Fig. 6.1B shows a complex synaptic arrangement called a glomerulus that involves both chemical and electrical synapses among the participating elements.
Much of what we know about chemical synapses comes from the study of two classic preparations, the frog neuromuscular junction (the synapse from a motor neuron onto a muscle fiber) and the squid giant synapse (the synapse from a second-order neuron onto third-order neurons that innervate the muscle of the squid’s mantle; i.e., the motor neurons whose axons were used to characterize the conductances underlying the action potential [see ]). The principles governing transmission at these synapses mostly apply to synapses within the mammalian CNS as well, at least with regard to synapses using what are called the “classic” neurotransmitters (see the section mitters). Thus, much of the following discussion will be based on results from these two preparations; however, some differences in CNS synapses will also be pointed out.
3 Gaseous transmitters Arginine NO synthase Citrulline Mitochondria Peptides diffuse in extracellular space and bind to synaptic and extrasynaptic G protein–complex receptors Gaseous transmitters diffuse out of cell of origin and directly into other cells. They can act inside cell of origin or in cells distant from point of release G protein– coupled receptors NO Activates variety of enzymes Ionotropic and G protein– coupled receptors Acetyl CoA + Choline Reuptake by transporter 1 Small-molecule neurotransmitters AChAcetyl cholinesterase Other small-molecule neurotransmittersSmall-molecule neurotransmitters diffuse across synaptic cleft and bind to postsynaptic receptors Vesicle transporter concentrates neurotransmitter into vesicles Postsynaptic cell Presynaptic terminal Ca++ channels Large electron-dense vesicles NO O2 Nitrogen oxide (inactive) 2 Neuropeptides •Fig. 6.2 Schematicofachemicalsynapticterminalreleasingallthreemainclassesofneurotransmitter.Foreach,themechanismsofrelease,sitesofaction,andmechanismsforterminationofactivityareshown.Realsynapsesreleasetransmitterfromoneormoreclasses.
Synaptic transmission at a chemical synapse may be summarized as follows. Synaptic transmission is initiated by arrival of the action potential at the presynaptic terminal. The action potential depolarizes the terminal, which causes Ca++ channels to open. The subsequent rise in [Ca++] within the terminal triggers the fusion of vesicles containing neurotransmitter with the plasma membrane. The transmitter is then expelled into the synaptic cleft, diffuses across it, and binds to specific receptors on the postsynaptic membrane. Binding of transmitter to receptors then causes the opening (or less often, the closing) of ion channels in the postsynaptic membrane, which in turn results in changes in the potential and resistance of the postsynaptic membrane that alter the excitability of the cell. The changes in membrane potential of the postsynaptic cell are termed excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) (
Fig. 6.3 ), depending on whether they increase or decrease, respectively, the cell’s excitability, which can be defined as its probability of firing action potentials. The transmitter acts for only a very short time (milliseconds) because reuptake and degradation mechanisms rapidly clear the transmitter from the synaptic cleft.