Unit 3 - Homeostasis (3) Flashcards
Ways to transmit information
direct contact between cells
diffusion of small molecules via junctions
slow and inefficient
endocrine system
quicker than gap junctions, but still relatively slow
a residual effect may remain until hormones are broken down
still somewhat inefficient as hormones travel throughout the body but only target specific effectors
nervous system
rapid transmission and response
effects are short lived
Neurons
highly specialized cells, functional unit of the nervous system
electrical transmission within neurons and chemical transmission between neurons
bundled together into nerves
neuron structure is not always the same, can differentiate based on their roles
Discovery of neuron function
much of what is known about neuron function was learned by studying the giant axons dissected out of squids
these are large enough to probe with electrodes to monitor their electrical activity
Action potential
when a resting axon is poked, there is a momentary reversal of polarization across the membrane
this creates a characteristic graph on an oscilloscope
Resting potential
the inside of a neuron is more negative than the extracellular fluid
the potential difference is about -70 mV (varies depending on the type of neuron)
the resting potential is caused by sodium/potassium pumps that use ATP to simultaneously pump 3 sodium ions out of and 2 potassium ions into the cells
Leak channels
there are sodium/potassium leak channels that allow these ions to leak back through the membrane
the leak channels are 100 times more permeable to potassium than to sodium
Voltage-gated sodium channels
there are voltage-gated sodium channels that open when the potential difference across the membrane reaches around -55 mV
if enough sodium ions can get back into the cytoplasm during the stimulus to lower the voltage from -70 mV to -55 mV, then the voltage-gated sodium channels open
this increases the sodium permeability of the membrane by 500 - 5000 times
sub-threshold stimuli do not let enough sodium ions in, so nothing happens
Depolarization
as sodium ions flood in through the voltage gated sodium channels, the potential difference across the membrane is temporarily reversed in the zone of depolarization
this means that the cytoplasm becomes positive compared to the outside
Voltage-gated potassium channels
as the membrane potential decreases from -70 mV to around 35 mV, voltage-gated potassium channels open to allow potassium ions to rush out of the cytoplasm
this allows the membrane to repolarize much more quickly than the sodium/potassium pumps
Propagation of impulse
after rushing into the cytoplasm, some of the sodium ions laterally diffuse along the inside of the cell membrane
these reduce the potential difference across the adjacent membrane enough to open the voltage-gated sodium channels
the adjacent membrane then depolarizes (chain reaction)
Refractory period
after depolarizing, the sodium/potassium leak channels take about 5ms to re-establish a resting potential
the neuron cannot be depolarized again during this refractory period
as a result, the wave of depolarization moves along the neuron membrane in one direction only (one-way flow)
neurons are normally stimulated at their end by sensors receptors anyways, so the wave wouldn’t move outwards in two directions from the middle
All or none response
neurons receiving a stimulus meeting or exceeding their threshold level will depolarize to the same extent and at the same speed
stronger stimuli do not produce larger action potentials or more frequent ones
Saltatory transmission
myelinated neurons don’t depolarize along their entire length
depolarization only occurs at the nodes of Ranvier between Schwann cells
this greatly reduces the amount of ATP required to reestablish a resting potential and speeds the transmission by 100x
multiple sclerosis takes out myelin sheaths, which destroys ability to use skeletal muscles
Neurotransmitters
allow a wave of depolarization to cross the gap (synapse) between neurons
the pre-synaptic neuron forms synaptic vesicles containing neurotransmitters
the arrival of an action potential causes vesicles of neurotransmitters to fuse with the cell membrane, releasing neurotransmitter into the synapse
neurotransmitter molecules diffuse across the synapse and combine with receptors in the postsynaptic cell
excitatory neurotransmitters depolarize and inhibitory ones prevent depolarization of the postsynaptic cell
theses are rapidly destroyed by enzymes to prevent residual effects
Neurotransmitter example
acetylcholine is excitatory in neuromuscular junctions (causes muscle contractions)
it is broken down by cholinesterase in the synaptic cleft
some insecticides and Sarin (nerve gas) kill by inhibiting cholinesterase