Neuroeffector Communication

Thus far we have described the effects of neurotrans-mitters released at synapses. Many neurons of the peripheral nervous system end, however, not at synapses on other neurons but at neuroeffector junctions on muscle and gland cells. The neurotransmitters released by these efferent neurons' terminals or varicosities provide the link by which electrical activity of the nervous system is able to regulate effector cell activity.

The events that occur at neuroeffector junctions are similar to those at a synapse. The neurotransmitter is released from the efferent neuron upon the arrival of an action potential at the neuron's axon terminals or varicosities. The neurotransmitter then diffuses to the surface of the effector cell, where it binds to receptors on that cell's plasma membrane. The receptors may be directly under the axon terminal or varicosity, or they may be some distance away so that the diffusion path followed by the neurotransmitter is tortuous and long. The receptors on the effector cell may be associated with ion channels that alter the membrane potential of the cell, or they may be coupled via a G protein, to enzymes that result in the formation of second messengers in the effector cell. The response (altered muscle contraction or glandular secretion) of the effector cell to these changes will be described in later chapters. As we shall see in the next section, the major neu-rotransmitters released at neuroeffector junctions are acetylcholine and norepinephrine.


I. An excitatory synapse brings the membrane of the postsynaptic cell closer to threshold. An inhibitory synapse hyperpolarizes the postsynaptic cell or stabilizes it at its resting level.

II. Whether a postsynaptic cell fires action potentials depends on the number of synapses that are active and whether they are excitatory or inhibitory.

Functional Anatomy of Synapses

I. A neurotransmitter, which is stored in synaptic vesicles in the presynaptic axon terminal, carries the signal from a pre- to a postsynaptic neuron. Depolarization of the axon terminal raises the calcium concentration within the terminal, which causes the release of neurotransmitter into the synaptic cleft.

II. The neurotransmitter diffuses across the synaptic cleft and binds to receptors on the postsynaptic cell; the activated receptors usually open ion channels.

a. At an excitatory synapse, the electrical response in the postsynaptic cell is called an excitatory postsynaptic potential (EPSP). At an inhibitory synapse, it is an inhibitory postsynaptic potential (IPSP).

b. Usually at an excitatory synapse, channels in the postsynaptic cell that are permeable to sodium, potassium, and other small positive ions are opened; at inhibitory synapses, channels to chloride and/or potassium are opened.

c. The postsynaptic cell's membrane potential is the result of temporal and spatial summation of the EPSPs and IPSPs at the many active excitatory and inhibitory synapses on the cell.

Activation of the Postsynaptic Cell

I. Action potentials are generally initiated by the temporal and spatial summation of many EPSPs.

Synaptic Effectiveness

I. Synaptic effects are influenced by pre- and postsynaptic events, drugs, and diseases (Table 8-6).

Neurotransmitters and Neuromodulators

I. In general, neurotransmitters cause EPSPs and IPSPs, and neuromodulators cause, via second messengers, more complex metabolic effects in the postsynaptic cell.

II. The actions of neurotransmitters are usually faster than those of neuromodulators.

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Neural Control Mechanisms CHAPTER EIGHT

Neural Control Mechanisms CHAPTER EIGHT


A substance can act as a neurotransmitter at one type of receptor and as a neuromodulator at another. The major classes of known or suspected neurotransmitters and neuromodulators are listed in Table 8-7.

Neuroeffector Communication

I. The junction between a neuron and an effector cell is called a neuroeffector junction.

II. The events at a neuroeffector junction (release of neurotransmitter into an extracellular space, diffusion of neurotransmitter to the effector cell, and binding with a receptor on the effector cell) are similar to those at a synapse.


excitatory synapse inhibitory synapse convergence divergence electric synapse chemical synapse synaptic cleft cotransmitter synaptic vesicle excitatory postsynaptic potential (EPSP) inhibitory postsynaptic potential (IPSP)

spatial summation presynaptic synapse presynaptic inhibition presynaptic facilitation autoreceptor neuromodulator acetylcholine (ACh) acetylcholinesterase cholinergic nicotinic receptor muscarinic receptor biogenic amine dopamine temporal summation epinephrine catecholamine adrenergic noradrenergic alpha-adrenergic receptor beta-adrenergic receptor serotonin excitatory amino acid glutamate aspartate GABA (gamma-aminobutyric acid)

norepinephrine (NE)

glycine neuropeptide peptidergic endogenous opioid beta-endorphin dynorphin enkephalin substance P

nitric oxide



Contrast the postsynaptic mechanisms of excitatory and inhibitory synapses.

Explain how synapses allow neurons to act as integrators; include the concepts of facilitation, temporal and spatial summation, and convergence in your explanation.

List at least eight ways in which the effectiveness of synapses may be altered.

Discuss differences between neurotransmitters and neuromodulators.

Discuss the relationship between dopamine, norepinephrine, and epinephrine.

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  • fre-swera welde
    Is the axon varicosities has neurotransmitter is stored and released form?
    8 years ago

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