Quiz 2 - chapter 12 problems

The afferent division of the nervous system has what two components?

Afferent division consists of sensory receptors and sensory neurons.

Chronic exposure to elevated concentrations of a signaling molecule usually causes receptor downregulation or desensitization, reducing the cell's responsiveness to the signal.

Define homeostasis.

Homeostasis is the maintenance of a relatively stable internal environment.

1. Connections between the sympathetic ganglia allow rapid communication within the sympathetic branch.

2. Antagonistic control: pupil of eye, heart (rate), bronchioles, digestive tract, endocrine and exocrine pancreas, and urinary bladder. Cooperative control: salivary glands, penile erection, and ejaculation.

A nerve that carries both sensory and motor information is called a(n) ________ nerve.

Mixed nerves carry sensory and motor signals.

Name the four regions of the spinal cord in order, starting from the brain stem.

The regions of the spinal cord are cervical, thoracic, lumbar, and sacral.

The three neurons that secrete ACh are cholinergic. The one neuron that secretes norepinephrine is adrenergic. The cell bodies of all preganglionic neurons are in the CNS; the cell bodies of postganglionic neurons are in a ganglion outside the CNS.

Nicotine acts as an agonist at nicotinic ACh receptors, opening ligand-gated cation channels and causing postsynaptic depolarization, similar to acetylcholine.

In what organelle is most intracellular Ca2+ stored?

Ca2+ is stored in the endoplasmic reticulum.

7. What enzyme

• (a) converts ATP to cAMP?

• (b) does cAMP activate?

• (a) Adenylyl cyclase converts ATP to cAMP.

• (b) cAMP activates protein kinase A.

Is the adrenal medulla most like the anterior pituitary or the posterior pituitary? Explain.

The adrenal medulla is neurosecretory and therefore like the posterior pituitary.

Predict whether chromaffin cells have nicotinic or muscarinic ACh receptors.

Chromaffin cells are modified postganglionic neurons, so they have nicotinic receptors.

3. Chronic nicotine exposure causes nAChRs to become desensitized, reducing their activity. Cells may compensate by upregulating nAChRs to maintain responsiveness to stimulation.

4. Voltage-gated Na⁺ channels.

5. Excessive nicotine causes prolonged activation and subsequent desensitization of nicotinic ACh receptors at the neuromuscular junction. This disrupts neuromuscular transmission and prevents the diaphragm and other respiratory muscles from contracting, potentially causing respiratory paralysis.

Is the ventral (anterior) horn of the spinal cord, which contains the cell bodies of somatic motor neurons, gray matter or white matter?

The ventral horn is gray matter.

Compare gating and ion selectivity of acetylcholine receptor-channels in the motor end plate with that of ion channels along the axon of a somatic motor neuron.

The nAChR of the motor end plate is a ligand-gated monovalent cation (Na+ and K+) channel. The axon contains voltage-gated channels, with separate channels for Na+ and K+

A nonsmoker who chews nicotine-containing gum might notice an increase in heart rate, a function controlled by sympathetic neurons. Postganglionic sympathetic neurons secrete norepinephrine, not ACh, so how could nicotine affect heart rate?

Postganglionic sympathetic neurons are activated by ACh from the preganglionic neuron acting on nicotinic receptors. This means that nicotine also excites sympathetic neurons, such as those that increase heart rate

Predict what will happen to ACh release from the axon terminal in Lambert-Eaton syndrome, where auto-antibodies cause removal of voltage-gated Ca2+ channels from the presynaptic membrane of the NMJ.

With less Ca2+ entry through Ca2+ channels, there would be decreased exocytosis of ACh-containing vesicles.

One treatment for muscle weakness in both myasthenia gravis and Lambert-Eaton syndrome is administration of acetylcholinesterase inhibitors. Why would these drugs help reverse the muscle weakness?

Acetylcholinesterase at the NMJ breaks down ACh. Leaving active ACh in the synapse longer helps offset the lower concentration of ACh in Lambert-Eaton syndrome or the loss of AChR in MG.