Although many neurotransmitters depolarize the postsynaptic membrane (produce EPSPs), some transmitters do just the opposite. The neurotransmitters glycine and GABA hyperpolarize the postsynaptic membrane; that is, they make the inside of the membrane more negative than it is at rest (fig. 7.30). Since hyperpolar-ization (from -70 mV to, for example, -85 mV) drives the membrane potential farther from the threshold depolarization required to stimulate action potentials, this inhibits the activity of the postsynaptic neuron. Hyperpolarizations produced by neuro-transmitters are therefore called inhibitory postsynaptic potentials (IPSPs), as previously described. The inhibition produced in this way is called postsynaptic inhibition. Postsynaptic inhibition in the brain is produced by GABA, while in the spinal cord it is mainly produced by glycine (although GABA is also involved).
Excitatory and inhibitory inputs (EPSPs and IPSPs) to a post-synaptic neuron can summate in an algebraic fashion. The effects of IPSPs in this way reduce, or may even eliminate, the ability of
Threshold for action potential
Inhibitory neurotransmitter from neuron ® Excitatory neurotransmitter from neuron (2
■ Figure 7.30 An IPSP hyperpolarizes the postsynaptic membrane. An inhibitory postsynaptic potential (IPSP) makes the inside of the postsynaptic membrane more negative than the resting potential—it hyperpolarizes the membrane. Subsequent or simultaneous excitatory postsynaptic potentials (EPSPs), which are depolarizations, must thus be stronger to reach the threshold required to generate action potentials at the axon hillock.
EPSPs to generate action potentials in the postsynaptic cell. Considering that a given neuron may receive as many as 1,000 presynaptic inputs, the interactions of EPSPs and IPSPs can vary greatly.
In presynaptic inhibition (fig. 7.31), the amount of an excitatory neurotransmitter released at the end of an axon is decreased by the effects of a second neuron, whose axon makes a synapse with the axon of the first neuron (an axoaxonic synapse). The neu-rotransmitter exerting this presynaptic inhibition may be GABA or excitatory neurotransmitters, such as ACh and glutamate.
Excitatory neurotransmitters can cause presynaptic inhibition by producing depolarization of the axon terminals, leading to inac-tivation of Ca2+ channels. This decreases the inflow of Ca2+ into the axon terminals and thus inhibits the release of neurotransmitter. The ability of the opiates to promote analgesia (reduce pain) is an example of such presynaptic inhibition. By reducing Ca2+ flow into axon terminals containing substance P, the opioids inhibit the release of the neurotransmitter involved in pain transmission.
Test Yourself Before You Continue
1. Define spatial summation and temporal summation and explain their functional importance.
2. Describe long-term potentiation, explain how it is produced, and discuss its significance.
3. Explain how postsynaptic inhibition is produced and how IPSPs and EPSPs can interact.
4. Describe the mechanism of presynaptic inhibition.
■ Figure 7.31 A diagram illustrating postsynaptic and presynaptic inhibition. These and other processes permit extensive integration within the CNS.
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