receptor in nervous system in at resting state - not stimulated
pacinian Corpuscle
mechanoreceptors - pressure + vibrations
sensory nerve ending wrapped in lamellae - end of sensory neurone
lamellae deform and press sensory nerve ending when stimulated
deform stretch-mediated sodium ion channels - open and Na diffuse into cell - generator potential trigger action potential
photoreceptors (light)
light enter via pupil
light rays focused by lens into retina (photoreceptors)
fovea contains most photoreceptors
nerve impulses carried from retina to brain by optic nerve - leaves eye via blind spot
photoreceptors convert light into impulse
light enters eye, hit receptors and absorbed by light sensitive optical pigments
light bleach pigment causing chemical change and alter membrane permeability to Na+
generator potential created and if exceed threshold nerve impulse sent along bipolar neurone
bipolar neurone
connect photoreceptors to to optic nerve which takes impulse to brain
Rods eye receptors
peripheral parts of retina
black and white
light sensitive
many rods join one neurone
many weak generator potentials combine to reach threshold and trigger action potential. Low visual acuity - light from 2 points close together cant be told apart
cone eye receptors
packed in fovea
colour - red/green/blue sensitive
less light sensitive
one cone joins one neurone
takes longer for more light to reach threshold and trigger action potential
high visual acuity - cones close together. can distinguish 2 points close together as two separate points
conduction system
SA node initiate impulse. (pacemaker) in right atria
Cause left and right atria to contract at same time
A band on non-conducting collagen tissue prevent impulse passing to ventricle
impulse transferred to AV node - delay impulse until atrial systole complete
Reach bundle of his split impulse to purkyne fibres
contract at base of ventricle
heart rate regulation
rate of SA release of impulse is unconsciously controlled by medulla oblongata
-baro/chemo receptors detect changes
-send impulses to SAN and (para)sympathetic neurones
neurones polarised at rest
resting state - outside membrane positive compared to inside (polarised)
-70mV
created and maintained by sodium-potassium pump
neurones membrane become depolarised when stimulated
stimulus - excite causing open, increase permeability to sodium (gradient)
depolarisation - potential difference exceeds threshold (-55mV), more sodium ion channels open and diffuse in
repolarisation - potential difference (+30mV) the Na channels close and K open (K diffuse out and return to resting)
Hyper-polarisation - K channels slow to close so slight overshoot ( p.d become more negative)
refractory period
neurone cell can’t be edited again straight after action potential
ion channels recovering and can’t be opened
Na+ channels closed during repolarisation and K channels are closed during hyper polarisation
factors affecting speed of conduction action potential
myelination
axon diameter
temperature
myelination
have myelin sheath - electrical insulator
sheath made of Schwann cells- between have small bare membrane - Node of Ranvier (Na channels conc)
depolarisation only occur at node of ranvier
cytoplasm conducts enough impulse to depolarise next node - saltatory conduction
Axon diameter
action potential conducted quickly along axons with bigger diameters because there’s less resistance to flow of ions.
less resistance, depolarisation reached other part of neurone cell membrane quicker
temperature
speed of conduction increases the temp increases
ions diffuse faster
40°C
Synapse
junctions between 2 neurones or between a neurone and an effector
synaptic cleft
tiny gap between cells at synapse
presynaptic neurone
before synapse
swelling - synaptic knob
contains synaptic vesicles filled with neurotransmitters
postsynaptic neurones
action potential reached end of neurone it causes neurotransmitters to be released into synaptic cleft
diffuse across to post synaptic membrane and bind to specific receptors
receptors only on post synaptic membrane - unidirectional
Ach transmits impulse at Cholinergic synapse
action potential reach synaptic knob and stimulate Ca+ channels to open (Ca diffuse in)
influx of Ca ions cause synaptic vesicles to move to presynaptic membrane and fuse together ( vesicle release Ach - exocytosis)
Ach diffuse across cleft and bind to cholinergic receptors on post synaptic
Na+ chanel open (Na diffuse in) - depolarisation
Ach removed so response doesn’t reoccur, broken down by acetylchokinesterase