Slow synaptic potentials

Dale used pharmacological criteria to distinguish two types of response to acetylcholine in peripheral tissues. Nicotinic responses are mimicked by nicotine and blocked by curare, whereas muscarinic responses are mimicked by muscarine and blocked by atropine. Correspondingly, we find there are two

Dendrite a b c

Fig. 8.7. Presynaptic inhibition. a (i) shows the EPSP produced in a motoneuron in response to stimulation (at time E) of the group Ia fibres innervating it. When a suitable inhibitory nerve is stimulated just beforehand (at I), the EPSP is reduced in size although there is no IPSP or other postsynaptic event associated with the inhibitory stimulation, as is shown in a (ii). b shows the probable nervous pathways and c shows the serial synapses which are thought to be involved. a From Eccles (1964).

Group la terminal

Interneuron terminal

Dendrite a b c

Fig. 8.7. Presynaptic inhibition. a (i) shows the EPSP produced in a motoneuron in response to stimulation (at time E) of the group Ia fibres innervating it. When a suitable inhibitory nerve is stimulated just beforehand (at I), the EPSP is reduced in size although there is no IPSP or other postsynaptic event associated with the inhibitory stimulation, as is shown in a (ii). b shows the probable nervous pathways and c shows the serial synapses which are thought to be involved. a From Eccles (1964).

distinct types of acetylcholine receptor, nicotinic and muscarinic. Nicotinic receptors occur at the skeletal neuromuscular junction, muscarinic receptors mediate the responses of heart muscle to vagal stimulation. Both types are found in sympathetic ganglia, where they produce different types of responses: let us have a look at them.

The postsynaptic cells in bullfrog sympathetic ganglia show a number of different types of synaptic activity, as is shown in Fig. 8.8. A single stimulus to the preganglionic fibres produces a fast EPSP which may be large enough to produce an action potential in the postganglionic fibres. The response is blocked by curare and can be mimicked by acetylcholine. Thus the mechanism of production of the fast EPSP is similar to that at the neuromuscular junction: it is mediated by nicotinic acetylcholine receptors in which a cation-selective channel opens when actylcholine is bound to it.

In some cells a slow EPSP with a much longer time course occurs after the fast EPSP. Similar responses are seen after application of acetylcholine. The slow EPSP is unaffected by curare but is blocked by atropine, hence the receptors which mediate it are muscarinic. Conductance measurements show that the slow EPSP is produced by the closure of ion channels selective for potassium ions.

In other cells the fast nicotinic EPSP is followed by a slow, hyperpolarizing IPSP. This also is muscarinic, and probably involves the opening of potassium channels. Finally, a long period of repetitive stimulation of the preganglionic

Als Repetitive Stimulation

Fig. 8.8. Fast and slow synaptic responses in a frog sympathetic ganglion neurons. The trace on the left in a shows the fast EPSP produced by a single preganglion stimulus; a stronger stimulus (right) excites more pre-ganglionic fibres giving a larger EPSP which is sufficient to produce an action potential. In b to d the fast EPSP is blocked by a curare-like compound; repetitive stimulation at various sites then produces three different types of slow response. Note the different time scales. From Kuffler (1980).

Fig. 8.8. Fast and slow synaptic responses in a frog sympathetic ganglion neurons. The trace on the left in a shows the fast EPSP produced by a single preganglion stimulus; a stronger stimulus (right) excites more pre-ganglionic fibres giving a larger EPSP which is sufficient to produce an action potential. In b to d the fast EPSP is blocked by a curare-like compound; repetitive stimulation at various sites then produces three different types of slow response. Note the different time scales. From Kuffler (1980).

fibres produces a depolarization which lasts for a few minutes; it is called the late slow EPSP. The neurotransmitter which produces this is a peptide similar in structure to the luteinizing hormone-releasing hormone.

Slow potentials are widely distributed. Their time course and their long latency could be explained if channel opening or closing is mediated by an indirect process involving intermediate steps between binding at the receptor and the response of the channel, rather than the direct link which occurs in fast-acting receptors with intrinsic channels. The intermediate steps involve the activation of G proteins and often the production of intracellular 'second messengers'.

The second messenger concept was first introduced to describe the role of cyclic adenosine monophosphate (cyclic AMP) in hormone action. Combination of a hormone with its receptor activates a G protein (so called because it needs to bind guanosine triphosphate to become active) which in turn activates the enzyme adenylate cyclase. This produces cyclic AMP which then alters the physiological properties of the cell in some way, such as by opening or closing ion channels. Neurotransmitters may act in a similar fashion, or may utilise a different second messenger such as inositol trisphosphate. In some cases the G protein may act directly on the membrane channel without producing a second messenger. Fig. 8.9 summarizes the various ways in which neurotransmitters may affect channels, and Table 8.1 outlines some of the various neurotransmitter receptors.

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  • darcy
    What are slow synaptic potentials?
    2 years ago

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