Neuronal Communication (Part 1)
determines if an action potential is produced or not
the net effect of the interaction between graded potentials
how do GPCRs affect post synaptic ion channels
they are transducers that indirectly affect ion channels
saltatory conduction
the propagation of action potentials along myelinated axons from one node of ranvier to the next, increasing the conduction velocity of action potentials
synapse
the region where an axon terminal communicated with its postsynaptic cell
What 2 major factors affect speed of AP in neurons
(1) the diameter of the axon and (2) the resistance of the axon membrane to ion leakage out of the cell. The larger the diameter of the axon or the more leak-resistant the membrane, the faster an action potential will move. Saltatory conduction thus is an effective alternative to large-diameter axons and allows rapid action potentials through small axons.
AP conduction in unmyelinated axons
1.
NT release at the synapse
1. AP depolorizes axon terminal 2. Voltage gated Ca2+ channels open, Ca2+ enters 3. Ca2+ triggers exocytosis 4. NT diffuses across synaptic cleft and binds with receptors on postsynaptic cell 5. Postsynaptic cell has response
2 factors that influence membrane potential
1. Concentration gradients of ions across the membrane. Normally, sodium (Na* ), chloride (Cl+ ), and calcium (Ca2* ) are more concentrated in the extracellular fluid than in the cytosol. Potassium (K* ) is more concentrated in the cytosol than in the extracellular fluid. 2. Membrane permeability to those ions. The resting cell membrane is much more permeable to K* than to Na* or Ca2* . This makes K* the major ion contributing to the resting membrane potential.
AP sequence of events
1. RMP 2. depolarizing stimulus 3. membrane depolarizes to threshold. Na+ channels open quickly. K+ channels open slowly. 4. Rapid Na+ entry depolarizes cell 5. Na+ channels close. SLower K+ channels open. 6. K+ moves from cell to ECF 7. K+ channels stay open and more K+ leaves. Hyperpolorization 8. K+ channels close 9. cell returns to RMP
AP conduction in myelinated axons
AP jump from one node of ranvier to next only the nodes have Na+ channels
absolute vs relative refractory period
Absolute: Na+ inactivation gate closes, activation gate still open Relative: Na+ inactivation gate reopens and activation gatecloses [de-inactivation] - ready to participate in AP again During the relative refractory period, a stronger than normal stimulus is needed to elicit neuronal excitation. After the absolute refractory period, Na+ channels begin to recover from inactivation and if strong enough stimuli are given to the neuron, it may respond again by generating action potentials.
Microglia
Act as phagocytes, eating damaged cells and bacteria, act as the brains immune system
How GPCRs act at the presynaptic neuron
Alter the function of voltage gated ion channels and modulate NT release
chemically gated ion channels
Chemically gated ion channels in most neurons respond to a variety of ligands, such as extracellular neurotransmitters and neuromodulators or intracellular signal molecules.
EPSP vs IPSP
EPSP is a depolarization (Na+ entering the cell). IPSP is a hyperpolarization (Cl- entering the cell)
Concentration of K+ in and out of cell
Extracellular - 5mM Intracellular- 150mM
metabotropic receptors
G-protein coupled receptors that activate heterotrimeric G-proteins; G-proteins dissociate to control ion channel activity or bind to other effector proteins
Effect that hypokalemia have on neurons
If blood K* concentration falls too low (hypokalemia), the resting membrane potential of the cells hyperpolarizes, moving farther from threshold. In this case, a stimulus strong enough to trigger an action potential when the resting potential is the normal +70 mV does not reach the threshold value (Fig. 8-19d). This condition shows up as muscle weakness because the neuron
mechanically gated channels
Mechanically gated ion channels are found in sensory neurons and open in response to physical forces such as pressure or stretch.
Astrocytes
Provide structural and metabolic support for neurons. blood brain barrier
tonic control
Regulates physiological parameters in an up-down fashion. The signal is always present but changes in intensity.
Where on neuron does integration occur
Soma integrates all incoming info and det's the net signal strength
Schwann cell
Supporting cells of the peripheral nervous system responsible for the formation of myelin. Each cell forms myeline around a segment of one axon
conductance
The ease with which ions flow through a channel
Explain Na+ channels
There are 2 gates: activation and inactivation. 1. at RMP activation gate is closed and inactivation gate is closed 2. Depolarization: AG opens. IG already open. 3. Na+ enters cell 4. at 30mV IG closes 5. during repolarization caused by K+ leaving cell, gates reset to their orig position
Oligodendrocytes
Type of glial cell in the CNS that wrap axons in a myelin sheath.
voltage-gated ion channels
Voltage-gated ion channels respond to changes in the cell's membrane potential. These channels play an important role in the initiation and conduction of electrical signals.
dendrites and soma
have responses that receive incoming neurotransmitter signals
resting membrane potential primarily determined by
[K+] gradient and the cell's resting permeability to Na+, K+, and Cl-
graded potential
a membrane potential that varies in magnitude in proportion to the intensity of the stimulus travel short distances and lose strength as they travel
normokalemia
a normal range of K+ in the blood; subthreshold graded potentials will not trigger action potentials
excitatory post-synaptic potentials
a small, local depolarization that make it easier for a neuron to fire
inhibitory post-synaptic potentials
a small, local hyperpolarization that make it harder for a neuron to fire
effect of subthreshold graded potential in normokalemia
a subthreshold GP creates no AP but a suprathreshold will
depolarizes the axon terminal
action potential
ligand-gated ion channel
an extracellular site and membrane-spanning ion channel; made of multiple individual protein subunits
What is the trigger zone
axon hillock all or non location for NET signal of AP
Why do AP's appear to jump from one node of Ranvier to next
because only the nodes have Na+ voltage gated channels
chemically-gated channels
bind chemical ligands
Glial cells
cells in the nervous system that support, nourish, and protect neurons
slow axonal transport
conveys axoplasm in one direction only - from the cell body toward the axon terminals. moves materials down axon and supplies new axoplasm needed for developing or regenerating neurons Used for things like enzymes and cytoskel. proteins
where in neuron does the input signal occur
dedrites and soma that have receptors to rcv incoming NT signals
Where are graded potentials found?
dendrites and cell body
neuron structure
dendrites, cell body, axon, myelin sheath, Schwann cells
intensity of a neurotransmitter
depends on the frequency of action potentials (more action potentials = stronger intensity)
opens voltage-gated Ca2+ channels
depolarization
Factors that affect speed of AP
diameter resistance to leakage
influences speed of action potential
diameter of axon and resistance of axon membrane to ion leakage out of the cell
lysosomes
digest old membrane components
Concentration of Na+ in and out of cell
extracellular- 145mM intracellular - 15mM
true or false, different action potentials can differ in strength
false
do ligand-gated ion channels control fast or slow responses?
fast
oligodendrocytes
form neuronal myelin sheaths in CNS; highly fatty myelin acts as an electrical insulator
What det'd stimulus intensity
frequency of AP
nodes of ranvier
gaps in myelin sheath along the axon between two Schwann cells
type of signal in graded potential vs action potential
graded - input signal AP- Regenerating conduction signal
decrease in strength as they spread out from the point of origin
graded potentials
ionotropic receptors
have two functional domains: an extracellular site that binds neurotransmitters, and a membrane-spanning domain that forms an ion channel both domains funct as a ligand gated ion channel (LGIC) Control fast responses
exocytosis
how neurotransmitters are relased
hyperkalemia
increased K+ in the blood; subthreshold graded potentials can trigger action potentials because the membrane has been brought closer to the threshold
function of voltage gated channels
init and regenerate AP VG Na+ channels are located in trigger zone and axon
voltage-gated channels
initiate and regenerate the action potential; are located in the trigger zone and in the axon
neurotransmitter binding
initiates a response in the postsynaptic cell
soma
integrates all of the information (determines net signal strength)
divergence
one presynaptic neuron branches to affect a larger number of postsynaptic neurons.
creates electrical signals
ion movement
do larger or smaller axons produce faster action potentials?
larger
convergence
many presynaptic neurons provide input to influence a smaller number of postsynaptic neurons
effect of subthreshold while someone has hyperkalemia
membrane is closer to threshold. So a subthreshold stimulus would trigger AP
G-protein coupled receptors
metabotropic receptors that activate heterotrimeric G proteins The alpha subunit interacts with GDP to GTP G protein dissociates to control ion channel activity or bind to other effector proteins that make 2nd messengers slow response
fastest type of axon
myelinated
patients with hyperkalemia
need more anesthesia because their threshold baseline is higher than it should be
Relationship between graded and action potention
net effect of graded potentials det's if a neuron produces AP
is the threshold voltage the same for all channels
no
only these have Na+ voltage-gated channels
nodes of ranvier
depolarization is this type of feedback cycle
positive
Output signal occurs at
pre-synaptic axon terminal
refractory period of the previously depolarized membrane
prevents backward action potential conduction
graded potentials
produced by stimulation of responses on dendrites and soma
Describe what happens to the Na+ and K+ channels
see slide 45 - Refractory period
mechanically-gated channels
sense distortion in their immediate membrane environment
voltage-gated channels
sense voltage changes in their immediate membrane environment
What affect does hyperkalemia have on neuron AP's
shifts the resting membrane potential of a neuron closer to threshold and cause the cells to re action potentials in response to smaller graded potentials
do GPCRs control fast or slow responses?
slow
neurotransmitters are synthesized and packaged here
soma
Satellite cells
surround neuron cell bodies in PNS
axon
the action potential is regenerated here until it arrives at the presynaptic axon terminal
axon hillock (trigger zone)
the all-or-none location for initiation of action potentials
resting membrane potential
the electrical potential difference across the plasma membrane of an unstimulated living cell measured in millivolts (mV) closest to the equillibrium potential for K+
what happens to the signal of graded potentials as they move
they decrease
G-proteins
transduers that indirectly couple GPCR-NT binding to the regulation of postsynaptic ion channels
neurotransmission
transmitting information via a neurotransmitter-initiated signal
calcium entry triggers
triggers exocytosis of synaptic vesicle contents
fast axonal transport
uses proteins that function as motors to move materials along the surfaces of microtubules in both directions in the axon either in an anterograde direction or in a retrograde direction
microtubule network
where fast axonal transport occurs
Schwann cells
wrap around axon and form insulating myelin sheaths in the PNS