Neurons & Synapses

Front 1

Where are EPSPs/IPSPs generated?

Back 1

dendrites

Front 2

Where are APs generated?

Back 2

The initial segment of an axon.

Front 3

What's the purpose of dendrites communicating somatic info backwards to synapses?

Back 3

Mediates plasticity

Front 4

What's the function of dendritic spines?

Back 4

Sites for synapse.

Front 5

What do dendritic spines contain?

Back 5

Molecules for synaptic maintenance/plasticity.

They compartmentalize these molecules to maintain unique synaptic function and plasticity.

Front 6

How big are spines? What are they made of?

Back 6

1 micron long; 0.1 micron diameter.

Made of actin microfilaments.

Front 7

How does Tay Sachs affect dendrites?

Back 7

It's a lipid storage disease, causes build up of meganeurites on cortical pyramidal cells. These cause MR, seizures, death.

Front 8

What could be an effect of chronic placental insufficiency on the CNS?

Back 8

Decreased dendrite length, stunted hippocampal neurons.

Front 9

What's a possible treatment for Fragile X involving dendrites?

Back 9

New drugs may be able to regulate the number of dendritic spines (reducing the number of them) with therapeutic effects.

Front 10

Most axons in the cerebral cortex talk to the:

Back 10

cerebral cortex.

Front 11

corticospinal axons travel through the ____ ____ to get to the spinal cord.

Back 11

internal capsule.

Front 12

C fibers contain ____ myelin and carry info about what 3 things?

Back 12

NO myelin.

Pain, temperature, itch.

Front 13

Fastest nerve fibers?

Back 13

A-beta fibers--~250mph

Front 14

What are "fast pain" fibers?

Back 14

A-delta fibers. Move faster than C fibers. Carry information about more severe pain (like the burn reflex).

Front 15

What happens in Guillain-Barre?

Back 15

Autoimmune; myelin is degraded in peripheral nerves. Comes on rapidly; often follows viral infection; often resolves on its own. Worst case: diaphragm is shut down.

Not clear why it happens.

Front 16

Where does MS happen? Describe it.

Back 16

Happens in the CNS. Demyelinating disease. Autoimmune. Axons are intact. Demyelination occurs in plaques.

Front 17

What are some consequences of demyelination?

Back 17

1) Slow and block conduction.
2) Causes crosstalk that can generate odd sensations/consequences.

Front 18

Main subunit of the V-dependent Na channel?

Back 18

Alpha subunit.

Front 19

How does lidocaine work?

Back 19

Blocks Na channels, blocking APs.

Must cross cell membrane and enter channel from the cytoplasm. Binds to the channel and plugs it up.

Front 20

Describe the selectivity of lidocaine.

Back 20

Blocks small pain carrying fibers; doesn't block larger touch and motor axons.

It does SLOW the larger axons. Since current flows more readily through the thick axon, it's able to recover from the lidocaine and transmit an AP.

Front 21

What else is lidocaine or similar drugs good for?

Back 21

Anticonvulsants, antiarrhythmics.

Front 22

What happens in hypoxia in regard to APs?

Back 22

It blocks axons in REVERSE order of lidocaine/other drugs.

Motor, touch, pain/temperature.

Front 23

Describe the use-dependence of local anesthetics.

Back 23

They work best on axons that are firing most rapidly. They don't work so well on axons that are slowly firing or resting.

(If the channels aren't open, the drug can't get to them)

Front 24

What's the relative frequency of pain-carrying axons?

Back 24

Really high frequency.

Front 25

How are pyramidal cells in the cerebral cortex organized?

Back 25

VERTICALLY. They're stacked in columns.

Front 26

Most epilepsy mutations affect ____ channels or ____ receptors.

Back 26

Ion channels and transmitter receptors.

Front 27

Glycine acts as a synaptic ____.

Back 27

inhibitor.

Front 28

____ ____ ____ converts glutamate to GABA.

Back 28

Glutamic acid decarboxylase (GAD).

Front 29

Even a small bit of loss of synaptic inhibition can cause:

Back 29

seizures

Front 30

GABA-A receptors are located on ___ channels.

Back 30

Cl-

Front 31

Receptor divergence:

Back 31

one neurotransmitter often activates multiple receptors, and thus multiple effectors.

GABA can activate GABA A,B, and C receptors; thus allowing conductance of Cl, K, or Ca.

Front 32

____ does NOT exhibit receptor divergence.

Back 32

Glycine. Only works on the glycine receptor.

Front 33

Muscimol is a GABA-A:

Back 33

Agonist

Front 34

Baclofen activates:

Back 34

GABA-B receptors. In clinical trials to treat Fragile-X. An anti-spastic.

Front 35

Some inhibitor antagonists:

Back 35

Strychnine blocks Gly-R.

Penicillin and other antagonists block GABA-A and GABA-B receptors, causing seizures.

Front 36

GABA-A receptor is a ____ (shape).

Back 36

pentamer

Front 37

GABA-A receptor has multiple ____ sites that ____ its function.

Back 37

Binding sites; modulate its function.

Sites for barbiturates, benzodiazepines, etoh, GABA, neurosteroids.

Front 38

How do barbiturates work?

Back 38

Bind to GABA-A receptor; agonize it by making the channel stay open for LONGER.

(changes the probability that the channel will be open in the presence of GABA)

Front 39

Name some disorders that involve imbalance of inhibition.

Back 39

Epilepsy, psych disorders, autism spectrum, stoke, huntington's, migraine, other neurodevelopmental disabilities.

Front 40

What's a possible problem with genetic variation in GABA receptors?

Back 40

One AA change in the GABA receptor can make enflurane (gaseous anesthetic) totally ineffective.

Front 41

2 ways anti-convulsant drugs work:

Back 41

Enhance GABA function or block GABA breakdown.

Front 42

What's hyperekplexia? What's wrong in hyperekplexia? How do you treat it?

Back 42

Increased startle response.

Disorder of GLYCINE inhibition. Mutation of Gly-R alpha 1 subunit. Treat with barbiturates or benzodiazepines.