Figure 141

Composite drawing of ganglionic neurotransmission. For simplicity, it has been divided into a type A synapse containing interneurons or small intensely fluorescent (SIF) cells and a type B synapse lacking interneurons. In the type A synapse, ACh is released from the preganglionic neuron and activates nicotinic and muscarinic receptors on the SIF cells (when present), leading to the release of a catecholamine, presumably dopamine. Dopamine subsequently activates a receptor on the postganglionic nerve. The insert depicts the temporal postganglionic action potential, consisting of a fast excitatory postsynaptic potential (EPSP) due to activation of nicotinic receptors by ACh, a slow inhibitory postsynaptic potential (IPSP) due to dopamine or another catecholamine activating the appropriate receptor, and a slow EPSP due to activation by ACh of an M± muscarinic cholinergic receptor on the postganglionic nerve cell body. The muscarinic receptor on the SIF cell is either an M± or M2 cholinergic receptor. The postganglionic nerve cell body also contains autacoid receptors that generate a late slow EPSP The broken line and X represent the appropriate receptor antagonists. The type B synapse is similar to type A but lacks interneurons and SIF cells. In this case, ACh activates both nicotinic receptors leading to the fast EPSP and muscarinic receptors leading to the slow IPSP and slow EPSP The receptor type leading to the slow IPSP is either M± or M2; that leading to the slow EPSP is M±. ACh, acetylcholine; DA, dopamine.

Type A Synapse Type B Synapse

Type A Synapse Type B Synapse

Chapter 28). Stimulation of nicotinic receptors in adrenergic nerve terminals leads to the release of norepineph-rine; and activation of nicotinic chemoreceptors in the aortic arch and carotid bodies causes nausea and vomiting. Nicotinic receptors in the central nervous system mediate a complex range of excitatory and inhibitory effects.

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