure.Neuromuscular junctions from frog sartorius muscle were flash-frozen milliseconds after high potassium treatment to increase synaptic transmission. Panel A. Synaptic vesicles are clustered at two active zones (arrows), which are sites where vesicles fuse with the plasma membrane to release their neurotransmitter. Panel B. At higher magnification and after stimulation, omega profiles of vesicles in the process of releasing their neurotransmitter are visible.Source. Reprinted from Schwarz TL: "Release of Neurotransmitters," in Fundamental Neuroscience, 2nd Edition. Edited by Squire LR, Roberts JL, Spitzer NC, et al. San Diego, CA, Academic Press, 2003, pp. 197–224; original source Heuser JE: "Synaptic Vesicle Endocytosis Revealed in Quick-Frozen Frog Neuromuscular Junctions Treated With 4-Aminopyridine and Given a Single Electrical Shock." Society for Neuroscience Symposia 2:215–239, 1977. Copyright 1977. Used with permission.

FIGURE 4–7. Steps in synaptic transmission at a chemical synapse.Essential steps in the process of synaptic transmission are numbered. Ca2+ = calcium.Source. Reprinted from Purves D, Augustine GJ, Fitzpatrick D, et al. (eds): Neuroscience, 3rd Edition. Sunderland, MA, Sinauer Associates, 2004, p. 97. Used with permission.

FIGURE 4–8. Molecular events in synaptic vesicle docking and fusion.A coordinated set of proteins is involved in the positioning of vesicles at the presynaptic membrane and in controlling release by membrane fusion. Panel A. Many of the recently cloned synaptic vesicle proteins are integral to this process. Some of these proteins interact with the cytoskeleton to position the vesicles at the terminal, while other proteins are integral to the fusion process. In addition, several of these synaptic vesicle proteins are targets for neurotoxins that function by influencing neurotransmitter release. Panel B. The current theory for how synaptic vesicles fuse with the membrane and release neurotransmitter is called the SNARE hypothesis. Both the synaptic vesicles and the plasma membrane express specific proteins that mediate docking and fusion: v-SNAREs (synaptic vesicles) and t-SNAREs (plasma membrane). Vesicles are brought close to the membrane through interactions between VAMP (synaptobrevin), syntaxin, and SNAP-25. N-ethylmaleimide-sensitive fusion protein (NSF) then binds to the complex to facilitate fusion. Calcium (Ca2+) influx is required to stimulate fusion, but the precise binding partner for calcium and the exact events leading to fusion remain obscure. Panel C. The crystal structure of the fusion complex, as shown here, is consistent with the SNARE hypothesis. BoNT = botulinum toxin; TeNT = tetanus toxin.Source. Adapted from Kandel ER, Siegelbaum SA: "Transmitter Release," in Principles of Neural Science, 4th Edition. Edited by Kandel ER, Schwartz JH, Jessell TM. New York, McGraw-Hill, 2000, pp. 253–279. Copyright 2000, The McGraw-Hill Companies, Inc. Used with permission.

FIGURE 4–9. Neurotransmitter transporters.Synaptic transmission in the CNS is terminated for the most part by reuptake of neurotransmitter by specific transporters with shared molecular motifs. These transporters carry neurotransmitters across membranes against concentration gradients, and thus require metabolic energy. Most often, this energy is provided by cotransport of an ion down its concentration gradient. Panel A. One family of transporters in synaptic vesicles serves to load neurotransmitter or transmitter precursors into synaptic vesicles. Panel B. A second family of transporters in the plasma membrane with eight transmembrane domains handles amino acid neurotransmitters, such as glutamate and -aminobutyric acid. Panel C. A third family of transporters in the plasma membrane with 12 transmembrane domains handles the monoamines dopamine, norepinephrine, and serotonin.Source. Reprinted from Schwartz JH: "Neurotransmitters," in Principles of Neural Science, 4th Edition. Edited by Kandel ER, Schwartz JH, Jessell TM. New York, McGraw-Hill, 2000, pp. 280–297. Copyright 2000, The McGraw-Hill Companies, Inc. Used with permission.

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