Chapter 44

1. 1. Refer to Figure 44.1.

   2. At a chemical synapse, a chemical signal crosses the synaptic space between neurons. A neurotransmitter released by the presynaptic nerve endings diffuses across the synaptic space to bind to receptors on the postsynaptic membrane.

2. A neuron can receive both excitatory and inhibitory input at multiple synapses located throughout its dendrites and on the cell body. Summation of inputs determines whether the postsynaptic neuron becomes sufficiently depolarized to initiate an action potential.

3. Astrocytes can take up neurotransmitters that have been released into the synapse and thereby control the postsynaptic response. Astrocytes can also directly release neurotransmitters that bind to receptors to affect the excitability of a neuron.

1. The Nernst equation calculates the membrane potential that will exist across a membrane due to the movement of a specific ion across that membrane, given the concentration difference of that ion on the two sides of the membrane. The dominant ion responsible for the membrane resting potential is K⁺, but the potential calculated from the K⁺ concentrations by the Nernst equation does not equal the measured membrane potential. This is because the membrane is also slightly permeable to other ions, and they contribute to the measured membrane potential. The Goldman equation predicts membrane potential more accurately because it takes into account all ions that have concentration differences across the membrane as well as the relative permeability of the membrane to those ions.

2. Inhibitory inputs to the dendrites of a neuron cause hyperpolarization of the dendrite membrane, and excitatory inputs cause depolarization. These changes in membrane potential spread to the neuron’s cell body. The resulting membrane potential of the cell body is a graded membrane potential because it is always reflecting the sum of the dendritic inputs. That graded membrane potential spreads to the base of the axon, which fires action potentials if its membrane potential reaches threshold for its electrically gated Na⁺ channels. Therefore the rate of action potential generation is a function of the graded membrane potential of the neuron’s cell body, hence an integration of all of the dendritic inputs.

3. When the voltage-gated Na⁺ channels open in a patch of membrane, that patch depolarizes. That local depolarization spreads by electrical conduction to neighboring regions of membrane, bringing them to threshold and thereby causing their electrically gated Na⁺ channels to open and regenerating that action potential. This process continues down the length of the axon.

4. If the axons of the motor neurons that stimulate the muscle are demyelinated, the conduction velocity will be decreased and reflected in a longer delay for the muscle to respond to the electrical stimulation.

1. The motor end plate contains chemically gated Na⁺ channels and voltage-gated Na⁺ channels. The chemically gated channels respond to the neurotransmitter acetylcholine to depolarize the motor end plate. The voltage-gated channels respond to that local depolarization by generating action potentials that spread to the adjacent muscle cell membrane.

2. The action of a neurotransmitter depends on the receptor types in the postsynaptic membrane, and they can initiate excitatory or inhibitory responses in the postsynaptic neuron.

3. Asphyxiation is the inability to breathe. Breathing requires regular activity in the motor neurons controlling the respiratory muscles. The inhibition of acetylcholinesterase by sarin results in the accumulation of acetylcholine in the synapses between the respiratory motor neurons and the respiratory muscles, reducing the ability of those muscles to relax between breaths.

4. Electrical synapses are fast but do not integrate information well. Electrical synaptic input does not allow temporal summation of inputs, as electrical synapses require a large area of contact between pre- and postsynaptic cells for effective transmission thus limiting the numbers of synapses that can be formed between two neurons. Finally, electrical synapses cannot provide inhibitory input.

1. Ganglia are collections of nerve cell bodies. They tend to be concentrated in the anterior region of many invertebrates because that is where large numbers of sense organs are located.

2. See Figure 44.14.

3. In the knee-jerk reflex the same stimulus can cause contraction of a muscle through an excitatory synapse and relaxation of the antagonist muscle because of an inhibitory interneuron.

4. The part of the vertebrate brain that increases the most in going from fish to reptiles to mammals is the most anterior part of the brain, the cerebrum.

1. Plugging the values in the table into the equation gives:

   Substituting 2.3RT/F log for RT/F ln:

   Assuming T = room temperature, 2.3RT/F = 58 (see Figure 44.5).

   So,

   V_m = 58 log 0.1118

   V_m = –55.2 mV

   If you use the Nernst equation:

   K⁺: E_K = 58 log (5/140) = –84 mV

   Na⁺: E_Na = 58 log (145/10) = +67 mV

   Cl^–: E_Cl = 58 log (110/20) = +43 mV

   Clearly the membrane potential is not due to K⁺ alone. The membrane permeabilities to Na⁺ and to Cl^– have a slight depolarizing influence on the resting potential of the mammalian neuron.

1. During the dark phase the WT mice had significant discrimination scores during testing, indicating that they learned to recognize the training object. The DS mice did not have significant discrimination scores and thus did not learn. These were the same results as obtained during the light phase.

2. When the experiment was done during the dark phase, the results for the saline-treated mice showed the same results as during the light phase—the WT animals learned to recognize the training object, and the DS mice did not. The results for the drug-treated mice, however, were different than they were in the light-phase experiment. PTZ treatment during the dark phase did not result in an improved ability of the DS animals to learn to recognize the training object. Thus the conclusion is that the drug has to be given during the light phase to have an effect.

1. The 1-second light stimulation of the hypocretin neurons caused depolarization of their membrane potentials and a large increase in the rate at which they fired action potentials. These results support the concept that ChR2 is a Na⁺ channel and that light increases the Na⁺ permeability of that channel, depolarizing the membrane and bringing the membrane potential to above the threshold potential for firing of APs.

2. The fact that the firing of the neurons followed precisely the trains of very short bursts of light (15 ms) indicates that the APs of the neurons were direct responses to the light.

3. The light stimulation of hypocretinergic neurons expressing ChR2 in sleeping mice shortened the latency to awakening. The same light stimulation had no effect on the mice not expressing ChR2. Above a frequency of 1 flash per second, the awakening response was not altered by the frequency of stimulation.

4. The fact that a blocker of the hypocretin receptor eliminated the awakening effect of the light stimulation supports the conclusion that the effect was mediated by the release of hypocretin by the stimulated neurons.