neur exam 1

DCML function

fine touch, vibration, propioception

STT function

crude touch, pain, temperature

SCT function

unconscious proprioception

corticospinal tract

voluntary control of skeletal muscle

extrapyramidal pathways

corticonuclear and subcortical pathways to brainstem and spinal motor circuits for involuntary/automatic skeletal muscle control

extrapyramidal pathways-name them

RuST, VST, TST, RST

visceromotor pathway example

autonomic nervous system

lesions in the spinal cord implications

we can affect motor axons coming out and sensory axons coming inwhat

what could go wrong in the DCML? LOF and GOF

LOF: absent sense of touch, vibration, proprioception

GOF: paresthesia (pins and needles), neurons fire APs when no actual physical stimulus

spinothalamic tract STT what info transmission

somatosensory info from peripheral sensory receptors to the CNS for sensation of crude touch, pain, itch, temperature, and visceral information

STT what could go wrong? LOF GOF

LOF: absent sense of pain, and temperature

GOF: pain sensation in absence of painful stimuli (neuropathic pain)

what ion channels STT open with extreme temp or chemicals

TRP ion channels

where does STT synapse?

dorsal root ganglia

STT neuron order

1: DRG synapses in dorsal horn, via anterior white commisure

2: dorsal horn

3: VPL thalamus

somatic motor system tracts

RuST, VST, TST, RST, corticospinal

visceral motor system

sympathetic and parasympathetic

what info transmission lateral corticospinal tract

-motor commands from motor cortex to alpha motor neurons in sc that control skeletal muscles underlying fine movementwh

what could go wrong LCT? LOF GOF

LOF: weakness (paresis) or loss of ability to move (paralysis)

GOF: spontaneous muscle contractions/spasms or twitches (fasciculations), spacitity, hyper-reflexia

where does LCT cross

pyramidal dessucation in medulla

autonomic vs other systems

ONLY MOTOR. others are sensory and motor

ANS analog of alpha motor neuron

pre-ganglionic neuron

pre-ganglionic neurons+location

send projections out to control motor state of visceral factors; lateral horn of SC

ganglia location sympathetic vs parasympathetic

SYM: near spinal cord

PARASYM: near organs

muscle stretch reflex + reciprocal inhibition

1) hammer tap stretches tendon, which stretches sensory receptors in leg extensor muscles

2a) sensory neuron synapses with and excites motor neuron in the spinal cord

2b) sensory neuron also excites spinal interneuron

2c) interneuron synapse inhibits motor neuron to flexor muscles

3a) motor neuron conducts AP to synapses on extensor muscle fibers, causing contraction

3b) flexor muscle relaxes because the activity of its motor neurons has been inhibited

4) leg extends

basal ganglia diseases

parkinsons, huntington, substance-use

thalamus disease

stroke, epilepsy

cerebellum diseases

ataxia, essential tremor

amygdala diseases

PTSD

hippocampus diseases

alzheimer’s, epilepsy

which brain parts contribute to epilepsy

thalamus and hippocampus

why would info go from cerebral cortex to basal ganglia and back through the thalamus

to form habits

why would info go from cerebellum to thalamus to cortex

motor implicit outputs ie playing piano

fast communication NS

employs excitatory NT ie glutamate or GABA that act by opening ligand-gated ion channels to produce rapid effects on postsynaptic cells

neuromodulation

employs nt that act on GPCRs for slower modulatory control and regulate the gain with which postsynaptic cells response to rapidly acting neurotransmitters

4 main neuromodulatory systems

norepinephrine, serotonin, dopamine, and acetylcholine

how are different types of info such as fine touch and noxious heat conveyed to the nervous system while preserving differences in the sensory info that is conveyed

Through distinct peripheral receptors (e.g., mechanoreceptors vs. TRP channels/nociceptors), labeled-line coding, and segregated anatomical pathways (DCML for fine touch vs. STT for noxious heat) projecting to specific central targets.

3 key neuronal electrical properties

1) resting potential

2) passive responses to stimulation

3) action potentials

membrane potential Vm

Vin-Vout

resting potential

the value of the membrane potential under resting conditions

can stick probe/electrode in normal solution as baseline then into the nerve cell, can see around -60mV resting potential

3 structural/molecular components that define intrinsic electrical properties of neurons

1) plasma membrane: separates inside from outside, permits regulation, separation of charge, electric potential difference called membrane potential

2) active ion transporters: use ATP or ATP gradients to move ions in an uphill direction to maintain nonequillibrium

3) ion channels: provide pathway for passive movement of ions across membrane over electrochemical driving force

how many na and k in pump

2K in 3Na out

relative amounts of K and Na to plasma

K high

Na low (salty banana)

2 functional properties of ion channels are

ion permation and gating

ion permeation

process by which ions move through open channels, depends on ions and pore properties of the channel

gating

process by which channels open and close, depends on the channel and the channel environment

when ion channel opens

depends on charge might go with or away from field

-flux of charge and max v due to resistance from other end from water molecules or other molecules

membrane potential steps

charge separation across membrane +Q -Q

creates electric field inside membrane (E=Q/Ac)

ions inside channel pore experience electric force (F=qE)

ions flow under influence of the electric force from a higher energy to a lower energy state

—> Vm, difference Vin-Vout

patch clamp technique

can measure signle channel current at constant Vm, tells us ion permeation

patch clamp current voltage relationship

Vm direct with iion

slope of iv relation graph is

measure of single channel conductance of channel

x intercept of iv graph voltage clamps

reversal/zero current potential, for channel Vrev

what info does Vrev provide

ion selectivity of channel

if channel perfectly selective for a given ion, Vrev=nerst potential

ohms law for ion channels

i,ion=single channel conductance*nernst potential for permanent ion

when membrane potential=nernst potential

no electrical driving force, 0 conc gradient, means current flows purely due to electric gradient/driving force

why are there both active and passive ion channels

allows electrical signaling via gated-ion channels

voltage gated vs leak channels

leak channels don’t have S1-4 voltage sensing regions, only pore forming S5/6

Gk vs GNa

K> Na> K> K>

K vs Na activation

K slower activation

Na conformations

resting open inactivated

K conformations

closed open

why Na inactivate vs close

inactivate or else Na will keep coming in neuron if a depolarization occurs

how does depolarization affect driving force on Na+

decrease, but driving force still favors inward Na current

how does depolarization affect driving force on K?

increases, favoring outward K+ current

factors that make voltage spread further

-large fiber diameter

-large conductance/area

small Ri/Rm

synaptic transmission role stretch reflex

graded receptor, AP/receptor P, ap, ap

stretch reflex releases..and does what

ACh, interacts with post synaptic nicotinic receptors

How do EPSPs and IPSPs explain the mono- and disynaptic stretch reflex?

• Monosynaptic: Sensory neuron releases neurotransmitter onto the motor neuron → causes an EPSP (depolarization) in the motor neuron → reaches threshold → motor neuron fires → stretched muscle contracts.

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• Disynaptic: Sensory neuron activates an inhibitory interneuron → interneuron causes an IPSP (hyperpolarization) in the motor neuron of the opposing muscle → makes it less likely to reach threshold → opposing muscle relaxes.

how many classes of neurottransmitters

4

how many classes of nt receptors

2

electrical synapse parts

gap junctions, pre and post synaptic cell

chemical synapse parts

synaptic vesicles, synaptic cleft, nt receptors, not directly touching

gap junction signaling example

for synchronized activity so the heart

what determines the direction and the magnitude of the current that flows from the pre to the post synaptic cell through gap junction channels?

the difference in Vm between pre and post synaptic cells and the total gap junctional conductance

what is the impact of this current on the membrane potential in pre and post synaptic cells?

Vm changes at a rate that depends on the net current flowing across the membranes of these cells and their respective membrane capacitances

main steps in neurotransmission

1) ap initiated at spike initiation zone at presynaptic neuron

2) ap propagates along axon to presynaptic terminal

3) ap depolarizes the presynaptic terminal

4) voltage sensitive ca channels in presynaptic terminal open and allow ca to flow into the terminal

5) ca conc rises, triggers NT release into synaptic cleft

6) nt molecules in the synaptic cleft bind to postsynaptic receptors, triggers postsyn response

7) nt molecules diffuse away, are degraded and/or taken up by presynaptic neuron or nearby glial cells

the message communicated via chemical synaptic transmission depends on three things:

1) specific neurotransmitter synthesized (excitatory vs inhibitory)

2) post synaptic receptors present, usually multiple types for one NT

3) postsynaptic effect of interaction between nt and its receptor

presynaptic effect diseases

-lambert eaton

-botulinum toxin

lambert eaton

auto antibody reduction in pre synaptic ca channels at skeletal NMJ, reduces ACh release at these synapses, w consequences for evoked muscle contraction including weakness

botulinum toxin

blocks NT release by cleaving syanpic vesicle proteins required for normal vesicle release

post synaptic effect diseases

myasthenia gravis

myasthenia gravis

auto antibody mediated reduction in functional nicotinic AChRs at the skeletal muscle muscle NMJ—>weakness, fatigue

4 main types of neurotransmitters are

ACh

Amino Acid

Neuropeptides

Monoamines

examples of each NT

ACh-ACh

amino acid- glutamate, GABA, glycine

neuropeptides-substance P, endorphins

monoamines-dopamine, serotonin, norepinephrine

two types of nt receptors are

ligand-gated and GPCR

ligand gated ion channel steps

nt binds, channel opens, ions flow across membrane

GPCR steps

nt binds, g protein activated, GP subunits modulate ion channels, ion channel opens, ions flow across membrane

ligand gated nonselective cation channel examples

nAChR, GluR

excitatory nt

glutamate ACh

inhibitory NT

Gaba, glycine

GABA and glycine IPSPs open

ligand gated Cl- channels

quantal analysis either

MEPP: miniature end plate potential

EPP: end plate potential

Quantal Size

postsynaptic electrical responses evoked by the neurotransmitter released from one vesicle

Quantal Content

number of vesicles that are released in response to a presynaptic action potential

postsynaptic response amplitude =

Quantal content x Quantal Size

how does quantal analysis work

we know quantal size from responses from one vesicle and we know the full amplitude of the EPSP. we can find # of vesicles by diving

same quantum size but smaller EPSP

pre synaptic issue

same quantum size but larger EPSP

post synaptic issue

one way to turn up or down excitability of neurotransmitter

add GPCR ie dopamine, ACh muscarinic receptors

what happens if you double the calcium concentration to exocytosis

multiply exocytosis rate by 16

synaptic plasticity: facilitation

postsynaptic responses to a second stimulus can be larger than the first if the interval between stimuli is too brief to permit complete recovery of presynaptic Ca2+