8 Flashcards
(111 cards)
nervous system
CNS (brain + spinal cord)peripheral NS (sensory nerves, motor nerves)autonomic NS (involuntary + stimulates smooth muscle, cardiac muscle and glands)Sympathertic NS ( preps body 4 fight or flight response)Parasympathetic ( preps body for rest and digest)somatic (voluntary+stimulates skeletal muscle)
motor, sensory and relay
motor-cell body situated within the CNS and axons extends out, conducting impulses from CNS to effectorssensory neurons- carry impulses from sensory cells to CNSrelay- these are found within the CNS- large no. of connections with other nerve cells
myelin sheath
fatty insulating layer around the axon- made up of Schwann cells wrapped around the axon
how resting potential of -70mV maintained
3 Na+ pumped out of the axon and 2K+ pumped into the axon against conc gradient using energy provided by hydrolysis of ATPonce conc gradient established by sodium potassium pump, K+ move out of the axon down the conc gradient, cell membrane more preamble to K+ then Na+- move through open channelsinside axon negative and outside axon positive creating a potential difference- polarized
what causes action potential
waves of depolarisation of the neurone- to pass electrical impulse down neurone once threshold stimulation occur action potential is caused by the change in permeability of axon membrane to Na+ and K+at resting potential voltage dependent gated channels are blocked by gates preventing the flow of ions through the,change in voltage across the membrane causes these gates to openwhen an impulse above the threshold is applied the PD across he membrane is locally reversed- depolarization- PD=+40 mV for brief instant- returns to -70 mV in repolarization
depolarisation
occurs when impulse stimulates neuronein receptor cells sodium voltage gated channels are opened by energy changes in environment, Na+ diffusionChange in PD across the membrane causes change in shape of Na+ gate, opening some of the voltage dependent sodium ion channels. small depolarisation has no effect on voltage gated channels, however, if depolarisation is large enough to reach threshold potential, it triggers the opening of more gates increasing depolarisation further causing a large influx of Na+thus a depolarisation of +40 mV is reachedpositive feedback loop- rapid opening of all Na+ gates- no way of controlling the degree of of depolarisationaction potentials are either there or they are not- all-or-nothing
hyperpolarization and repolarization
after about 0.5ms volatge gated Na+ channels spontaneously close and the permeability of the membrane to Na+ return to normal levelsdue to depolarisation of the membrane K+ voltage gated channels open and K+ ions flow out down eletrochemical and concentraton gradientinside axon becomes -ve again in comparison to outsidemembrane is now highly permeable to K+ and more ions move out than occurs at resting potential making PD more neg- hyper- resting potential re-established by closing the volatge dependent K+ channels and K+ diffusion into the axonif lots of action potentials occur in the neurone the Na+ conc inside cells rises significantly- sodium potassium pump starts to function restoring the og ion conc across the cell membrane - not used frequently if cell not transmitting many action potentialsrefractory period- immobilsies all ions channels- no further depolarisation
how an impulse is passed along an axon
stimualted neurone triggers a sequence of AP at resting potential there is a postive charge on the outside of the mebrane and a negative charge on the isnide, with high Na+ conc outside and high K+ conc inside when stimulated votlage dependent nA+ channels open, and soidum ions flow into the axon depolarisng the membrane - localsied electric currents are generated in the membrane- sodium ions move to the adjacent polarised resting region causing a change is PD at this part of the membrane the chnage in pd in the membrane adjacent to the first action potential initiates a second action potential- at the site of the first action potential the voltage dependent sodium ion channels close and voltage dependent potassium ion channels open- K+ leave the axon repolarisng the membrane - membrane becomes hyperpolarised a third action potential is initiated by the second - in this way local electric currents cuase nerve impulses to move along the axon- at site of 1st action potential potassium ions diffuse back into the axon resotring the resting potentiala new action potential cannot be generated in the same section of the membrane for a bout 5 miliseconds- refractory period- lasts until all the voltage dependent sodium and potassium channels have returned to their normal resting stage and the resting potential is restored- ensures impulse only travels in one direction
control of speed of impulse
diameter of axon- wider the dimaeter the faster the impulse
myelnation- myleniated neurones conduct impulses faster, mylein shiefs act as electrical inulators preventing the flow of ions, so depolarisation only occurs at the node sof tavier- salatory conduction
saltatory conduction
the insulatin mylein seath prevents curents from passing through the memebrane, except in gaps between Schwann cells- nodes of ranvier- areas of membrane hat become dpeolarised- this forces the current to travel down the axon to the next gap- AP jump from one gao to thenext
synapse structure
a
how synase trnasmits impulses
arrival of AP at the presynaptic membrane causes the release of neurotransmitter into the synaptic cleft- the neurotransmitter diffuses across the gap, reslting in events that cause the depolarisation of the postsynaptic membrane and hence the propagation of the impulse along the next cell the presynaptic cell expends a considerable amont of enrgy to produce the neurotransmitter and packag it inot a vesicles reay for transport out of the cell
synaptic transmssison
an action potential reaches terminal end of pre-synaptic neuronthe membrane depolarises causing voltage gated calcium channeles to open Ca2+ rush inca cuase synaptic vesicles conatining neurotransmitter to fuse with the presynaptic membraneneurotransmitter s released into the synatic cleft- exocytosis- trvale down conc gradientneurotransmitter binds with receptors on the pstsynaptic membrane- cation channels open- sodium ionsflow through the channelsthe membrane depolarises and initiates an APwhen released from the receptor the neurotrnasmitter will be taken up acoss the presynaptic membrane or it can diffuse aay and be brokendownenzyes in the synaptic gap then breakdown the NT- products taken up by presynaptic neuron by AT
stimulaton if the postsynaptic membrane
0.5 ms to diffuse across synaptic cleft and reach postsynaptic membrane
in postsynaptic memrane are specific receptor proteins that have binding sites with a complemntary shape to part of the acetylcholne molecules0 AM binds to receptor, chaninging the shape of theprotein, opening cation cannels and making the membrane permeale to sodium ions- flow of sodium ions across psotsy membrane causes depoarisation and if tehre is sufficent depolarisation an AP will be roduced and propgated along the postsynaptic neurone
the extent of the depolarisation will depedend on the amout of acetylcholine rraching the postsynaptic memane- depend on the frequency of impulses reaching the pre synaptc membrane- several required to generate enough neurotrsmitter to depolarise the ost synap membrne - no. of functioing receptros in post will alsoe influence degree of depolar
inactivaton of neurotransmitter
some neurotrnsmitter are actively taken up byre syanptic membrane and the molecules are used again- with others the neurotrnamitter rapidly diffuses away from the synaptic cleft or is taken up by other cells of the nervous system- in case of acetylcholine a specific enzyme at the psotsynaptic membrane, acetylcholinesterase, breaks down the acetylcholine so that it can no longer bind to receptors- some of the breakdownproducrs are then reabsorbedby the presynatic membrane and reused
role of synapses
control nerve pathways allowing flexibility of response
integration of info from diff neurones, allowing a coordinated response
factors thata ffect likelood of postsynaptic cell to depolarise
type of synapse
the no. o impulses reived
postsynatic cell likely to be recievig input from many synapses at the same time- the overall effect of thses synapses will determine whether or not the post synaptic cell generates an action potential
inhibitory and excitatory
make less likely for postsy membrane to depolarise and stimulate AP- post synaptic cll have manyof both so whether an AP result depends upon balnce of the two
Inhibitory: net decrease of neurotransmitters produced in post synaptic neurones
-Associated with parasympathetic nervous system, eg acetylcholine
Excitatory: net increase in NTs produced in post synaptic neurones
-Associated with sympathetic nervous system, eg adrenalin
excitatory synapses
make postsy mem more permable to NA- single synapse does not typically depolarise mem to produce AP but several arriving in a short period of time produces sufficent depolar via the relase of neurotransmitter to produce an AP in pstsy cell- each impulse adding to effect known as summationspatial summation- impulses from diff synapses usually from diff neurones - no. of diff sensory cells stimulated can be reflected in the control of the responsetemporal ummation- several impulses arive at synapse having travelled along a single neurone- combined release of neurotransmitter generates an AP n post sy membrane
inhibitory synapses
make it less likely for AP to result in post sy cell - neurotransmitters from these synapsesopen chanels for cl- and K+ in post sy membrane and these ions will move through the chanels down their diffusion gradient - cl_ will move into the cell carrying a negative charge an k+ move out cell caryying a pos charge - gretaer PD across membrane as inside becomes more neg than usual -90mV: hyperpolarisaton- makes subsquent depolarisation less leikely- more excitatory synapses required for depoalr
nervous v hormonal coordination
nervouselectrical transmission by nerve impulses and chem trans at synapsefats actinshort term changes- muscle cotractionAP carried by neurones with conections to specific cells local espnsehormonalchem trnasmission through the bloodslower actinca control long term chnagesblood carries hormone to all cells but only traget cells are able to repsond reponse may be widespread such as in growth and devlopment
cooridnation in plants
lack nervous system so must use chems to coordiante growth, development and repsosne to the environment
auxins
chems made in the tip of a plany passed down the coleptile- deonstarted by removin the tip, placing it on a small block of agar jelly ad putting the agar on top of the cut end- coleptile started to grow again showing auxin has diffused down through the agar jelly
auxons stimuale growt resulting in cell elongation
measurment of he amount of chems produced on the shaded and unshaded side of shoot found that total mount produced did not chnage compared wth a shoot illuminated from all sides- instead auxins had passed dwon the shaded side - increased conc on shaded side increased cell elongation, reduced inhibited cell elongation- shoot grew towards light
auxins such as IAA ae synthesied in actively growing roots and shoots tips and in developing seeds, leaves and fruits. They are transported from these sites to sites of action
transpoted long distances in phloem and short distances between cells via carrier proteins in the cell membrane- auxins bind to protein receptors in target cells- activates intracellular second messanger signal molecules which activate tracription fcators - control transciption of auxin reguated genes and the protein prduced bring about metabolic chnages that reuslt in a range of resposne through changes in cell expansion, division and differentiation
auxins cause acidifcation f cell wall by stimualting the activvityof proton pumos that move H+ out of the cytoplasm and into the cell wall here the low ph activates proteins called expansis- disrupt the bonds that old cellulose microfibrils and hemicellulose together- loseining of cell wall ; slippage o polysacchardes relaive to each other, bonds form in new locations allowing expansion of the cell
acidification of cll wall increases the PD across the membrane: enhances uptake of ions io cell- in turn the presence of these ions causes water uptake by osmosis causing cell to swell- elongation
plant growth involves cell division and elargemnt in the eristem cells are actively dividing , most of these cells enlarge, forming a region of elongation adjacent to the meristem- cells go on to mature and differentiate
cholodny-went model
circised due to small smaple size and diffuclty of measung small conc