Answers to A2 Bilge Book - Chapter 13 Assignment

A2 BIOLOGY

NERVOUS SYSTEM AND RECEPTORS
CHAPTER 13 ASSIGNMENT ANSWERS

Baker, Indge and Rowland Book

(Nervous Receptors)

1. (a) An action potential is created when the sodium channels in the membrane of the nerve open to allow a sudden influx of sodium ions. (Normally, of course, the cell actively pumps out sodium ions, creating a ‘resting potential’ of around – 92 mV (c. 1/10th volt) within the cell.) ‘Voltage-sensitive’ refers to the fact that the gate only opens when a stimulus above a certain critical value reaches it.

(b)Each ion has a different diameter (particularly when associated with water molecules as in the human body). The ion channel protein will only allow ions of the appropriate charge and diameter to enter. It is not 100% accurate: strontium is accepted as a substitute for calcium, which can be a problem if the strontium is radioactive (Sr90) – this then becomes concentrated in bone tissue leading to cancer.

2. (a) Tetrodotoxin. [An aminoperhydroquinazoline poison]

will block sodium channels so that they will not open to allow the action potential to be generated. This will have the effect of incapacitating the nerve, leading to paralysis (motor neurones) or numbness (sensory neurones).

Tetrodotoxin (or)

Octahydro-12-(hydroxymethyl)-2-imino-5,9:7,

10a-dimethano- 10aH-(1,3) dioxocino(6,5-a)

pyrimidine-4,7,10,11,12-pentol

1. The large number of mitochondria immediately next to the pre-synaptic membrane. Presence of what look like microvilli (?), implying secretion.

1. Bungaratoxin is a polypeptide, so it will be digested in the stomach. It is too large to be absorbed intact (unless you have gastric ulcers).

1. (a) Bungaratoxin would be injected in low dose into a large animal (e.g. horse). A few days later another injection would be made. These stimulate the horse into producing large quantity of the specific antitoxin, which can then be extracted from a citrated and centrifuged sample of horse blood. When these antibodies are mixed with a fluorescent dye (attached other than to the toxin binding site), they can then be injected into a hapless iddy-bitty mouse that had earlier been injected with bungaratoxin (you know he really did have a bad day!) This animal is then killed (swing round by the tail and bang head on edge of bench – no, not you, the mouse!) and the neuromuscular junctions examined. The fluorescent antibodies will only bind to the bungaratoxin, which had itself attached to the neuromuscular junctions.

(b)No information in part (a) is of any relevance that I can see. Breathing involves two main sets of muscles, the intercostals and the diaphragm. Both sets are under the control of the autonomic nervous system i.e. they need nervous stimulation before they will contract. If krait venom (bungaratoxin) has the effect of blocking the secretion of neurotransmitter from the neuromuscular junctions, then these muscles will be paralysed. The heart would not be affected, so the individual would suffocate, or be eaten alive, but paralysed....hmmm!

1. Black widow spider venom. The supply of acetylcholine in the pre-synaptic vesicles is limited. If it is all released under the influence of the toxin, then there will be no more available and neurotransmission will cease.

Organophosphate insecticides. These stimulate the parasympathetic nervous system, by binding to acetylcholinesterase and so leading to acetylcholine remaining in the synapse for far longer than normal.

W-conotoxin from cone shells. By preventing Ca2+ ions from crossing the pre-synaptic membrane, the vesicles containing the neurotransmitter are no longer stimulated to fuse with the membrane and so remain intact. No neurotransmitter = no nerve impulse!