3g Flashcards
Inhibitory and excitatory synapses
Subsynaptic Receptors (on dendrites or cell body of the next neuron)
Some channels may change permeability to Na+
, K+
or even Clto create Excitatory or Inhibitory synapses
(activate or inhibit the next neuron through diverse
changes in ion permeability)
The receptor itself can be an ion channel
= ionotropic receptors…
… or the receptor can indirectly act on an ion channel
(G protein, second messenger)
= metabotropic receptors
These ion channels are distinct from the
voltage-gated channels, and are called
‘ligand-gated channels‘
Excitatory synapses
The post-synaptic response to the neurotransmitter is a depolarization.
Due to the concentration gradients and to the electrical
gradient => Typically, net movement of positive charges inside the cell => Slight depolarization called an Excitatory
postsynaptic potential or EPSP
Inhibitory synapses
Inhibitory synapse
Na+ permeability is not affected
K+ and Cl- channels can open
IPSPs can hyperpolarize the membrane by increasing
membrane permeability to K+ or Cl
Chloride active
In this way, some neurons can actively alter Cl
to modify membrane potential:
Still inhibitory via IPSPs (hyperpolarize by importing Clto ICF but via active transport)
Or even excitatory via EPSPs (depolarize by exporting Clto ECF via active transport)
Application: some tick medications for pets inhibit active Cltransport (GABA-A receptors) to
interfere with neural function
cl passive
Passive diffusion of Cl- will depend on its equilibrium potential relative to membrane potential (varies across types of neurons)
Unlike the previous example (last slide), some cells have a Cl- equilibrium potential that is equal to the resting
membrane potential (-70mV)
High Cl- concentration in ECF relative to ICF, but negative ICF repels Cl- at resting membrane potential = no flux
However, if membrane potential changes, Cl- will naturally move in whatever direction that will bring it to -70mV
Free movement of Cl- serves to stabilize membrane potential to help counter leak of other ions and decrease the
likelihood of reaching threshold (an IPSP that ‘stabilizes’ the membrane potential like a brake pedal)
Notion of synaptic delay
The complexity of the neural pathway (chain of neurons) determines the total number of synaptic delays
The sum of the synaptic delays determines our Total Reaction Time
(the time required to respond to a particular event)
Neurotransmitter removal
There is an equilibrium between bound neurotransmitters and the unbound form.
= if the unbound neurotransmitters are removed from the cleft, the number of occupied receptors will
decrease.
1) Actively transported back into
the presynaptic axon terminal =
Reuptake
2) Diffuse away from the receptor site and the cleft
3) Enzymatically transformed into inactive
substances (and eventually recycled into the
presynaptic axon terminal)
Synaptic integration
Sum of these IPSP and EPSP = GPSP = Grand PostSynaptic Potential
The temporal summation
2) The spatial summation
=> Spatiotemporal summation
Presynaptic inhibition / facilitation
A third neuron (B) can influence the level of activity between
the presynaptic axon terminal (A or D) and the postsynaptic
neuron (C).
If the level of neurotransmitter released by (A) is increased
presynaptic facilitation
Opposite = presynaptic inhibition