neural communication & plasticity

Question 1

nissl stain vs golgi stain

Answer 1

nissl: stains all cell bodies
golgi: stains a %, shows dendrites more clearly

Question 2

brain layer 1

Answer 2

molecular layer

Question 3

brain layer 2

Answer 3

outer granular layer

Question 4

brain layer 3

Answer 4

outer pyramidal layer

Question 5

brain layer 4

Answer 5

inner granular layer

Question 6

brain layer 5

Answer 6

inner pyramidal layer

Question 7

brain layer 6

Answer 7

multiform layer

Question 8

central sulcus (forward & behind)

Answer 8

forward: action
behind: perception

Question 9

broadman’s cortical map

Answer 9

began to map certain functions to certain brain areas

Question 10

afferent

Answer 10

info to brain

Question 11

efferent

Answer 11

info from brain

Question 12

dorsal roots

Answer 12

afferent
sensory info

Question 13

ventral roots

Answer 13

efferent
movement info

Question 14

Wilhelm von Waldeyer defined what?

Answer 14

defined a neuron as communication cell in NS
named: dendrite & axon

Question 15

charles sherrington’s discovery ( 3 reasons supporting)

Answer 15

synapse exists b/c:
1. degeneration was discrete, not continuous
2. reflexes were slowed down by a junction
3. something makes reflex conduction unidirectional

Question 16

1897: cajal & sherrington

Answer 16

synapse!!
(only theoretical)

Question 17

george oliver & henry dale

Answer 17

naturally occurring substances mimic nerve stimulation
chemical?

Question 18

loewi (vagusstoff)

Answer 18

stimulation of one heart activates the other heart in a connected chamber (inhibitory effect observed)
therefore: chemical

Question 19

how many neural impulses is there a second? chemical synapse

Answer 19

1000-2000

Question 20

have neurotransmitters changed over time?

Answer 20

primitive animals had the same neurotransmitters as we do now
it is the WAY the NT’s act that changes via evolution

Question 21

what can you infer about a NT’s function from their chemical structure?

Answer 21

nothing!

Question 22

cajal’s discovery (relating to synaptic plasticity)

Answer 22

discovered “growth cones”
how fixed is the NS?

Question 23

how many inputs can one neuron have?

Answer 23

50,000

Question 24

why was hippocampus studied? (& hippocampus deficit)

Answer 24

studied to further understand synaptic connections (in rat brains)
deficit = memory

Question 25

CA3 -> CA1 experiment

Answer 25

stimulate pathway one (CA3 -> CA1)
pathway 1: stronger epsp post-tetanus
pathway 2: same epsp post-tetanus
therefore -> more stimulation = strengthens a pathway

Question 26

long term potentiation

Answer 26

frequent use of one synapse strengthens the synapse long-term
(this can have no affect on adjacent neurons OR it can have little affect on adjacent)

Question 27

LTP: specitivity

Answer 27

only one synapse strengthened
How? NMDA channels are opened only active synapses, confining LTP to these sites.

Question 28

LTP: associativity

Answer 28

adjacent synapses strengthened as well
How? strong neighbouring inputs depolarise & remove Mg2+ block

Question 29

how does LTP occur?

Answer 29

depolarisation inside (state of LTP) = Ca2+ influx via NMDA receptors
Ca2+ = production of more receptors via CAMKII & CKP = stronger synapse

Question 30

NMDA receptors

Answer 30

internal depolarisation = more positive inside = repels Mg2+ away