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23 Cards in this Set

  • Front
  • Back
What is an integrating synapse and what are some characteristics?

e.g. # of synaptic connections, type of input, variety of neurotransmitters, safety factor
It is a central neuron

# of synaptic connections per cell: many

Type of input: excitatory and inhibitory

Variety of neurotransmitters: Many (Ach, GABA, Gly, Glu, etc). Ionotropic or metabotropic

Safety factor: Low (many synaptic potentials are necessary to fire an action potential
What is a non-integrating neuron and what are some characteristics?

e.g. # of synaptic connections, type of input, variety of neurotransmitters, safety factor
It is a neuromuscular junction

# of connections: innervated by one neuron

Type of input: excitatory

variety of neurotransmitters: only Ach. Ligand gated ion channel

Safety factor: high - one AP, one synaptic potential, muscle excitation
How do EPSPs and IPSPs transmit their signals?
The neurotransmitter binds to its postsynaptic receptor/channel, which causes it to open and generate a transmembrane current. These are known as ionotropic synaptic receptors
What type of signals do axodendritic and axosomatic synapses produce?
Axodendritic are excitatory - EPSPs

Axosomatic are usuall inhibitory -IPSPs
What is a metabotropic receptor? Where is it found? Is it direct or indirect?
These receptors gate ion channels indirectly and are typically found at modulatory axoaxonic synapses. When the neurotransmitter binds, these receptors activate second messenger systems that cause ion channels to either open or close.

This causes the post synaptic response to be slower than that found at gated synapses, where neurotransmitters act on ionotropic receptors directly.
How do EPSPs work?
Glu causes the opening of a channel that is highly permeable to Na and K, and relatively insensitive to differences in these ions.
What are the two types of Glu-gated receptors? How is each opened?
1. NMDA receptors- opened by NMDA

2. non-NMDA receptors - opened by AMPA, kainate, and quisqualate
What are some characteristics of non-NMDA receptors?
-Similar to ACh receptors at the NMJ
-Open channels have similar permeation properties in that they are nonselectively permeable to K and Na
-Usually not permeable to divalent cations (Ca and Mg)
-They are the major postsynaptic players in FAST EPSPSs
What are some characteristics of NMDA receptor channels that make them differ from non-NMDA channels?
NMDA receptor channels are permeable to Ca and blocked by extracellular Mg
How does low frequency stimulation in NMDA receptors differ from high frequency stimulation?
Low - The postsynaptic response is limited to a regular EPSP. Moes non-NMDA receptors remain blocked by Mg

High - Mg block is relieved by a greater depolarization of the postsynaptic membrane potential, and Ca enters the postsynaptic neuron through the NMDA receptors. This rise in Ca can enduce enzyme systems, such as Ca calmodulin kinase, and thereby induce long - term changes in the dendrite
How does Glu excitotoxicity occur?
During epilepsy or stroke, neurons may die as a result of excessive Ca influx through NMDA receptors in depolarized neurons
What is the diff b/t an EPSP and IPSP?
The reversal potential is more hyperpolarized than the threshold for an AP in IPSPs.
What causes an IPSP?
An increase in G(Cl). In the brain GABA is the transmitter that opens Cl channels; in the spinal cord, Gly is the common inhibitory transmitter
What type of pharmacological agents can open GABA(A) receptors?
Valium, librium, barbiturates, Benzodiazipines, Ethanol
How do IPSPs work, and what happens if they fire simultaneously with an EPSP?
They work by driving the membrane potential to a voltage more negative than threshold.

If an EPSP and IPSP occur simultaneously, the IPSP will inhibit the depolarization beyond E(Cl)

Depends on the relationship between Vrev and Vthreshold
What is the relationship between Vrev and Vthreshold?
If Vrev > Vthreshold, then the synapse is excitatory

If Vrev < Vthreshold, then the synapse is inhibitory
What is an example of a Glycine pharmacological agonist and what does it do?
Strychnine, it acts as an inhibitory agent in the spinal cord
What is shunting inhibition?
It is when an IPSP attenuates the EPSP by behaving as a leak conductance g(LEAK). Therefore EPSP = I(EPSP)/g(LEAK)
What are some diseases associated with Glu, GABA(A), and Gly receptors?
Glu - intoxication by excitotoxins, MSG, neurodegeneration

GABA(A) - Angelman disease

Gly - Startle disease
What are 4 factors that affect the strength and influence of a particular synaptic input?
1. whether it's EPSP or IPSP

2. location of the synapse on the postsynaptic neuron

3. size of the input

4. proximity and strength of other synergistic and antagonistic synapses
Where do APs normally initiate and why?
At the axon hillock b/c the threshold is lowest there.
T or F? 2 asynchronous EPSPs can summate to bring a neuron to AP threshold?
T

... if the time constant of the cell is big enough

By contrast, cells with small time constants (usually small cells with small capacitance) are better able to discriminate individual inputs that arrive in rapid succession. These inputs get blurred in neurons with larger time constants
What is spatial summation? What does it depend on?
Two synaptic inputs occur in close succession at two distinct dendritic locations. They propagate electronically toward the soma and undergo attenuation with distance. If this attenuation is modest, the resulting EPSPs undergo spatial summation, the excitation reaches Vthreshold and triggers an AP at the axon hillock.

Depends on the affective length constant of the postsynaptic neuron.

The closer the input is to the axon hillock, the stronger it will be.

As inputs are integrated from all over the cell, spatial summation occurs