Lecture 5 Flashcards
Do neurons have action potentials without sensory input?
Yes. Some express channels that generate ongoing spiking without stimuli
The firing rate is sensitive to change in sensory input, inhibitory or excitatory so they can convey a broader range if information.
If neurons spike at a steady state in the absence of sensory input do they have a resting potential?
It is defined as the membrane potential they sit at when all voltage-gated Ka+ channels are blocked and there is no sensory input
If neurons keep firing all the time, how long do they maintain their ionic concentration gradient across their membranes?
Until death
Receptor protein
Protein that is sensitive to and can communicate a signal. Can be ionotropic or metabotropic
Ionotropic receptor
Receptor protein that has an ion channel.
Direct effect is always short lived and immediate change to the permeability of the membrane to certain ions
Metabotropic receptor
Receptor proteins that is not an ion channel
Signal intracellular signaling cascades, usually with g proteins which can change gene expression, or open/close a g protein gated ion channel
The effects are slow and long lasting as they rely on signaling cascades and diffusion
Trophic means
Turn towards
ionotropic turn towards ions to mediate their effects
metabotropic turn towards metabolism
Metabotropic receptors and g proteins
Metabotropic receptors use metabolism to affect changes. The use g proteins to start a cascade.
g proteins use GTP instead of ATP.
When they are bound to GTP they are on and catalyze things. WHen the g protein clips off a P from GTP it becomes GDP and is inactivated.
Inactivated g proteins cannot release GDP. When a ligand binds to the extracellular part of a metabotropic receptor, it changes its intracellular configuration. This then binds to the g protein and allows it to release its GDP. Then the g protein can bind GTP and become active again.
G-protein ion channels
Are activated by g proteins
Metabotropic receptor is activated, cleaves GDP from a g protein which then binds GTP, becomes active, binds with the ion channel and activates it
Why use metabotropic receptors when you already have ionotropic ones?
While the metabotropic receptor is active, it can activate many g proteins.
While the g protein is active, it can catalyze many things.
ie gene expression, ion channels, secretion from the cell (anything more or less)
So scats to amplify many things.
It is slow to act >30ms but has a bigger, longer effect.
Synapses can form between the axon terminals and (4 things)
Dendrites (dendritic shafts) - led toward cell body
Dendritic spines
The soma (cell body)
Other axon terminals cause presynaptic inhibition or facilitation
presynaptic inhibition or exitation
Inhibition - causes the synapse to release less neurotransmitter. hyperpolarizes presynaptic axon terminal so that less voltage gated Ca2+ channels open
Excitation -depolarizes it so more ca2+ comes in
Autoreceptors
On pre synaptic membranes
Sensitive to the neurotransmitter the presynaptic neuron releases
Usually metabotropic and inhibitory
prevent excess release
A strong source of presynaptic inhibition.
2 parts to nervous systen
central nervous CNS = brain and spinal chord
Peripheral (PNS) everything outside the CNS including the bits attached to it
Oligodendrocytes in CNS … in PNS
Schwann cells
