Exam 3: Signaling Across Synapses

A series of critical experiments showed the properties of chemical synaptic transmission at the neuromuscular junction. One of these is shown in Figure Q3-1 in which the voltage across the membrane was recorded with an intracellular electrode. Figure Q3-1 A. What happened when the motor axon was stimulated? B. The investigators then applied ACh to the muscle via iontophoresis in the presence of TTX. Why did they use TTX? C. The elicited response of ACh iontophoresis was similar to nerve stimulation. What did this tell the investigators?

Myasthenia gravis is an autoimmune neuromuscular disease that results in muscle weakness caused by circulating antibodies that block acetylcholine receptors. People with the disease are treated with acetylcholinesterase (AChase) inhibitors or immunosuppressants. Why do AChase inhibitors work?

Which molecules activate the ionotropic AChR? Choose all that apply.

The presynaptic active zone must line-up with the postsynaptic density. What is one molecular mechanism that contributes to this alignment?

One way that nociception (the sensation of pain) is modulated is by presynaptic inhibition of transmitter release from the nociceptive sensory neuron onto its postsynaptic target that takes information to the central nervous system (Figure Q3-48). Endogenous opioids (endorphins) are released onto the presynaptic terminal of the nociceptive sensory neuron. Figure Q3-48 A. If endorphins eventually result in an increased probability of Ca²⁺ channel closure, what will happen to the amount of glutamate release from the sensory neuron? Increase or decrease? B. What would happen to Ca²⁺ channels if a G protein were activated in the absence of endorphin release? C. Would endorphin result in synaptic facilitation or depression?

In Figure Q3-52, a 5-ms depolarizing current pulse was injected into the soma, which produced a single action potential that was recorded in the cell body. Right after that, the distant dendrites of the neuron were activated, which generated a dendritic spike, which propagated to the cell body and resulted in two additional somatic action potentials. What would happen to (A) the first and (B) the second two action potentials if you blocked the dendritic action potentials? Figure Q3-52

Syt1 point mutation is a point mutation in synaptotagmin-1. How did the experiment shown in Figure Q3-12 show that synaptotagmin was probably the Ca²⁺ sensor? Figure Q3-12 B. What would the synaptotagmin-1 mutant response look like if synaptotagmin was not the Ca²⁺ sensor?

What are the three main SNARE proteins?

Flies with the Shibire mutant become paralyzed at high temperatures as this destabilizes dynamin. Why would this result in paralysis? Select all that apply.

What is a reversal potential (E_rev)?

Norepinephrine (NE) can bind to the β-adrenergic receptor and speed up heart rate through the cAMP signaling cascade. The cAMP cascade results in the phosphorylation of a voltage-gated Ca²⁺ channel, which increases its open probability. For each situation below state if the Ca²⁺ channel open probability increases, decreases, or does not change. A. Intracellular addition of cAMP, in the absence of application of NE B. In the absence of NE application, the inability of GTP to dissociate from Gα C. In the presence of NE application, the inability of GDP to dissociate from Gα

You identify a new neurotransmitter and call it Jerrionin. In order to characterize the actions of this neurotransmitter, you conduct an experiment in which you stimulate the Jerrionin-containing neuron while recording the postsynaptic current using voltage clamp. You get the following results: Figure Q3-27 A. Draw the I-V curve for this response. B. What is the reversal potential for the Jerrionin receptor? Why did you choose that value? C. What ion/s is/are most likely to have a high conductance through the Jerrionin channel?

You identify a new neuron in the Drosophila brain and find it contains acetylcholine. Based on this identification this neuron is ________. Explain your answer.