Nervous System Flashcards
which animals dont have nervous systems?
sponges.
jellyfish have “nerve nets” but this still counts. many animals lack cephalization (a brain), so instead have clustered ganglia that act as integrating centres.
how do neurons communicate?
chemical and electrical signals
which are the 3 main divisions of neurons
afferent sensory
integrating
efferent motor
which division of neurons are in the CNS?
integrating centres
which division of neurons are in the PNS
efferent and afferent
how do afferent neurons transmit information?
they send information from the stimulus to the integrating centre
how do efferent neurons transmit information
information from integration centre to the effector
describe the vertebrate nervous system
high degree of cephalization (large brains)
unique hollow dorsal nerve cord (spinal cord)
part if nervous system encased in bone/cartilage (CNS)
part of nervous system extends into periphery of body (PNS)
nervous system, top to bottom
cerebrum
cerebellum
brainstem
cervical nerves
spinal cord
thoracic nerves
lumbar nerves
sacral nerves
coccygeal nerves
draw it! (slide 14)
what is in the CNS?
brain and spinal cord
(interneurons perform integrating functions of CNS, including processing sensory info from afferent neurons and sending commands to efferent neurons)
draw the organization of the nervous system!
slide 15
CNS feeds into two divisions:
afferent and efferent
efferent branch has two divisions:
somatic (voluntary) and autonomous (involuntary)
what does the somatic nervous system feed into
skeletal muscle, since it’s voluntary control
what are the 3 divisions of the autonomic system?
sympathetic nervous system
parasympathetic nervous system
(both are smooth muscle, cardiac muscle, exocrine glands and some endocrine)
enteric nervous system (digestive organs)
2 major cell types in nervous system
glia and neurons
describe glial cells
not electrically excitable!
important for development and support, homeostasis of extracellular fluid around neurons and synapses, and helps with electrical insolation (forms myelin sheaths)
more abundant than neurons, ~90% of NS
describe neurons
fundamental, electrically excitable cells (signal via APs)
make up only 10% of NS
structurally and functionally distinct
carry out electrical and chemical communication
5 main types of vertebrate glial cells
ependymal cells
astrocytes
microglia
oligodendrocytes
schwann cells
ependymal cells
line fluid filled cavities of CNS, which circulate cerebrospinal fluid
astrocytes
transport nutrients, remove debris in CNS, regulate neurotransmitter levels around synapse.
*in PNS, neurotransmitter levels are controlled by satellite cells
microglia
neuronal maintenance, remove debris and dead cells from CNS
oligodendrocytes
forms myelin on neurons of CNS to increase electrical insulation and increase electrical conduction speed. one oligodendrocytes may wrap around the axon of several neurons
schwann cells
deposit myelin on motor and sensory neurons of PNS
increase electrical conduction speed along the axon
what do oligodendrocytes and schwann cells do for their respective neurons?
they reduce electrical/ion lead across the membrane, increasing AP signal transmission
draw the different kinds of neurons on slide 20!
most important:
purkinje cell
motor neuron
retinal neuron
olfactory neuron
efferent and afferent sensory neurons
interneurons
how do 3 functional classes of neurons differ in structure?
draw them from slide 20!
efferent neurons look like the typical neurons with their cell body and dendrite position
interneurons are all cell body and dendrites
afferent/sensory neurons are p much all axon, cell body off to the side
4 functional zones of the vertebrate neuron
signal reception
signal integration
signal conduction
signal transmission
Draw it! (Slide 21)
what structure is responsible for signal reception?
dendrites and cell body
what structure is responsible for signal integration ?
axon hillock
what structure is responsible for signal conduction?
axon
what structure is responsible for signal transmission?
axon terminals
explain membrane potential
all animal cells maintain a voltage difference across their cell membranes. this voltage difference is the membrane potential.
explain voltage difference
a source of potential energy for the cell, 2 functions:
- provide energy for membrane transport
- change in membrane potential is used by cells in cell-to-cell signalling
what can excitable cells do with their cell permeability?
they can alter cell permeability to generate changes in membrane potentials over time
what is the difference between non-excitable and excitable cells?
excitable cells have the ability to significantly change their electrical activity and propagate a signal.
explain the electrical properties of neuron membrane
cell membranes have varying degrees of permeability to different ions with varying concentrations across the membrane.
which ions are most influential on membrane potential? why?
K+
Na+
Cl-
they move readily across the cell membrane and have differences in extra/intracellular concentrations
what is the function of the sodium potassium pump?
running on ATP, it maintains Na+ and K+ gradients across the membrane
explain chemical gradient
concentration gradient for an ion across the plasma membrane
describe electrical gradient
created by attraction between opposite charges (+/-) or repulsion between like charges (+/+ or -/-)
describe electrochemical gradient
form of potential energy determined by the combination of an ion’s chemical and electrical gradients
describe equilibrium potential
membrane potential at which an ion’s electrical and chemical gradients are in balance. No net movement of ions across the membrane.
what sort of signal is in the cell body?
chemical
what sort of signal is in the axon hillock?
electrical
what sort of signal is in the axon?
electrical
what sort of signal is in the axon terminals?
chemical
draw the neuron electrical/chemical diagram!
ok!
slide 15
how to measure membrane potential in resting cell?
glass micropipette filled with saline and placed in extracellular solution. electrode placed into resting nerve cell.
Interior of cell is more electronegative than the exterior of the cell
describe electrochemical gradient
a combination of both chemical and electrical forces that act upon ions across a cell membrane
when neurons are excited, gated ion channels open. all ions move in an attempt to reach their equilibrium potential.
what is equilibrium potential
the membrane potential when the electrical gradient for an ion is in balance with the chemical gradient and there is no net movement of the ion
how do we calculate the equilibrium potential of a cell?
NERNST equation.
Eion = 58mV/z log [ion]o/[ion]i
z is valence
ion conc outside and inside the cell.
what is Na+ equilibrium potential? how is it reached?
+70
when Na+ channels open and Na+ floods into the cell and depolarizes the membrane.
What is K+ potential? how is it reached?
-90
When channels open and the membrane is hyperpolarized, K+ leaves
Resting membrane potential: potassium ion channels
membrane resting at -70.
K+ chemical gradient wants it out, electrical gradient wants it in. the electrochemical gradient wants it out.
the equilibrium potential for both gradients to balance is -90 mV.
resting membrane potential: Sodium ion gradients
membrane rests at -70
chemical gradient wants Na+ in, electrical gradient also wants it in. electrochemical gradient wants it in. lack of balance, all in one direction
when equilibrium potential is reached so the electrical gradient wants Na+ out. Sits at 66-70mV
explain how to maintain resting membrane potential
requires passive forces (diffusion of Na+ and K+ through leak channels driven by gradients)
and active processes (sodium potassium pump)
how to establish resting membrane potential?
difference in voltage is due to difference in concentrations of ions, called the resting membrane potential (-70mV)
at rest, the membranes are mostly permeable to K+, because there are more leak channels, and the ion channels are left open at rest. these channels mostly determine resting membrane potential.
sodium potassium pump also maintains resting membrane potential with ATP
how does opening Na+ channels contribute to membrane potential?
they depolarize the cell when they open as Na+ comes in. cell becomes more positive inside.
how does opening K+ channels contribute to membrane potential?
they hyperpolarize the cell and K+ leaves. this means the cell becomes more negative on the inside.
what are the two types of electrical signals in neurons?
graded potentials and action potentials
explain graded potentials
occur in the dendrites and the cell body
can cause depolarization or hyperpolarization
travel short distances
decrease in intensity with distance
can initiate the firing of action potentials
explain action potentials
rapid changes in membrane potential
triggered by net graded potential at axon hillock, and threshold increase (depolarization) in membrane potential
caused by opening/closing of voltage gated ion channels
are all or none events that can travel long distances along the axon, to the axon terminal
do not degrade over distance or time
explain stimulus strength and graded potentials
graded potentials vary in magnitude depending on strength of stimulus
more neurotransmitter means more ion channels open, and larger magnitude of graded potential
(binding of neurotransmitters causes the ion channels to open, so more binding triggers more opening). this means the shift in membrane potential is greater when theres more neurotransmitter/open channels. (Ex. more depolarization)
explain electrical signals and polarization types
neurons are excitable, meaning they can rapidly change their membrane potential.
depolarization: membrane potential becomes more positive
hyper polarization: membrane potential becomes more negative
repolarization: membrane potential returns to resting value
explain how graded potentials travel and change with distance
the membrane potential sees biggest change at site of stimulus, where the ligand gated ion channels open and ions move across the membrane. This is in the dendrites and cell body,
this results in graded potential, which decays with distance (ex. charge leaks out thru leak channels)
graded potentials are integrated at axon hillock, and summation of graded potentials will determine if AP will occur.
explain the threshold membrane potential
if sum of graded potentials causes the membrane potential at the axon hillock to depolarize beyond threshold potential, the action potential occurs.
subthreshold is a graded potential not large enough to trigger AP
explain spatial summation of graded potentials
graded potentials at different sites take place at the same time, influencing a net change in membrane potential. if depolarizing and reaches threshold, it causes AP.
spatial summation can also prevent APs if the membrane is hyperpolarized. it depends on which ion channel is open.
explain temporal summation of graded potentials
graded potentials that occur at slightly different times, influencing a net change in membrane potential. if depolarizing and reaches threshold, can cause AP.
build off of each other if they occur before the resting potential is restored again.
can also prevent APs!
explain how graded potentials are integrated at the axon hillock
neurons received excitatory and inhibitory synaptic inputs.
excitatory: excitatory post synaptic potential
inhibitory: inhibitory post synaptic potential.
the combined inputs lead to a change in membrane potential, and an AP will or will not occur
describe action potentials!
large changes in membrane potential in axons
3 phases
changes in Na+ and K+ permeability due to the opening/closing of voltage gated channels results in movements of ions and charge.
ions always move in effort to make the membrane potential their personal equilibrium potential.
at rest, K+ ions are most permeable, followed by Cl- and then Na+
K+ leak sets resting potential.
describe the phases of action potentials
Phase 1: rapid depolarization
- graded potentials depolarize the membrane to threshold, there is rapid opening of voltage gated Na+ channels. Na+ entry is more than K+ exiting, so the membrane potential approaches Na+ equilibrium
Phase 2: rapid repolarization
- after the Na+ channels open, the K+ channels open, around the same time the voltage gated Na+ channels become inactivated and close.
- K+ exit now exceeds Na+ entry. Membrane potential approaches K+ equilibrium
Phase 3: after-hyperpolarization
- voltage gated K+ channels are slow to close, so K+ permeability stays high, which means the membrane potential dips below the resting potential. Afterwards, the voltage gated K+ channels close, and the membrane potential slowly returns to rest
go over the 3 states of voltage gated ion channels during an action potential
there are 2 gates: activation and inactivation gates within one Na+ channel
- Closed (Resting), the inactivation gate is open, activation gate closed. after depolarization, this opens the activation gate
- open (Activated), ion can pass through the channel, both gates open.
- inactivated, the inactivation gate closes and is unable to open until resting state. this leads to repolarization.
rapid activation followed by slow inactivation induced by initial depolarization.
voltage gated K+ channels only have one gate that opens slowly after depolarization
explain the propagation of action potentials
when an AP is initiated at the axon hillock (trigger zone), the depolarization produces a current that spreads to adjacent areas of the membrane.
positive charges at region of depolarization are attracted to negative charge of neighbouring regions. the current spreads and depolarizes adjacent regions.
soon the neighbouring region is depolarized enough to generate an AP, and the positive current moves down the axon.
AP cannot move backward because the previous region is in the absolute refractory state.
how does axon diameter affect AP conduction?
larger diameter increases speed of AP conduction, since it decreases resistance to current flow along the axon.
difference between oligodendrocytes and schwann cells? what are they?
Oligodendrocytes in the CNS, and schwann cells in the PNS.
they insulate axons, covering 99% of the axon.
The myelin makes it harder for the current to leak out through open ion channels.
myelin sheath= internode
what are the nodes of ranvier?
the spaces between the myelin sheath on an axon, taking up less than 1% of the axon. they are exposed parts of the axon, where voltage gated Na+ and K+ channels are concentrated. APs leap from one node to another through saltatory conduction
propagation of action potentials in myelinated axons
APs are generated by depolarizing current flowing over long distances much quicker thanks to the myelin insulation. Nodes of ranvier are spaced so there is enough current remaining to bring the next node to threshold.
why myelinate?
myelination increases conduction velocity. Some animals make up for lack of myelination by increasing axon diameter (ex. median giant axon)
explain the absolute vs. relative refractory periods
If a second stimulus is applied during/after an AP and no AP is triggered, the cell is in an absolute refractory period. (1-2 ms long). This is because Na+ channels are inactivated.
If stimulation is a bit later, then AP may be triggered as long as the stim is more intense. this is the relative refractory period (3-4 ms). this AP may have a smaller amplitude. this is because Na+ channels are no longer inactivated.
why are absolute refractory periods necessary?
allows for propagation of closely spaced, yet discrete APs
limits the number of APs that a neuron can produce per unit time (varies amongst different neurons)
how is signal intensity determined?
By AP frequency.
a large stim is more likely to generate AP during relative refractory period, so frequency is higher and then so is intensity.
strong, long lasting graded potentials produce more APs in bursts.
describe the opening/closing of channels during an AP, and when the absolute/relative refractory periods are
A graded depolarization brings an area of excitable membrane to threshold. Voltage gated Na+ channels open, ions move into the cell which depolarizes. The membrane potential rises. We’re now in the absolute refractory period.
at the peak, Na+ channels begin to close, voltage gated K+ channels begin to open, and those ions move out. repolarization begins.
now in the relative refractory period.
voltage gated K+ channels begin closing, near threshold the voltage gated Na+ begin reactivating, and the membrane returns to resting state.
how is information integrated?
a single neuron may receive information (both excitatory and inhibitory) from thousands of synapses. the axon hillock integrates all stimuli, determines rate of AP generation at initial segment.
the hillock is closest to initial segment where AP starts. threshold at hillock is lower than anywhere else on the cell body.
describe the structure of a synapse
draw it too! (slide 12)
telodendrion turns into the synaptic knob.
within the synaptic knob there can be ER, or mitochondria, and many synaptic vesicles.
the presynaptic membrane releases chemical signals into the synaptic cleft, and the postsynaptic membrane on the other neuron takes that up
describe electrical synapses
direct flow of electrical current from one cell to another through gap junctions
fast, bidirectional
postsynaptic signal is similar to presynaptic signal
excitatory
electrical signalling throughout
describe chemical synapses
secrete neurotransmitter molecules that activate receptors
slower, one way. pre and postsynaptic signals can differ
excitatory or inhibitory
electric, but is chemical in the synaptic cleft. neurotransmitters and receptors
transmission of signal at chemical synapse
postsynaptic cells have specific receptors
binding of neurotransmitter to receptors alters ion permeability, leading to change in membrane potential.
postsynaptic cell response is dependent on:
- density of receptors on postsynaptic cell
-amount of neurotransmitter (determined by AP frequency)
-rate of removal
what are the effects of intracellular calcium?
they regulate neurotransmitter release
AP arrives at axon terminal and voltage gated Ca2+ channels open, Ca2+ enters the cell and signals to vesicles, which move to membrane and release neurotransmitter via exocytosis. Neurotransmitter diffuses across synaptic cleft and binds to receptors which activates signal transduction pathway
AP frequency influences amount of neurotransmitter released. low AP frequency leads to fewer synaptic vesicles releasing contents. more APs, more vesicles.
draw it! (slide 15)
how is chemical synaptic transmission terminated?
neurotransmitter is removed from synaptic cleft.
can be degraded by enzymes
reuptake into presynaptic terminal (degraded/recycled)
diffusion out of synaptic cleft, and reuptake/metabolism by surrounding glial cells
what are some characteristics of neurotransmitters
synthesized in neurons (amino acids, peptides, amines, acetylcholine, gases, purines, etc)
released at presynaptic cell following depolarization (single neuron can produce and release more than one neurotransmitter)
binds to postsynaptic receptors
describe excitatory neurotransmitters c
cause depolarization of postsynaptic membrane
excitatory postsynaptic potentials (EPSPs)
postsynaptic cell is more likely to generate an AP
describe inhibitory neurotransmitters
cause hyperpolarization of postsynaptic membrane
inhibitory postsynaptic potential (IPSP)
postsynaptic cell less likely to generate AP
describe ionotropic neurotransmitter receptors
ligand gated ion channels in post synaptic membrane
excitatory neurotransmitters: acetylcholine, glutamate
inhibitory: GABA, glycine
describe metabotrophic neurotransmitter receptors
receptor changes shape and activates signalling pathway
forms a 2nd messenger, which alters opening of an ion channel. then modifies existing proteins, activates or releases gene expression.
slow neurotransmission
ex. norepinephrine, serotonin (amines) or oxytocin, proctolin, acetylcholine, glutamate (peptides)
what affects can drug action have on synapse (pharmacology)
alters uptake by presynaptic neuron
antagonist
agonist
increase release from presynaptic terminal
alter breakdown
which drugs affect acetylcholine synapses?
acetylcholine: excitatory. control of vertebrate skeletal muscle
caffeine- depolarize axon hillock
nicotine- agonist in nicotine receptors
nerve gas- inhibits acetylcholinesterase
which drugs affect GABA synapses
inhibitory in CNS of vertebrates, GABA release inhibits anxiety
substances that reduce anxiety enhance GABA’s effect
-tranquilizers, either increase release or act as agonist
-alcohol, increases action of GABA
- anti anxiety drugs increase action of GABA
which drugs affect enkephlin synapses
enkephlin- opioids, pain relief. inhibitory in CNS
opiates (opium, heroin, morphine, etc) are agonists
compare somatic vs autonomic nervous systems
somatic: neurons from CNS directly coordinate voluntary control of skeletal muscles. upper motor neurons in primary motor cortex
autonomic: motor neurons of CNS will synapse on visceral motor neurons in autonomic ganglia, and these ganglia coordinate involuntary control of visceral effectors (ex. smooth muscle, glands). visceral motor nuclei in hypothalamus, and autonomic nuclei in brainstem.
how does the autonomic system maintain homeostasis?
the autonomic control areas receive afferent neural input from sensory receptors, and then homeostasis is balanced using efferent pathways, without the need for conscious thought :
sympathetic nervous system: stressful, physical activity
parasympathetic nervous system: most active during rest, rest and digest system
enteric nervous system: affects digestion
where are autonomic control centres in vertebrates?
hypothalamus and brainstem
what does dual innervation refer to
the autonomic system and the sympathetic vs. parasympathetic divisions. they innervate the same organs, but with different/opposing effects. Complete structural separation
sympathetic goes to thoracolumbar division
parasympathetic goes to craniosacral division
describe the anatomy of the autonomic nervous system
preganglionic and post ganglionic neurons, that synapse onto effector organs
preganglionic neuron has its cell body in the CNS, with an axon that projects into the autonomic ganglia in PNS, next to vertebral column (sympathetic) or near target organ (parasympathetic)
postganglionic: cell body in autonomic ganglia, axon projects to effector organ
what are some differences in autonomic pathways
sympathetic: short preganglionic neuron, closer to spinal cord, with long postganglionic neuron.
parasympathetic: long preganglionic neuron, with short postganglionic neurons, closer to effector organ
length of neurons
transmitter of pre (ach in both)
receptors on post (nicotinic, Ach)
transmitter on post (NE in symp, Ach in parasymp)
different receptors on target tissue. (adrenergic in symp, metabotropic in parasymp)
describe the sympathetic nervous system
efferent signals transmitted via spinal nerves
pre-ganglionic neurons exit spinal cord and synapse with postganglionic neurons in SNS ganglia in sympathetic chain, which then leave to innervate target tissue.
last neurotransmitter usually norepinephrine
compare sympathetic vs parasympathetic
2 neurons in chain, both Ach
cell bodies (thoracic and lumbar spinal cord symp, hindbrain and sacral spine parasymp)
ganglia location (spinal cord symp, effector organ parasymp)
preganglionic neuron (short symp, long parasymp)
postganglionic neuron (long symp, short parasymp)
synapses per neuron (many SNS, few PSNS)
final neurotransmitter (NE in SNS, Ach in PSNS)
what is the vagus nerve
a superhighway of information that innervates many organs
why do some effectors only get sympathetic innervation?
theyre alarming/stress responses. ex. arrector pills of skin, blood vesssels, etc.
autonomic reflex arcs, explain
many autonomic changes use simple neural circuits with no input from brain
