Nervous Communication Flashcards
Resting potential
Sodium potassium pump transports 3 sodium ions out of the axon and 2 potassium ions into the axon.
Active transport – against a concentration gradient.
Concentration of sodium ions outside the cell increases.
Potassium ions diffuse out of the axon
The sodium ion gate is closed.
The sodium ions cannot diffuse into the axon. Positive charge on the outside of the axon
Action potential
Sodium ion channel protein opens.
Sodium ions diffuse into the axon along the concentration gradient.
Potassium ion channel protein closes.
Inside of the axon becomes positively charged.
Outside of the axon becomes less positive (-) charged.
Repolarisation
Potassium ion channels open
Potassium ions diffuse out of axon
Sodium ion channels close.
More positively charged outside axon.
Sodium ions actively transported outside the axon.
Pacinian corpuscle
Increase pressure deforms stretch mediated sodium on channels
Sodium channels open
Sodium ions flow in
Depolarisation
Leads to a generator potential
Rod cells
Rhodopsin breaks down when light shines on it.
Rhodopsin → retinal + opsin
Results in a series of reactions
Generator potential being produced.
ATP is needed to re-synthesise rhodopsin.
Synapses
Action potential reaches end of sensory neurone. Na+ enters the axon.
Calcium ion channels in the presynaptic membrane open allowing calcium ions to diffuse into the presynaptic knob.
Ca2+ ions cause vesicles containing acetylcholine to fuse with the presynaptic membrane.
Neurotransmitter is released into the synapse.
Acetylcholine diffuses across the synapse.
Binds to the receptor proteins on post synaptic membrane –
Causes sodium ion channels to open on post synaptic membrane.
Sodium ions enter relay neurone.
Action potential generated at next Node of Ranvier.
Acetylcholinesterase breaks down acetylcholine which leaves the receptor protein. Acetyl and choline diffuse across the synapse.
Acetyl and choline reabsorbed into the presynaptic knob
Condense to form acetylcholine.
Muscle contraction
Action potential arrives in the muscle cell membrane.
Actin potential travels down a T tubule.
Action potential causes calcium ions to be released from the ER in the muscle cell. Calcium ions bind to the troponin
Tropomyosin to move and reveal the myosin binding sties.
Myosin head binds to the actin to form an actinomyosin bridge.
Myosin moves in power stroke
Myosin pulls the actin.
ADP is released from the myosin head.
Attachment of ATP to the myosin head causes actinomyosin bridge to break
ATP is hydrolysed
Energy released used to ‘recock’ the myosin head.
Calcium ions reabsorbed into the ER of the muscle cell by active transport
Myosin binding sites are hidden preventing myosin binding to the actin.
Control of cardiac cycle/heart beat
SAN sends wave of electrical activity over the atria
Atria contract
Non-conducting tissue prevents impulses reaching the ventricles
AVN delays impulse blood leaves atria into ventricles
AVN sends wave of electrical impulses down
Bundle of His or Purkyne fibres Ventricles contract from base up sending blood into arteries
Increasing heart rate due to increased respiration
Rate of respiration increases in muscles
Chemoreceptors detect rise in CO2 / H+ / acidity / carbonic acid / fall in pH Receptors in aortic arch or carotid bodies
Send impulses to cardioaccelerator centre in medulla
Increased frequency of impulses to SAN
Along sympathetic nervous system to SAN
Release of noradrenaline increase impulses frequency from SAN
Reducing heart rate due to increase blood pressure
Pressure receptors or baroreceptors detect increase in blood pressure Baroreceptors in aortic arch or carotid arteries
Send impulses to cardioinhibitory centre in medulla
Increased frequency of impulses to SAN
Along parasympathetic nervous system
Release of acetylcholine decreases frequency of impulses from SAN;
