Synapses

Question 1

Synapses

Answer 1

Junction between two neurons

Primary means by which one neruon directly interacts with another neuron

Pre synaptic
Synapse
Post Synaptic

Question 2

Converge and Divergence

Answer 2

Converge: many neurons into one

Divergence: one neuron into many

Question 3

Synapse steps

Answer 3

1. Action potential arrives at terminal end
2. Voltage gated calcium channels open
3. Calcium moves into knob (where synaptic vesicles are)
4. Arrival of Calcium triggers the release of neurotransmitters
5. NT migrate across synapse
6. Binds to receptor sites
   -opens ion gates
   -triggers graded potiental

Question 4

Neurotransmitter release

Answer 4

Calcium binds to synaptotagmin
-stimulates snare proteins which release NT
- Vesicles migrate down

Question 5

Post synaptic membrane

Answer 5

Activates
-Ionotropic receptors- action ion charnels, first response
or
- Metabotropic receptors - 2nd messenger activation of channel

Synaptic delay
0.2msec for Ionotropic
0.5msec for metabotropic

• bigger delay then would think

Question 6

Synapses in terms of IPSP or EPSP

Answer 6

Signal at synapse either excites or inhibits the postsynaptic neuron

Two types of synapses (binds to)

-Excitatory synapses (Na+ or ion gates)
-Inhibitory synapses (K+ gates or Cl- gates)

Question 7

Direction of flow

Answer 7

Excitatory Synapse: out ward from synapse

Inhibitory Synapse: back towards the synapse

Refer to slide 65 if needing help

Question 8

Size of post synaptic potential

Answer 8

Depends on:

Calcium levels (fatigue) (not enough neurotransmitter released)
NT levels
Desensitization / hypersensitization (desense= same message over and over, hypersense=small impulse high release)
Pre-synaptic inhibition or facilitation

Question 9

Spatial vs temporal summation

Answer 9

Spatial:

Summation of many EPSP’s occur at
different locations on the dendrites at the same time

Temporal Summation:

Summation of many EPSP’s occurring at
the same location over a very short
period of time

Need both to reach threshold?

EPSP and IPSP interaction: some neurons have 200k terminals

Question 10

Pre synaptic facilitation/inhibition

Answer 10

ex: Opiates, endorphins meaning they inhibit release of neuro transmitter

Neuron A releases neurotransmitter that can either increase or decrease release from neuron B

Question 11

Neurotransmitters

Answer 11

Vary from synapse to synapse:

-Same neurotransmitter is always released at a particular synapse
-Quickly removed from the synaptic cleft

Some common neurotransmitters:
Acetylcholine
Dopamine / Serotonin
Norepinephrine / Epinephrine
Histamine
Glutamate
Gamma-aminobutyric acid (GABA)

Question 12

Neuropeptides

Answer 12

Large molecules consisting of from 2 to 40 amino acids

Neuropeptides:

Substance P (pain)
Enkephalins /Endorphins
Dynorphins
Hypothalamic releasing
and inhibiting hormones
Angiotensin II (BP)
Cholecystokinin (gut)

Question 13

Characteristics of Neurotransmitters and Neuropeptides

Answer 13

Neurotransmitters:

Small, one amino acid or smilier chemical. Rapid, brief response

Neuropeptides:

Large, 2 to 40 amino acids in length. Slow, prolonged response

Question 14

Acetylcholine (Ach)

Answer 14

Cholinergic receptors
* Parasympathetic system / muscle
* Muscarinic vs nicotinic receptors
(agonists)
* Broken down by acetylcholinesterase
and recycled (send it out and then take it back)
⬧ Sarin – inhibits this enzyme
* Alzheimer’s Disease

Question 15

Catecholamines

Answer 15

Epinephrine / norepinephrine
- Affect consciousness, mood,
attention
-BP, HR (fight or flight)

Adrenergic / noradrenergic
receptors
Broken down by MAO
(monoamine oxidase)
MAO inhibitors increase epi
levels in synapse
* Anti-depressant (affect mood and conciseness)

Question 16

Serotonin

Answer 16

From tryptophan / modulates (slow onset)
Excitatory on muscle control
Inhibitory on sensory mediation
Mood, anxiety, wakefulness
-role with dopamine too
Block reuptake with
Paxil (anti-depressant)
Also LSD

Serotonin and dopamine work together

Examples:

Parkinson’s Disease
Decrease release of L- dopa (dopamine) from basal nucleii
Tremors / muscle rigidity

Question 17

Synaptic drug interactions

Answer 17

Possible drug actions:

-Altering the synthesis, axonal transport, storage, or release of a neurotransmitter

-Modifying neurotransmitter interaction with the postsynaptic receptor

• Influencing neurotransmitter reuptake or destruction
• Replacing a deficient neurotransmitter with a substitute transmitter

Question 18

Possible drug effects on synaptic effectiveness

Answer 18

A. release and degradation of the
neurotransmitter inside the axon
terminal
B. increased neurotransmitter release
into the synapse
C. prevention of neurotransmitter
release into the synapse.
D. inhibition of synthesis of the
neurotransmitter.
E. reduced reuptake of the
neurotransmitter from the synapse.
F. reduced degradation of the neurotransmitter in the synapse.
G. agonists (evoke same response as neurotransmitter) or antagonists
(block response to neurotransmitter) can occupy the receptors.
H. reduced biochemical response inside the dendrite

Question 19

drug interactions

Answer 19

Agonists – mimic NT when they bind
Eg. Morphine (opiates), block pathway

Antagonists- bind but don’t activate
receptor – blocks site
Eg. Atropine (Ach), block binding site

Question 20

drugs that alter synaptic transmission

Answer 20

Cocaine:
Blocks reuptake of neurotransmitter dopamine at presynaptic terminals, doesn’t take dopamine back

Strychnine
Competes with inhibitory
neurotransmitter glycine at
postsynaptic receptor site
* convulsions

Tetanus toxin
Prevents release of inhibitory
neurotransmitter GABA, affecting
skeletal muscles
* (destroys SNARE proteins)

Botulism
Interferes with SNARE proteins for
excitatory NT
-Muscle paralysis (can’t breath)