You are not signed in. Sign In / Register.

MCQ

Bookmark

Personalize Website

Account

About

Sign In

A2 Level

AS Level

A2 Human Biology Unit 11

Text questions

P227/Q1		Motor/effector neurones stimulate muscles/glands (effectors).
P228/Q2		Cell body, nucleus, dendrite, synoptic knobs; Schwann cells/nodes of Ranvier absent in relay neurone but present in sensory neurone.
P229/Q3		Because there are two polar regions present: Cytoplasm inside neurone (-) Tissue fluid outside neurone (+)
P230/Q4	a)	-70mV
	b)	+40mV
	c)	4ms
P232/Q5		Blue
P233/Q6		Nerve impulses can only travel in one direction along the neurone, because an action potential can only depolarise the membrane "in front". (The membrane "behind" is in its refractory period and cannot be depolarised again).
P234/Q7		Surface Area/Volume ratio in neurones having small diameter is larger than S.a./V. ratio in neurones having large diameter. Consequently, diffusion/leakage of ions in "thin" neurones is greater than leakage in "thick" neurones.
P235/Q8		Exocytosis.
P236/Q9		Simple reflex: In-born (not learned); Always results in the same (fixed) response to a particular stimulus (e.g.dilation of a pupil).
P238/Q10		Heat receptor → sensory neurone → relay neurone in the spinal chord [→ relay neurone up the ascending tract to brain → various centres in the brain, e.g. memory centre (the impulse may be cancelled here; if not cancelled, then:] → relay neuron down the descending tract from the brain) → motor/effector neurone → muscle in the arm (biceps).

Assignment

P241/Q1	a)	As a result of a stimulus/impulse, V-sensitive Na⁺ gates open and the resulting influx on Na⁺ ions will cause an action potential (= an abrupt/sharp change in the concentration of Na⁺ ions between the outside and the inside of the axon, which consequently brings about an abrupt change/reversal of the potential difference (from -70mV to + 40mV).
	b)	Each of the voltage sensitive gates is specific to a particular ion (Na⁺, K⁺, Cl^-) because of the presence of an "ion filter" in their molecule.
P241/Q2	a)	As a result of tetrodotoxin blocking the Na⁺ ion gate, no Na⁺ ions will be able to move across the gate into the neurone. This movement of Na⁺ ions is normally the cause of an action potential, therefore no action potential is possible = insensitivity to stimuli = paralysis.
P242/Q3		Presence of vesicles (containing neurotransmitter) is a feature of the presynaptic membrane.
P242/Q4		Bungaratoxin, if swallowed, will be digested in the gut. If injected, it will be transported by blood/tissue fluid onto the postsynaptic membrane on the neuromuscular junction.
P242/Q5	a)	(Fluorescent) antibodies will bind on the bungaratoxin in the neuromuscular junction. Their fluorescent properties can be used to trace their position at the neuromuscular junction.
	b)	Muscles associated with breathing are stimulated by neurones. If the postsynaptic membrane of the neuromuscular junction is covered by bungaratoxin, (= receptor molecules blocked by the toxin), then, consequently, neurotransmitter released by the presynaptic knob will not bind to the receptors and the postsynaptic membrane will not be depolarised.
P242/Q6		Black widow spider venom: large amounts of acetylcholine released (→ lack of acetylcholine in the presynaptic knob) → ACh not available to stimulate action potential in the postsynaptic neurone (= temporary paralysis). Organophosphate insecticides: inhibit enzyme acetylocholinesterase → ACh not deactivated by acetylcholinesterase → ion channels in the postsynaptic membrane remain open (= influx of Na+) → action potential continually generated → effectors (tear/salivary glands) overstimulated → continuous production of saliva/tears). W-conotoxin: prevents Ca²⁺ ions from crossing the presynaptic membrane (yet influx of Ca²⁺ ions necessary for release of ACh) → ACh not released → no action potential generated in the post- synaptic membrane.

Examinations

P243/Q1	a)	(i) ATP → ADP + energy (for active transport). (ii) Na⁺ and K⁺ ions can move across the membrane of the neurone via open ion channels. The movement of, for example, K⁺ ion is determined by its electrochemical gradient. (Electrochemical gradient = electrical gradient + concentration gradient of K⁺ ions across the membrane). K⁺ ion concentration inside the cell is higher than outside. However, K⁺ ions will not move out of the neurone down the concentration gradient, because the build up of positive charges (Na⁺ ions and K⁺ ions together) on the membrane outside the neurone eventually repels the movement of any more K⁺ ions, preventing their outward movement. An equilibrium is reached. (NB. The same applies to Na⁺ ions).
	b)	Stimulus/impulse arrives → Na⁺ gate(s) open → influx of Na⁺ ions: the tiny part of the membrane (where the change occurs) becomes depolarised (: action potential) → adjacent Na⁺ gate(s) open → influx of Na⁺ ions (etc.). At the same time K⁺ gates open (: K⁺ flow out of the neurone, thus restoring the resting potential). Although the resting potential has now been restored, the balance of Na⁺ and K⁺ ions has not. This is done by structure A (Na-K pump) using ATP.
P243/Q2	a)	(i) pH (the higher CO2, the lower pH) (ii) Medulla oblongata (iii) The accelerator nerve: Impulses travelling down this nerve to the SAN increase the heart rate; Impulses travelling to the heart muscle increase the strength of the contraction; (Vagus nerve: opposite action). (iv) High % CO2 in blood → chemoreceptors (aortic & carotid bodies) → sensory nerves → cardiovascular centre in medulla oblongata → accelerator nerve → increased heart rate & strength of contractions (stroke volume) → increased cardiac output → increased blood flow through the lungs → increased gaseous exchange in alveoli → less CO2 in blood (sensed by chemoreceptor of the aortic body) → sensory neuron → cardiovascular centre in m. oblongata → vagus nerve → decreased heart rate & strength of contraction (stroke volume) → lower gaseous exchange in alveoli → more CO2 in blood.
P244/Q3	a)	Stimulus/impulse arrives → Na⁺ gates open → influx of Na⁺ ions: the tiny part of the membrane (where the change occurs) becomes depolarised (: action potential) → adjacent Na⁺ gates open → influx of Na⁺ ions (etc.). At the same time K⁺ gates open (: K⁺ flow out of the neurone, thus restoring the resting potential). Although the potential difference has now been restored, the balance of Na⁺ and K⁺ ions has not. This is done by Na-K pump using ATP.
	b)	Step 1: The arrival of a nerve impulse at the end of the presynaptic axon causes an influx of Ca²⁺ ions and induces the vesicles to release their neurotransmitter into the synaptic cleft. Step 2: The neurotransmitter diffuses across the synaptic cleft to receptors on the postsynaptic membrane. This delays the impulse transmission by about 0.5 ms. Step 3: The neurotransmitter binds to receptors on the post- synaptic membrane. Step 4: Ion channels in the membrane open, causing an influx of Na⁺. This response may or may not reach the threshold required to generate a nerve impulse. Step 5: The neurotransmitter is deactivated by acetylcholinesterase enzymes located on the membrane. Components of the neurotransmitter are actively reabsorbed back into the synaptic knob, recycled, and repackaged.
	c)	Stimulus: pin prick → pain receptors in the skin → action potential up the sensory neurone → synapse → the relay neurone (spinal cord, sensory impulse interpreted) → action potential across the synapse to the motor neurone → action potential down the motor neuron → motor end plate → muscle contraction (response).
P244/Q4	a)	(i) Resting potential: the inside of the neurone is -70mV. Action potential: Na+ gates open → Na+ diffuse inside the neurone changing the potential difference across the membrane from the inside being -70 mV, to the inside being now +40 mV (= action potential). (ii) The resting potential is restored as a result of K+ ions, diffusing across the membrane (through open V-sensitive K+ gates) from the inside to the outside of the neurone.
	b)	If the next action potential is to be generated, different gradients of Na⁺ and K⁺ concentrations (between the inside and outside of the neurone) are necessary. This is achieved by Na-K pump which uses ATP for active transport of Na⁺ (outside of neuron) and K⁺ (inside). ATP is produced by mitochondria during respiration, hence high metabolic rate in active neurones.

Bluecounter Website Statistics

Bluecounter Website Statistics