Discussion for

Weekly Sample Exam Unit 2, No. 1

True/False

Explanation of false statements...

6. The resting potential of neurons is around -70 mv, closer to the K+ equilibrium potential than the Na+ equilibrium potential. This is because the axon membrane is much more permeable to potassium ions than to sodium ions at rest.

8. A decrease in extracellular Ca++ tends to enhance the influx of sodium ions, hence tends to depolarize (made less negative) the resting potential of a neuron.

10. The cerebellum is mainly associated with motor skills. Strictly speaking, the, damage to the cerebellum would not mainly produce anesthesia.

12. Damage to the neuromuscular junctions would disrupt communication between motor neurons and skeletal muscle cells. The result would be some form of muscle weakness or paralysis. Sensation would not be altered.

13. If inhibitory synapses in the CNS were destroyed, excitatory synapses would prevail and lead to inappropriate transmission along sensory and motor pathways. This would lead to heightened sensation (paresthesias) rather than anesthesia.

15. Action potentials travel faster along axons with more myelination. This is because myelin tends to concentrate and improve current flow between nodes. And if the speed between nodes is improved, so will the overall propagation velocity along the nerve

Terminology

K+ equilibrium potential

1. A voltage that exists across the axon (cell) membrane when potassium ions are in a state of electochemical equilibrium. It is determined by the concentration gradient and the degree to which the membrane is permeable to K+. The greater the concentration gradient or permeability "favoritism", the greater this voltage. Normally, it is about -90 mv.
2. The K+ equilibrium potential, along with the Na+ equilibrium potential determine the overall esting potential of nerve and muscle cells. Anything that increases the K+ equilibrium potential will increase the resting potential, making the cell less excitable and vice versa. Furthermore, without a K+ equilibrium potential there might not be any resting potential, hence no possibility for action potentials, hence no sensory function (anesthesia) or motor function (paralysis).

Dual motor innervation

(a) This refers to smooth and cardiac muscle that receive both sympathetic and parasympathetic nerve fibers, one tending accelerate activity, one tending to inhibit. Neither of these cause the muscle to contract (they're both autorhythmic). Rather they control the rate and strength of contraction.

(b) Just as the speed of a car can be affected better by the action of brakes and accelerator, the value of this system is that it provides more immediate and efffective control over such actions as glandular secretion, peristalsis and heart rate.

EPSP

1. An excitatory postsynaptic potential is a voltage created on a post- synaptic membrane by the action of an excitatory transmitter substance (TS). The size of this voltage is variable, and determined by the amount of TS released. The amount of TS released is based on the amount of Ca++ allowed into the presynaptic terminal which is based on the frequency of presynaptic APs. The greater the EPSP the greater the depolarizing action on the resting potential of the postsynaptic membrane. Some excitatory TS molecules include acetylcholine, norepinephrine and serotonin.
2. EPSPs work in conjunction with IPSPs in determining when and to what degree an action potential will be transmitted. Factors that increase EPSPs would tend to accentuate sensory and motor or interneuronal activities and vice versa. Without EPSPs, IPSPs would effectively block AP transmission, hence shutting down sensory and motor function. Lights out, game over!

Refractory Period

1. This is the time during which a nerve or muscle cells is insensitive to further stimulation and will not produce an action potential. It begins as the cell is first depolarized from its resting potential and ends when the cell repolarizes to its normal value. A cell cannot produce and action potential during its refractory period because an action potential is basically in progress.

(b) The length of the refractory period determines the number of action potentials that can be produced in a period of time (its maximum frequency response). Hence a cell with a shorter refractory period can generate more APs per second. In addition, the refractory period prevents APs from reversing as they advance along a neuron because the earlier nodes of an axon are in a refractory state.

Situational

1.Occupation of postsynaptic reactive sites by strychnine means the poison blocks the action of the inhibitory transmitter substance and prevents the formation of IPSPs. Therefore EPSPs will dominate at the synapse and the resting potential of the postsynaptic membrane will be depolarized (brought closer to threshold). This will tend to promote transmission across sensory and motor synapses. The former would lead to bizarre sensations (paresthesia) such as tingling or burning in an extremity, the latter would lead to twitches or involuntary contraction in skeletal muscles. High doses could be lethal because it would cause sustained contraction of the diaphragm (a skeletal muscle) which would amount to respiratory arrest.

2. Blocking the operation of the Na+ channels of peripheral nerves would prevent the influx of sodium ions. This would nullify the sodium equilibrium potential (+60 mv) and so cause the resting potential to be entirely determined by the K+ equilibrium potential. In other words the resting potential would be become more negative, farther from threshold. Sensory symptoms would be degrees of peripheral anesthesia (numbness of the extremities) and motor symptoms would be degrees of weakness. In high doses the diaphragm would not be able to contract and breathing would stop. In fact a number of people die each year in Japan as a result of gambling with the puffer fish.