9.2- the mammalian nervous system Flashcards
2 divisions of the nervous system
1.CNS- brain and spinal cord
2.PNS-sensory and motor neurons
the peripheral nervous system
-made up of somatic and autonomic
-autonomic is further divided into sympathetic (arousing) and parasympathetic (calming)
-somatic is further divided into sensory and motor
autonomic- sympathetic Vs parasympathetic
symp= speeds up activity
para=slows down/ inhibits activity
function of sensory Vs motor neuron
-sensory carries impulses from receptors towards CNS
-motor carries nerve impulses away from the CNS to effectors
motor nervous system sub divisions
1.voluntary- carries nerve impulses to the bodies muscles under conscious control
2.autonomic- carries nerve impulses to glands smooth or cardiac muscle and is involuntary
autonomic nervous system sub divisions
-sympathetic and parasympathetic
-these systems act antagonistically
functional comparison parasympathetic Vs sympathetic
symp
-produces noradrenaline at synapses
-often involved in fight or flight
-activated in times of stress
para
-slower inhibitory effect
-acetylcholine produced
-maintains normal functions, rest and digest
brain functions- cerebrum
-controls voluntary behaviour including movement, intelligence, memory, personality and ability to reason
brain functions- cerebellum
-coordinates smooth movements, using info from muscles and ears the maintain balance and posture
brain functions- medulla oblongata
-contains reflex centres that control functions such as breathing and heart rate
brain functions- hypothalamus
-thermoregulation and osmoregulation
-coordinates autonomic nervous system
-involved in thirst, hunger etc
sensory neuron structure
-cell body in centre
-synaptic bulbs at end to pass on impulses
-receptor e.g. pressure receptor at other end connected to dendrites
-direction of nerve impulse is from receptor end to bulb end
relay neuron structure
-cell body in centre
-very short axon either side
-not myelinated
-no Schwann cells or nodes
-impulse travels from dendrites end to synaptic bulbs
motor neuron structure
-cell body on end
-other end has synaptic bulbs attached to effector e.g. muscle
-dendrites coming off cell body
-myelinated axon
-nodes and Schwann cells
myelination and its purpose
-means they are wrapped in a Schwann cell
-this cell forms a fatty layer
-protects nerve from damage
-speeds up transmission of impulse by stimulating it
-gaps between are nodes of ranvier
what is resting potential?
-when the inside of the axon is negatively charged compared to the outside
-we describe the axon as polarised
-resting potential is around -70mV
when does an action potential occur
-when a neuron sends information from its cell body down its axon
stages of action potential
1.depolarisation- movement of Na+ ions into neuron reduces potential difference across the membrane +40mV
2.repolarisation- movement of K+ ions out of neuron reduces depolarisation
3.hyperpolarisation- K= channels stay open too long, gradually ion concs go back to resting
the sodium potassium pump
-requires ATP
-3 Na+ ions move out for every 2K+ in
-ATPase in pump uses ATP to move ions
how resting potential happens
1.Na ions are actively transported out by Na-K pump
2. K ions actively transported in by pump
3. active transport of Na is greater than K 3-2
4. Na will naturally diffuse back into axon and potassium out
5. however, most Na channels are closed and most K channels more permeable
6. so gradient maintained
steps of AP in detail
-stimulus causes some Na gates to open so sodium ions diffuse in, they trigger depolarisation, becomes +
-as Na diffuses in, more Na channels open increasing diffusion (pos feedback)
-once around +40mV, sodium ion channels close and excess pumped out by Na K pump
-K channels open so they diffuse out of axon moving down conc gradient axon is repolarised
-outward diffusion of K ions causes overshoot, with inside being more neg that usual (hyper)
-gates on K channels close and once again Na pumped out and K in
-RP -70mV again
refractory period
-recovery time of an axon
-neurons can generate nerve impulses at many frequencies, limited by;
1.absolute refractory period- neuron inexcitable
2.relative refractory period- less excitable than normal
-when line on graph lies flat
absolute refractory period
-left part of graph before AP
-sodium channels completely blocked and RP has not been restored
-milliseconds
-second stimulus will not trigger second AP no matter how strong
relative refractory period
-when potassium channels are open to repolarise the membrane
-normal RP cannot be restored until these are closed
-greater then normal stimulus required to initiate AP
purpose of refractory periods
- ensures APs are only propagated in one direction
-produces discrete impulses so Aps are separate
-limits number of Aps
transmission in unmyelinated axons
-current occurs in part of the neuron
-this is detected in an adjacent part of membrane
-causes voltage gated channels to open when threshold is reached
-nerve impulse is transmitted as self propagating wave of depolarisation
propagation in myelinated axons
-myelin sheath acts as electrical insulator
-current can only be set up between adjacent nodes of ranvier
-more sodium channels are open at these nodes
-depolarisation leaps from one node to next (saltatory conduction)
-therefore nerve impulses can be transmitted very quickly and efficiently
factors affecting nerve impulses- myelination
-only vertebrates have this
-increases speed
-100 times faster
factors affecting nerve impulses- axon diameter
-wider axon can transmit impulses faster
-myelination means there is no need for wide axons
-therefore takes up less space
factors affecting nerve impulses- temperature
-higher temp means faster conduction, within limits
-this is because propagation involves diffusion of ions and rate of diffusion increases with temperature
-therefore ions have more kinetic energy
-temp also effects enzymes involved in active trasnport to maintain RP
-at very high temps, they denature, disrupting nerve conduction
events at a synapse
-Action potential depolarises the presynaptic neuron.
-Calcium channels open and calcium diffuses in.
-Synaptic vesicles move to and fuse with the pre-synaptic membrane.
-The neurotransmitter is released into the synaptic cleft.
-Neurotransmitter moves across cleft by diffusion.
-Neurotransmitter binds to specific protein receptors on the sodium channel on the post synaptic membrane..
-Sodium channels open and sodium diffuses in.
-This causes a change in the potential difference of the membrane and an excitatory post-synaptic potential (EPSP) to be set up.
-If there are a sufficient number of these EPSPs, the positive charge in the post-synaptic cell exceeds the threshold level and an action potential will occur.
inhibitory post synaptic potential
-kind of synaptic potential that makes postsynaptic neuron less likely to generate AP
-different channels open in membrane allowing inward movement of neg ions
-makes it more neg than RP
-means AP less likely to occur
synapse- breakdown of neurotransmitters
-broken down by hydrolytic enzymes
-they then move back across the cleft, back into synaptic knob and are recycled
acetylcholine
-neurotransmitter found at majority of synapses
-it is broken down by an enzyme called acetylcholinesterase.
-acetyl and choline diffuse back across the cleft into presynaptic
-this allows neurotransmitter to be recycled
2 types of synapses
1.adrenergic
-often found in sympathetic nervous system
-uses noradrenaline as neurotransmitter
2.cholinergic
-mostly found in parasympathetic
-only uses Acth
specific drug examples need to know
-nicotine -cobra venom
-lidocaine
effects of drugs- nicotine
-mimics effects of acetylcholine
-triggers dopamine release which can be associated with pleasure sensations
-triggers AP in post synaptic but receptors remain unresponsive for a while
-has stimulating effect at low doses but lethal in high doses
effects of drugs- lidocaine
-used as local anaesthetic by dentists
-blocks voltage gated Na channels so preventing AP
-also prevents some heart arrhythmias so preventing early action potentials
effects of drugs- cobra venom
-toxic and often fatal
-binds reversible to acetylcholine receptors, preventing an impulse
-can be used to relax trachea muscles in low doses
-means muscles are not stimulated to contract so person becomes paralysed
function of eye parts- cilliary muscle
-pulls lens for focusing
function of eye parts- cornea
-lets light in eye and begins focusing
function of eye parts- iris
-controls amount of light entering eye
function of eye parts- lens
- focuses light onto retina
function of eye parts- optic nerve
-sends signals to brain
function of eye parts-pupil
-lets light through to lens
function of eye parts-retina
-light sensitive layer, sends messages to optic nerve
function of eye parts- suspensory ligaments
-holds lens in plae
transduction in the eye
-converts light into pattern of nerve impulses
-takes place in retina by layer of photosensitive cells at back of eye
rod cells
-spread evenly across retina except fovea
-show black and white images
-cannot distinguish between different wavelengths of light
-detect light at very low intensity
-threshold must be detected before potential can occur
-generator potential is generated in bipolar cell
-multiple to one bipolar (retinal convergence), threshold more likely to be reached through summation
rod cells- visual acuity
-cannot distinguish 2 close together dots
-because light received only generates one impulse
-
rod cells in low light
-rhodopsin must be broken down to create generator potential
-low light intensity has enough energy to break this down
cone cells
-tightly packed at fovea
-3 diff types for diff wavelengths
-own seperate bipolar neurons
-only respond to high light intensity as summation cannot occur
-brain can distinguish between separate light sources
-iodopsin requires higher light intensity to break down
-contain diff types od iodposin for diff light wavelengths
the fovea
-part of the retina which light is focused on
-receives greatest intensity of light
-therefore cone cells found here
how does rhodopsin work?
-Rhodopsin is formed from opsin and retinal.
-Retinal exists as 2 different isomers: cis-retinal & trans-retinal.
-In the dark all retinal is in the cis form.
-When a photon of light hits the rhodopsin, it converts from cis to trans form.
-This changes the shape of the retinal and puts strain on the bonding between opsin and retinal, breaking up the molecule.
-This is known as ‘bleaching’.
bleaching
-Rod cells are usually quite permeable to sodium ions.
-When rhodopsin is bleached, this causes the -Na ion channels to close, making it less permeable to sodium.
-However, the sodium pump continues to work and so sodium ions are removed from the cell.
-This makes the inside of the rod cell more negative than normal.
-This hyperpolarisation is known as the ‘generator potential’.
HR control by baroreceptors
-found in carotid arteries in neck and aorta, when exercise starts;
1.blood vessels dilate in response to adrenaline, bp falls
2.reduces stretch in baroreceptors
4.cardiac control centre sends messages along sympathetic nerve to stimulate heart rate and increase bp by vasoconstriction
HR control by chemoreceptors
-found in walls of carotid arteries
-sensitive to CO2 levels which cause changes in pH
1.when blood has high CO2 conc, pH is lowered
2.they detect this and inc frequency of impulses to medulla
3.this increases frequency of impulses via sympathetic to SAN so hr increases
4.inc blood flow means more CO2 is removed from lungs
HR control by hormones
-when stressed, sympathetic nerve stimulates adrenal medulla to release adrenaline
-binds to receptors on target organ, including SAN
-increases excitation and so increasing hr
-more oxygen and glucose are supplied to muscles for fight or flight
cardiac output calculation
stroke volume* heart rate
