Brain & Behavior - Week 2

Front 1

For each form of intracellular neuronal transport, list the direction, main t-port molecule and the cargo:
- Anterograde
- Retrograde

Back 1

Anterograde:
- from soma to button
- vesicles containing: NT, macromolecules & mitochondria
- Carried by fast (500mm/day) and slow (4mm/day) Kinesins

Retrograde:
- from terminal end to soma
- endosomes, mitochondria, SER, etc, all carried by dyneins
- allows nerve to detect growth facotrs but also suck up viruses (tetanus, etc).

Front 2

What happens to the equilibrium potential if you decrease the [gradient] of an ion?

Back 2

If you decrease the [gradient] of an ion, then you will need a smaller electrical force to oppose it's movement = smaller equilibrium potential!

Front 3

What 2 things regulate the extracellular [K] in the brain?

Back 3

The BBB and Astrocytes which act as K+ sponges!!

Front 4

What channels are responsible for creating the contour of the action potential curve ( ie the rise, fall, AHP, and refractory periods)

Back 4

Rise: opening of fast Na+ channels leads to rapid influx, but can't get cell to Na+ e- potential b/c influx opposed by K+ efflux
Falling: d/t opening of slow K channels and closing of Na+ channels
Hyperpolarization: No Na+ channels but have ++ extra K leak channels open
Abs refractory: inactivated Na channels, no amount of stimulation will open them.
Relative refractory: requires more stimulation to reach threshold

Front 5

What happens in the cell (ions & channels) at or around threshold?

Back 5

Threshold is the point at which K+ leak channels can no longer compensate and the Na+ influx >> K+ efflux. This changes the membrane potential and opens more Na+ channels

Front 6

What 3 things will determin the velocity of conduction in a neuron?

Back 6

1. Axon diameter: ↑ing the diameter will ↓resistance (think of pushing water through a pipe), and this will ↑velocity
2. Membrane resistance: ↑ the memb resistance will mean that more current flows through the axoplasm = moves faster
3. ↓ the capacitance of the cell membrane so that it doesn't attract the current as it flows past

Front 7

What type of cell makes myelin? (2)

Back 7

In the PNS - schwann cells
In the CNS - oligodendrocytes
Cell membrane acts as a capacitator - 2 plates separating a charge - this causes it to attract the charge going past it. Myelin insulates this membrane thus separating the "plate" of membrane which ↓ it's attractive field

Front 8

LMN nuclei can be found in the brainstem, associated with CNs or in what 2 areas of the spinal cord?

Back 8

1. Medial motor column - the medial aspect of the ventral horn, spans the length of the column.
** axial muscles **

2. Lateral motor column - lateral aspect of the ventral horns at the cervical and lumbar enlargements only.
** limb muscles **

Front 9

What is a primary myopathy? What is a primary neuropathy and how are they different?

Back 9

1 Myopathy: the # of MU's is constant but the size ↓'s (ie muscle fibers die). The loss of fibers will eventually lead to the death of their LMN's b/c of trophic interdependence.
Same # but smaller!

2. Primary neuropathy - the LMN dies leaving orphan msk fibers that will secrete trophic subtances and induce collateral sprouting in adjacent LMNs.
Smaller # but bigger size!

Front 10

What are the 5 symptoms of a LMN lesion?

Back 10

1. Weakness - ipsilateral, paresis or paralysis (if all MNU's damaged). Usually individual muscles.
2. Hyporeflexia - ↓ or absent b/c LMN are the efferent part of the arc
3. Flaccid paralysis - loss of tone
4. Atrophy - d/t trophic interdependence of the LMN & msk fiber
5. Fasciculations - twitching in early stages of wasting d/t spontaneous release of NT from LMN

Front 11

In addition to the cerebral cortex, what are 3 other sources of UMNs (ie nuclei)?
What is the function of the UMN from each of these?

Back 11

1. Vestibular nuclei - maintenance of posture & balance
2. Reticular formation - locomotion & postural control
3. Red Nucleus - positions the joints of the upper limb to facilitate fine motor skills
** UMNs in the cerebral cortex are involved in voluntary control of sk msk

Front 12

What modulates the UMNs?

Back 12

input from the basal nucle and the cerebellum, both via the thalamus!

Front 13

<50% of the axons in the corticospinal tract originate in the 1 motor cortex (precentral gyrus).
If not there, then where do the other axons of the CST come from (4 places)?

Back 13

In addition to the primary motor cortex, axons of the CST originate within:
1. premotor cortex (pre-pre-central gyrus)
2. supplementary motor area
3. primary somatosensory cortex
4. superior parietal lobe

Front 14

Cell bodies of UMNs in 1 motor cortex give rise to axons which traverse the subcortical white matter of the cerebral hemispheres (2 structures). They then go through what structures of the brain stem?

Back 14

white matter: corona radiata ---> internal capsule
brainstem: cerebral peduncles ---> ventral pons ---> medullary pyramids

Front 15

After leaving the brainstem what to the axons of UMNs do?

Where do they meet LMNs?

Back 15

At the junction of the medulla & spinal cord, most fibers of th CST decussate and descend contralaterally in the lateral funiculus.
UMN axons will synapse with LMNs in the lateral motor column and from there the LMNs go to innervate distal limb musculature.

Front 16

What are the 5 signs of an UMN lesion?

Back 16

1. Hemiplegia that is contralateral for a supratentorial lesion, and ipsilateral for a spinal cord lesion.
2. Reflexes will be intact and may be hyperactive b/c of a loss of modulation.
3. No atrophy (only mis-use atrophy)
4. No fasiculations
5. Will get dorsiflexion (jnstead of plantar) with a Babinski

Front 17

Which cranial nerves have motor nuclei that are controlled bilaterally? Ipsilaterally?

Back 17

Bilateral nuclei: CN V, IX, X
Ipsilateral nuclei: CN XI

Front 18

Which cranial nerves have motor nuclei that are controlled bilaterally? Ipsilaterally?
What deficit would result from an UMN lesion? LMN lesion?

Back 18

The UMN in the face region of the primary motor cortex innervate masticator LMN bilaterally, and the LMNs leave to control ipsilateral msks of mastication.
LMN lesion = ipsilateral deficit
UMN lesion = no deficit

Front 19

What do the LMN of the nucleus ambiguus control? (hint: 2 CN)
What is the UMN pattern of innervation for this nuclei?
LMN lesion?
UMN lesion?

Back 19

LMNs in the nucleu ambiguus control the ipsilateral muscles of the larynx (CN X) and pharynx (CNs IX & X)
UMNs from the 1 mCTX innervate these LMNs bilaterally.
LMN lesion - ipsilateral paralysis
UMN lesion - no deficit b/c other side can compensate!

Front 20

What do the LMNs of the accessory nucleus control?
What is the UMN pattern of innervation for this nuclei?
LMN lesion?
UMN lesion?

Back 20

The LMNs of the accessory nuclei contro the ipsilateral sternomastoid and trapezius muscles via CN XI (accessory).
UMN in corresponding 1 mCRTX innervate these LMNs ipsilaterally.
LMN lesion - deficit on side of lesion
UMN lesion - deficit on side of lesion

Front 21

What do the LMNs of the facial nucleus innervate?

Back 21

LMNs of the facial nucleus innervate msks of facial expression via the facial nerve:
- rostral part does forehead, caudal part does eyes and mouth

Front 22

The 2 parts of the facial nucleus are innervated by the 1 mCTX differently. Describe the innervation of the rostral and caudal parts.
LMN lesion = ?
UMN lesion = ?

Back 22

Rostral - innervated bilaterally
Caudal - innervated ipsilaterally
LMN lesion will paralyze 1/2 the face
UMN lesion
- forehead will be spared b/c innervated bilaterally. contralateral face will be paralyzed!

Front 23

What do LMNs in the hypoglossal nuclei control?
What muscle is controlled contralaterally?

Back 23

LMNs in the hypoglossal nuclei control the ipsilateral int&extrinsic muscles of the tongue via CN XII.
The genioglossus subnucleus is controlled by the contralateral 1 motor cortex and all others are innervated bilaterally.

Front 24

What would be the deficit if you had a
- LMN lesion
- UMN lesion
(both in the hypoglossal nuclei)

Back 24

LMN = deficit in whole tongue on ipsilateral side
UMN = deficit in contralateral genioglossus muscle ONLY (all other muscles are innervated bilaterally!)

Front 25

Define an electrical synapse. What does it do? When would it be shut down?

Back 25

The flow of ions through channels between cells with direct physical contact. It is rapid and bidirectional - used to synchronize thins like respiration. If pH↓ or [Ca] ↑ then channels will close

Front 26

What 2 things does the active zone have and how are these structures involved in synaptic transmission?

Back 26

+++ V-gated Ca+ channels and docking proteins. When an AP depolarizes the active zone, the channels open and the influx of Ca+ causes the docking proteins to contract = vesicle fusion and exocytosis of NT

Front 27

What determines the post-synaptic effects of ionotropic receptor activation?

Back 27

Postsynaptic effects of ionotropic channels opening is determined by the ion selectivity of the channel:
- Na+ influx = excitatory
- Cl- in / K+ out = inhibitory
*** effects of each ionotropic R will be graded

Front 28

What NT is released onto skeletal muscle?
What NT is an inhibitor in the CNS?
What NT is common among CNS inter-neurons?

Back 28

ACh is released onto skeletal muscle.
Glycine is a major inhibitory NT of the CNS (opens Cl- channels)
Glutamate is a major NT of interneurons in the CNS?

Front 29

What are the 2 types of synaptic integration?

Back 29

1. Temporal - same presynaptic neuron that ↑'s its frequency of firing
2. Spatial - multiple presynaptic neurons that all start firing together

Front 30

How do metabotropic receptors work?

Back 30

The receptor is an integral transmembrane protein w/ an extracellular ligand-binding site, and an intracellular G-protein that is linked to 1o effector enzyme. This enzyme will alter [2nd messanger] which:
- binds other proteins directly
- activates a protein kinase which P-lates the target!

Front 31

For the NT Glutamate, list the:
- source & distribution
- 2 types of receptors and their affects

Back 31

Glutamate:
- Most common in CNS; From α-ketoglutarate
- Inotropic: non-NMDA = ↑ Na/K perm = excitatory
- Metabotropic: NMDA =↑ perm to Na/K/Ca but @ Vrest Mg will block channel,thus cell must be a little depol for NMDA to work

Front 32

For the NT GABA, list the:
- source & distribution
- 2 types of receptors and their affects

Back 32

GABA:
-Widely distributed in CNS, from glutamate
Inotropic - A: open Cl- channels = inhibitory
Metabotropic - B: use G-proteins to open Cl- channels or to close pre-syn Ca+ channels (via autoreceptors)

Front 33

How are the NT Glutamate and GABA recycled?

Back 33

Direct at pre-synaptic or via adjacent astrocyte

Front 34

For the NT Glycine list their:
- location
- effects
- recycling

Back 34

- Inhibitory interneurons of the spinal cord
- Inhibitory – provides tonic negative feedback on LMNs in the brainstem and spinal cord
- Rapid re-uptake, reused by synaptic terminals

Front 35

How does tetanus poisoning work?

Back 35

Retrograde axonal T-port from wound to s.cord --> taken up by glycinergic neurons esp. in B.stem that controls mastication = lock jaw.

Front 36

How does stychnine poisoning work?

Back 36

Strychnine will cause convulsions and an agonizing death by blocking glycine receptors --> LMNs loose their inhibition

Front 37

What enzyme is the rate limiting step in catecholamine synthesis?
What are the remaining steps in the synthesis p-way?
What breaks down catecholamines?

Back 37

Tyrosine hydroxylase converts tyrosine to L-DOPA.
L-DOPA --> Dopamine (in vesicle) ---> NE (by DbH) ---> EP (by PNMT)
MAO and COMT will break down catecholamines

Front 38

How are small-molecule NT packaged into vesicles?
What are the small-molecule NTs?

Back 38

Vesicular ATPase will pump H+ into the vesicle to create a pH gradient across the membrane which is then used to drive the NT into the vesicles, against their [gradient]. Enzymes that make the NT's reach the terminal by slow axoplasmic flow. Packaging happens in terminal.
Glutamate, GABA, glycine, srotonin, ACh, and catecholamines

Front 39

What tract carries pain, temperature and simple touch sensation?
What tract carries fine touch, vibration, and proprioception?

Back 39

Spinothalamic Tract

Dorsal columns (lateral lemniscus)

Front 40

Name the tracts and the senses they carry!

Back 40

Woo

Front 41

How could you get a suspended sensory loss? What is it?

Back 41

Lesions at the centre of the spinal cord will cause anesthesia over that spinal segment ONLY! This is because the ascending and descending fibers are at the peripheries and would be left untouched.

Front 42

The spinal thalamic tract is somatotropically arranged. What would be the first part of the body affected from an intramedullary lesion? What about extra-medullary?

Back 42

Front 43

What would happen if you had a compressive midline lesion at the spino-medullary junction?

Back 43

will affect lower limb sensation first and will ascend up the body as the lesion gets bigger