Neuro Block I- Synapses and Spinal Cord and Brainstem Flashcards

electrical: current flows freely through open gap junctions

chemical: NTs are released from the presynaptic cell, traverse the cleft and bind to receptors on the post synaptic cell

ions and small molecules (no proteins)

ion flow bidirectionally; current is rectifying (only flows on direction)

1. excitatory

2. inhibitory

we get synchronozation of activity in a network of interconnected neurons

fast and synchronized

help to regulate extracellular potassium concentration

note: some epilepsies are due to breakdown in this regulation causing depolarizations

1. ionotropic (channel linked)- the channels and receptor are part of the same protein

2. metabotropic (G protein linked)- receptor is GPCR whose response opens nearby channels

1. axodendritic
2. axoaxonic
3. axosomatic
4. dendrodendritic

when we see several connections on a single postsynaptic cell

commonly found on autonomics of smooth muscle

light core
- small molecular NTs (epi and norepi)
-made in soma, but some may be recyclced in the axon terminal

dark core
-peptide (larger molecules)
-always made in soma and brought to the terminal via transport along the MTs

each of the 3 major problems with diabetes leads back to vascular problem

(vasoconstriction, atherosclerosis, hyperplasia blood vessel endothelial cells)

adv: amplification of singla within the cell

disad: too many pieces of puzzle can go wrong and energetically expensive

but the advantages must outweigh the disad because this is a common mechanism in the body

the first axon synapses on the second axon to modulate whether the signal the second axon sends willl be excitatory or inhibitory

when multiple signals are sent to the same neuron, they can combine spatial (as a function of distance to one another) or spatially (as a function of time in between separate signals)

say you grab a mug of hot coffee and it begins to burn; brain says hold ont the mug, but withdrawal refelex may tell same neurons to let go

excitatory and inhibitory potentials combine in neuron of focus and summartion is detected at initial segment to determine AP or not

Na-channels (NOT IN THE AXON TERMINAL)

1. nicotinic (PNS)
2. nicotinic (PNS)
3. muscarinic (PNS)
4. muscarinic (CNS)

tyrosine->DOPA->dopamine->norepi->epi

tryptophan->sero

1. glutamate
2. aspartate

both excitatory

conventional receptors work as normal ionotropic receptor

NMDAs have a Mg2+ ion that block the channel. this means that you need a larger depolarization to activate this channel, but once activated it leads to lasting changes in the synapse

LTPs are involved in learning and memories. the NMDA can be activated to cause LTPs to lead to long term changes in how the membrane responds to potential changes

excitotoxicity- this is when excitation occurs too much for too long causing damage or even killing the neuron

GABA
glycine

glutamate->(glutamic acid decarboxylase)->GABA

substance P

endogenous opioids

NO (nitric oxide)

1. interact with receptor
2. breakdown
3. re-uptake (back into cell from which it was secreted)
4. uptake (it's a different cell; usually glial)
5. diffusion-it simply diffuses out of synaptic cleft

communication

synapses

...

electrical and chemical synapses

opposed plasma membranes of cells in near contact

proteins acting like membrane spanning pores align in adjacent cells from multiple

6 connexins, forming a connexon

ions
small molecules

bidirectional or rectifying (only allows in one direction and not the other

PNS and CNS

excitatory: inferior olive, thalamus, hippocampus
inhibitory: cerebral cortex

rapidly through no neurotransmitters, no synaptic delay; at most direct level, straightforward effects

in the network of interconnected neurons

says the individual nerve cells comprise the nervous system instead of a syncitium

they are the functional link between glial cells

play a role in helping astrocytes regulate EC K because they are linked by gap junctions; epilepsy could be from this

they also play a role in intracellular transport within Schwann cells

if something goes nucleus to membrane to get there, it would have to go around, but it can take shortcuts through membranes to get there quickly

CMT disease family

CMT X chromosome is gene, conduction of APs break down

probably most common cause of peripheral neuropathy
- high foot arch, paresthesis, arched foot, atrophy of muscle in legs, inverted champagne bottle leg

more common
seemingly better understood

involvement of chemical molecule to carry signal from one signal from one cell to next

channel linked chemical synapses- ionotropic
G protein linked chemical synapses- metabotropic

axodendritic
axoaxonic
axosomatic
dendrodendritic
boutons en passage (multiple boutons on postsynaptic cell; when one works, they all exert effect)- typical of how postsynaptic autonomic cells synapse on smooth muscle cell

AP in presyn neuron
depol of axon terminal
entrance of Ca ions into axon terminal
exocytosis of NT
diffusion of NT across synaptic cleft
binding of NT to receptor molecules of postsyn cell
initiates response in postsyn cell
-hyperpol: inhibitor
-depol: excitatory
removal of released NT

Ca entrance due to Ca channel opening due to depolaritzation of terminal

synapta bregmen and synapta tagin on vesicle
synaptataxon and synap 25 on synaptic cleft

small clear vesicles with small molecule NTs, ACh, GABA, glutamate, glycine

amines
dopamine
epi
norepi
serotonin

peptide NTs
endogenous opiates
beta endorphin
enkephalins
neuropeptide Y
can be found many places because made many places

NT in ECF in synaptic cleft
receptor on membrane
G protein with alpha, beta, gamma subunits with GDP on alpha
adenylate cyclase in membrane

Galpha switches GDP for GTP and it goes to activate adenylate cyclase, which produces cAMP and can amplify response

ions will not be able to cross synaptic cleft

ACh, present in PNS at NMJ (nicotinic), pregang autonomic motor receptors (nicotinic), postgang parasym receptors (muscarinic)

in CNS: brain stem and basal forebrain receptors (muscarinic)

epi and norepi from tyrosine

serotonin from tryptophan

enzyme: dopa decarboxylase takes DOPA dihydroxyphenylalanine to dopamine

glutamate and Asp

channel linked with receptor site and ion channel that works fast as an excitatory NT; if it goes, it lets Na into cells and cells depolarize

but there

NMDA receptor with a narrow throat with Mg lodged in it; if a glutamate does bind, it still does not allow things in because of Mg; if there is a big depolarization with the normal glutamate receptors, then the NMDA receptors change and they allow Ca ions through which changes cells in a way that a regular glutamate channel depolarization does not

excitation of this cell when Ca comes in can last a longer time than when just regular glutamate cells come open

downside of these is excitotoxicty: when Ca ions come in it is risky because high Ca levels are bad, cells can go through self induced suicide and they can be excited to death

from glutamate, which via glutamic acid decarboxylase becomes GABA (gamma amino butyric acid)

inhibition

substance P
endogenous opioids

dilation of BVs

inactvation
reuptake
uptake
diffusion
interaction of NT and receptors

excitatory postsynaptic potential (EPSP)
inhibitory postsynaptic potential (IPSP)

affect at initial segment on the axon

axoaxonic or axodendritic or axosomatic summation

this is where VG Na channels are most concentrated

motor centers in brain have inhibitory synaptic input from descending spinal tract and sensory input from the hand has a withdrawal reflex on muscle, these combine and you can override the reflex for a while

caudal portion of neural tube

alar plate to sensory
basal plate to motor

C1-C7 above corresponding vertebral bone
T1 and below all below corresponding vertebral bone

cervical enlargement is C5-T1

lumbosacral enlargement is L2-S3

first it is present at the coccygeal vertebral level
next it is present at S3
at birth it is present at L2-L3
a few months after birth it is present at about L1-L2
bones grow at a faster rate than the spinal column, so they take spinal nerves with it

side 1: posterior
side 2: anterior
a. dorsal root
b. ventral root
c. dorsal ramus
d. ventral ramus
e. gray rami communicantes
f. white rami communicantes
g. sympathetic ganglia

C5

C6

C7

C8

T4

T10

L5

S1

S2

thoracic

lumbar

cervical

sacral

a. Lissauer's tract
b. posterolateral sulcus
c. posterior intermediate sulcus
d. posterior median sulcus

e. gracile fasciculus
f. cuneat fasciculus
g. dorsal funiculus
h. lateral funiculus

i. ventral funiculus
j. anterior median fissure
k. anterior white commissure

can be any of the three, travel elsewhere in Lissauer's tract

thin diameter axons more likely to go up or down

a. cuneate fasciculus
b. gracile fasciculus
c. lateral corticospinal tract
d. dorsal spinocerebellar tracts
e. ventral spinocerebellar tracts
f. anterolateral system

a. substantia gelatinosa
b. nucleus propria
c. Clarke's nucleus
d. dorsal horn
e. lateral horn
f. intermediate gray horn
g. ventral horn

parasympathetic nucleus is only in the cervical and sacral

always at anterior horn, lower motor/alpha motor neurons that innervate muscle cells

Dorsal Column Pathway
anterolateral system
corticospinal tract
dorsal spinocerebellar tract also considered

Ia, Ib, II
large diamater heavily myelinated sensory afferent axons

organization that reflects that of the body

a. S5-T6
b. T5-C1
c. substantia gelatinosa
d. above T5

a. S5-T6, running outward
b. substantia gelatinosa

ascending pathway
located in dorsal funiculus
origin: primary and sensory afferent neurons with cell bodies in dorsal root ganglion
terminate in dorsal column nuclei
ipsilateral organization
somatotopic organization within the tract with the lower body control being more medial and the upper body control being more lateral

a. gracile nucleus
b. cuneate fasciculus
c. gracile fasciculus
d. gracile fasciculus

e. cuneate fasciculus f. cuneate nucleus
g. cervical
h. thoracic (lateral horn) below T6
i. sacral/lumbar

carry proprioceptive
fine touch and vibration sense
pallesthesia: vibration

ascending
location is in ventral-lateral funiculus
originates in substantia gelatinosa and nucleus proprius
terminates in thalamus
contralateral
lower body is more dorsal and lateral while upper body is more ventral and medial

spinothalamic tracts

pain, temperature, crude touch

Adelta and C

a. nucleus proprius
b. Lissauer's tract
c. substantia gelatinosa
d. still substantia gelatinosa
e. lissauer's tract can synapse either in substantia gelatinosa or nucleus proprius
f. thalamus
g. anterolateral system
h. anterior white commissure

more ventral and medial
legs more dorsal and lateral

a. cerebral cortex
b. motor decussation
c. no difference between arm and leg
d. no difference between arm and leg
ARM MORE MEDIAL, LEG MORE LATERAL

descending pathway
origin in pyramidal cells in cerebral cortex
termination: spinal cord gray matter
contralateral: R side cortex controls L side
somatotropic: to upper body is more medial, lower body more lateral

1. carry motor instructions down to spinal cord
2. modulate sensory processing in cord- can tone down reflex

a. due to inferior cerebellar peduncle
b. cerebellum
c. Clarke's nucleus

ascending
in margin of lateral funiculus (posterior part)
origin: cells of Clarke's nucleus
terminate in cerebellum
ipsilateral

convey proprioception from the lower body

Ia, Ib, II

large diameter, heavily myelinated sensory afferent axons

anterior cord syndrome (at cervical cord)
fine touch, proprioception, vibration sense
- not affected because the dorsal columns are not affected by the anterior spinal artery

pain and temperature
- bilateral at and below level of lesion, clinically it is one or two levels below

motor
- flaccid paralysis at the level
- spastic paralysis at lower levels

Brown Sequard Syndrome (at any level)
fine touch, proprioception, vibtration sense
- same side lost

pain and temperature
- opposite side loss

motor
- flaccid at level, same side
- spastic at levels below, same side

syringomyelia/syringomyeliac syndrome (cervical cord takes place more than others)

fine touch, proprioception, vibration sense
- no effect

pain temperature
- cavitation at anterior white commissure
- loss only at level of injury

motor
- maybe some flaccidity but paresis (weakness) first and possible paralysis later if lesion works itself over

tabes dorsalis

tertiary syphillis

loss of fine touch, vibration sense, proprioception, which can be shown through a positive Romberg test (swaying) because together with visual and vestibular input coordinates balance

polio

viral infection of poliovirus

loss of alpha motor neurons at the particular level, which leads to either paresis or flaccid paralysis with time

ALS

combination of flaccidity or spasticity depending on whether upper MNs or lower MNs are affected; if you lose lower motor neurons, you have a more immediate problem

a. medulla
b. pons
c. midbrain
d. tegmentum
e. tectum
f. tectum
g. tectum
h. cerebral peduncles (crus cerebri) that contain pyramidal tract axons and corticospinal axons
i. red nuclei
j. substantia nigra
k. corticospinal and corticobulbar axons
l. pontine nuclei
m. inferior olive (inferior olivary nucleus)
n. pyramids (pyramidal tract axons), corticospinal axons
o. tegmentum
p. tegmentum

a. upper midbrain
b. lower midbrain
c. pons
d. high medulla
e. low medulla

a. diencephalon
b. CN III
c. CN IV
d. vestibular nuclei
e. CN VI
f. spinal cord
g. MLF

axons can drop in, go with spinal cord, and get off the track at a particular place

they can also cross the midline
these things communicate across the MLF to make eye movements compensate for head movements

they help innervate the movement of the eye

receive information from vestibular apparatus about head movements

every time we move our head, we make eye movements that compensate for head movement, and eyes will move in the opposite direction of the turn to help stabilize the visual world

coordination breaks down like in MS

when you see repeated movements in the eye but then they flip back really fast to the direction you move, slowly move usually then flip when their eyes cant move the right way any more

always named for the direction of fast eye movement

can be pathological

Lateral Corticospinal tract
a. cerebral cortex
b. LTA lateral to medial
c. dorsal column nuclei
d. LTA lateral to medial and it is the pyramid
e. spinal cord
f. motor decussation
g. cerebral peduncles
h. pontine nucleus

medial lemniscus
a. thalamus
b. ATL medial to lateral
c. ATL medial to lateral
d. ATL posterior to anterior
e. dorsal column nuclei

Anterolateral system
a. thalamus
b. LA post to ant
c. LA post to ant
d. spinal cord

nondescript part of center of brainsteam

lateral (mostly in medulla)
medial
raphe (gets most mention, in midline)

breathing, swallowing, cardiovascular control, coughing, gagging, vomiting

in or around reticular formation

a place that takes input from spinal cord and forebrain and also passes through the brainstem and the bulk of a cranial nerves run out of brainstem and thus relay response

send projections ramified throughout the forebrain and correlate arousal or excitement; they set this level

some brainstem neurons are extensive in their projections

norepinephrine
dopamine
serotonin

famous in having cell bodies in one spot: locus ceruleus (blue spot, more important) and lateral reticular nuclei (near medulla)

below and lateral to ventricles

sets wakefulness, elevates level of attention to fit current situation

substantia nigra (pars compacta is the important part of SN to remember) and ventral tegmental area

midbrain

locus ceruleus

just deep to cerebral peduncles in midbrain

VTA is ventral to that

parkinson's and motor problems

mostly movement, cognition, and pleasure related

discussing projections from ventral tegmental area using dopamine to limbic areas in cerebral hemispheres or just cerebral hemispheres altogether

midline of brainstem reticular formation

serotonin

general level of arousal (morning vs. evening) not moment to moment

part of pain control pathway in nervous system (makes life more bearable), also called descending pain control pathway

basal forebrain, basal ganglia

most of medulla except posterior lateral section

most of pons
anterior medial midbrain

much of midbrain, except anterior medial part