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Neurology 1- M2 > 08 27 2014 Neurotransmission > Flashcards

08 27 2014 Neurotransmission Flashcards

1
Q

What type of neuron responds to sensory inputs?

A

Pseudo-unipolar and Bipolar

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2
Q

What type of neuron resounds to other synaptic inputs

A

Multipolar and bipolar neurons

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3
Q

What is the resting potential of a neuron and how is this produced/maintained?

A

-65mV (-40mV to -90mV) Produced by osmotic and electrical forces, AND selective permeability Maintained by Na+/K+ ATPase

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4
Q

RECALL: Are the concentrations of the following ions greater inside a cell or outside a cell: Ca2+ Cl- Na+ K+

A

All are greater outside except for K+ who is greater inside.

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5
Q

what is a graded potential in a neuron?

A

response of neurons to inputs – reaches threshold and caused depolarization In sensory neurons a graded potential is called a receptor potential. Response can change based on potential.

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6
Q

What causes a neuron to detect a more intense stimulus?

A

Action potential firing rate increases a sensory neuron’s response to a more intense stimulus. Higher firing rate = more neurotransmitter released = detect a more intense stimulus.

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7
Q

What is a graded potential at a synapse?

A

electrical responses to synaptic input. changes in membrane potential that vary in size, as opposed to being all-or-none.

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8
Q

What are the types of graded potentials?

A

-excitatory postsynaptic potentials (EPSPs) -opening of Na+ or Ca+ channels -cause depolarization -Inhibitory postsynaptic potentials (IPSPs) -opening of Cl- or K+ channels - hyperpolarize

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9
Q

Describe ability of graded membrane potentials to impact system?

A

attenuate rapidly with distance from the point of stimulation. “impact factor” depends on their location and strength of synapse. ** has more of an impact if closer to where trigger is **

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10
Q

Where is the trigger zone for sensory vs motor neurons?

A

Sensory neuron = near the “dendrite” end of a sensory neuron. Anatomoic axon/physiological dendrite – node of Ranvier? Motor neuron = axon hillock.

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11
Q

Since graded potentials are summed, what is the threshold needed to initiate AP?

A

about 10mV at initial segment.

If threshold is reached at the trigger zone, one or more action potentials will occur.

Recall: if input is large, the firing rate of action potentials increase.

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12
Q

What are the two types of summation?

A
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13
Q

Spatial Summation?

A

refers to the number of inputs

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14
Q

Temporal Summation?

A

refers to the timing of inputs.

Can add on and create even bigger responses.

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15
Q

Example of inputs that modulate sensory signals in the spinal cord?

A
  1. motivation/ attention
  2. Arousal/anxiety levels
  3. other sensory inputs
  4. intesnity of input (comes in through DRG)
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16
Q

Location of Synaptic inputs?

A

AD– Axodendritic

AA– Axoaxonal

AS– Axosomatic

DD– Dendrodendritic

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17
Q

Where does PRE-synaptic inhibition occur?

A

Axon terminals

  • axon projecting onto another axon
  • affects one collateral
    1. an excitatory neuron fires
    2. an action potential is generated and travels down the axon
    3. an inhibitory neuron fires, blocking neurotransmitter release at ONE synapse (aka a collateral)
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18
Q

Where does post-synaptic inhibition occur?

A

Prevents neuron from firing action potential –blocks at dendrites/cell body

  • all outputs are affected.
    1. an excitator and an inhibitory presynaptic neuron fire.
    2. modified signals in post-synaptic neuron is below threshold
    3. no action potential triggered.
    4. no response from target cell.
19
Q

Review of channels when AP is created

A

Resting: Na+ inactivated

             K+ closed -- but they are leaky

Threshold: Na+ open– fast activaiton of Na+ channels

                K+  closed

Depolarization Peak: Na+ is inactivating

                                 K+ are opening -- slower activation

Refractory period: Na+ inactivated

                              K+ open

                              Na+ and K+ are closed again.
20
Q

How are AP propagated down an axon?

A

** Recently depolarized regions become refractory so that action potentials move unidirectionally.

  1. Na+ channels locally open in response to stimulus = generate AP
  2. depolarizing current flows passively down axon
  3. local deplarization causes neighboring Na+ channels to open and generate AP.
  4. Na+ channels there were once active are now inactive– refractory phase
  5. process repeats down axon potential
21
Q

What does Action Potential conduction velocity depend on?

A

Myelination and axon diameter

  • Myelination = increases speed
  • Thicker axons have less resistance to current flow
22
Q

Name two demyelinating diseases:

A
  1. Multiple Sclerosis
  2. Guillain - Barre
23
Q

Multiple Sclerosis

A

Autoimmune inflammatory disorder.

  • genetic/environmental factors
  • Oligodendroglial myelin attacked – makes sense becuase oligodendrocites make myelin.
  • CNS disease. usually begins with sensory loss

Diagnosed:

History of 2 or more deicits separated in neuroanatomical space and time.

  • supported by MRI evidence of white matter lesions
  • slowed CV (conduction velocity – EMG)
  • CSF oligoclonal bands.
24
Q

Guillane- Barre?

A

Inflammatory- induced demyelination in peripheral nerves

Usually seen 1-2 weeks after a viral infection (can last for months)

Motor> sensory

Autonomic is also affected

Ascending pattern of weakness

Decreased nerve conduction velocity– measure in PERIPHERAL NERVES

Elevated protein in CSF w/o increase in WBC.

25
Q

Chemical Synaptic transmission

A

Pre-synaptic neuron releases one neurtransmitter into synaptic cleft. Neurotransmitter binds to receptors on post-synaptic neuron and can open/close post-synaptic channels (excitatory or inhibitory AP generation).

Neurotransmitters are removed by glial uptake or enzymatic degradation

26
Q

Two types of post-synaptic receptors?

A
  1. Ligand-gated ion channels
    • Ionotropic
  2. G-protein coupled receptors
    • Metabotropic
27
Q

Ionotropic Receptor

A

Receptor linked directly to ion channels

  • ligand-gated ion channel

Enable FAST responses.

Provide information about what,when, where?

28
Q

Metabotropic receptors?

A

Receptor does not have a channel directly linked to it.

  • slow, long-term changes.
  • G-protein-coupled receptors
    1. G-protein activation
    2. G-protein dissociation and interaction (directly or indirectly) with ion channel.

Responsible fro neuromodulation

  • slow = they hang around long enough that they can change the resting membrane potential = more excited/more inhibitory
29
Q

Ionotropic receptors: Excitatory vs. inhibitory neurotransmitters?

(CNS vs. PNS)

A

Major Excitatory neurotransmitters

PNS: ACh (nicotinic)

CNS: glutamate

Major Inhibitory neurotransmitters

CNS: GABA or Glycine (spinal cord)

30
Q

Excitatory Amino Acid group neurotransmitters

  • Action and Location
A

Glutamate

Location:

CNS: everywhere; PNS: spinal ganglia

Action in CNS:

Fast and Slow excitation

Slow inhibition (metaboropic)

31
Q

Inhibitory Amino Acid Group Neurotransmitters

-location and Action

A

GABA

location: CNS: everyhwere

             PNS: ganglia, gut

Action in CNS: Fast and slow inhibition

Glycine

location: Brainstem AND spinal cord

Action in CNS: Fast inhibition

32
Q

Glutamate

  1. Type of neurotransmitter
  2. Origin (location of cell bodies)
  3. Function
  4. receptor subtype
  5. Location of receptor
  6. receptor functions
  7. Glutamate toxicity
A
  1. Major excitatory amino-acid neurotransmitter
  2. Entire CNS
  3. Fast and slow excitation; slow inhibition (metabotropic). Requried for long-term potentiation of (learning and memory)
  4. AMPA and NMDA
  5. Location of cell bodies: Entire CNS

6.

AMPA– ionotropic Na+/K+ passage – net effect =excitatory

NMDA –Mg2+ plug that is released when glutamate is present. Na+, K+ and Ca+ passage (Na+ and Ca2+ go into cell, K+ comes out of cell)

  1. Glutamate toxicity

Trauma/disease impaire ATp-generation = increased glutamate release or decrease glutamate reuptake.

-NMDA channels allow Ca2+ to leak into cells–> autodigestion. Leads to multiple seizure

Disease thought to be assocaited with glutamate toxicity: ALS, Alzheimer’s, tumors, oxygen deficiency, ischemia trauma.

33
Q

GABA

  1. Type of neurotransmitter
  2. Origin (location of cell bodies)
  3. Function
  4. receptors
  5. Location of receptor
  6. receptor functions
  7. Molecules that act on GABA receptors
A
  1. amino acid – inhibitory
  2. Everywhere in CNS
  3. Fast and slow inhibition
  4. GABA- gated Cl- channels (GABA a receptor): Ionotropic recepotrs that open Cl- channels

GABA b - metabotropic receptors open K+ or close Ca 2+ channels

  1. CNS: everywhere; PNS: Ganglia and gut
  2. Inotropic opening of Cl- channels
  3. molecules that can act on GABA receptors: Benzodiazepine (anti-anxiety), Ethanol, Barbituate, and Neurosteroids, GABA.
34
Q

Glycine

  1. Type of neurotransmitter
  2. Origin (location of cell bodies)
  3. Function
  4. receptors
  5. Location of receptor
  6. receptor functions
A
  1. Amino Acid- inhibitory
  2. Spinal cord (maybe brain stem too)
  3. Fast inhibition in CNS
  4. Glycine receptors
  5. Location: spinal cord and brainstem
  6. Ionotropic: ligand-gaited Cl- channels (Similar to GABA a receptor)
    - inhibitory!
35
Q

Catecholamines that come from Tyrosine?

A

Norepninephrine, epinenphrine, and dopamine

36
Q

Norepinephrine

  1. Type of neurotransmitter
  2. Origin (location of cell bodies)
  3. Function
  4. receptors
  5. Location of receptor
  6. receptor functions
  7. Drugs that stimulate NE release?
A
  1. Biogenic Amine– Catecholamine from tyrosine
  2. Locus ceruleus and Lateral tegmental areas (Pons)
  3. Slow excitation; Modulates pina, role in sleep-wake cycles and attention; post-synaptic ganlian.
  4. alpha and beta subtypes
  5. CNS: everywhere; PNS: sympathetic ganglia
  6. Neuromodulation AND sympathetic functions
  7. Amphetamines, Methylphedinate (Ritalin)
37
Q

Dopamine

  1. Type of neurotransmitter
  2. Origin (location of cell bodies)
  3. Function
  4. receptors
  5. Location of receptor
  6. receptor functions
  7. three projections? (just name them)
A
  1. Biogenic Amine– Catecholamine from tyrosine
  2. Substancia Nigra, ventral tegmental are, pars compaccta (Midbrain)
  3. Slow inhibition or excitation

motor control

memory

motivation

reward

addiction

maternal behavior

sensory processes

  1. D1- D5
  2. CNS: Everywhere
  3. Neuromodulation

7.

  • Mesostriatal (nigrostriatal) pathway
  • Mesolimbic pathway
  • Mesocortical pathway
38
Q

Dopamine pathway– Nigrostriatal Pathway

where does it start –> where does it go

  • functions
  • what happens when dysfunction?
  • treatment
A

arises from substantia nigrapars compacta —> cuadate and putament (thalamus)

control of movement

disfunction= Parkinson’s disease

Treatment: dopamine agonists

39
Q

Dopamine pathway – Mesolimbic

  • where does it start –> where does it go
  • functions
  • what happens when dysfunction?
  • treatment
A

Arises from ventral tegmental area (some from substancia nigrapars compacta) to limbic structures:

- Medial orbital frontal cortex
- Nucleus accumbens
- Cingulate cortex
- Hippocampus and parahippocampal gyrus
- Amygdala

Reward pathway (addiction)

Damage = positive symptoms of schizophrenia –> hallucinations

Treatment: dopamingeric antagonists

40
Q

Dopamine pathway – Mesocortical pathway

  • where does it start –> where does it go
  • functions
  • what happens when dysfunction?
  • treatment
A

ventral tegmental area (some from substancia nigrapars compacta) to prefrontal cortex.

Functions: working memory and atttional aspects of motor initiation.

Damage: cause cognative deficitis and hypokinesia (decrease movement) in Parkinson’s disease. Can also cause NEGATIVE symptoms of Schizophrenia

41
Q

Seratonin (5-HT):

  1. Type of neurotransmitter
  2. Origin (location of cell bodies)
  3. Function
  4. receptors
  5. Location of receptor
  6. receptor functions (aka how does receptor work)
  7. Drugs that affect 5HT systems?
A
  1. Biogenic Amines
  2. Raphe nuclie – midbrain, pons, and medulla
  3. Slow inhibition or excitation, fast excitation, sleep-wake cycle, mood, depression, anxiety, pains
  4. N/A
  5. CNS: everywhere
  6. N/A
  7. Prozac : blocks 5-HT reuptakeMDMA, MDEA (“ecstacy”) increases 5-HT efflux and increses sensory experiences and affect social relationships.
42
Q

Acetylcholine:

  1. Type of neurotransmitter
  2. Origin (location of cell bodies)
  3. Function
  4. receptors
  5. Location of receptor
  6. receptor functions (aka how does receptor work)
  7. What happens when Ach is blocked?
A
  1. Biogenic Amines
  2. Nucleus Basilis of the basal forebrain, septal nuclei, and nucleus of diagonal band, and tegmentum of the pons
  3. Fast excitation (nicotinic ionotropic), Slow excitation or inhibition (muscarinic metabotropic), memory, alertness
  4. Nicotinic and muscarinic
  5. CNS: cortex and spinal cord; PNS: parasympathetic ganglia (muscle)
  6. N: ganglion, skeletal muscles

M: Smooth musle, contraction, sweat gland secretion

  1. causes delirium. Nucleus basalis degerates in Alzheimer’s disease
43
Q

Opiates

  1. Type of neurotransmitter
  2. Origin (location of cell bodies)
  3. Function
  4. receptors
  5. Location of receptor
  6. receptor functions (aka how does receptor work)
  7. 3 classes?
A
  1. Neuropeptides
  2. Periaqueductal grey of the midbrain, Thalamus, Ventral tegmental area, nucleus accumbens, amygdala, spinal cord
  3. regulates pain
  4. Mu, Kappa, Delta
  5. (same as number 2)
  6. N/A
  8. Enkephalin– spinal cord–> periaqueductal grey (PAG) – regulates pain
  9. Endorphins– hypothalamus–> PAG –> Spinal Cord – regulates pain-analgesia
    • morphine is agonist
  10. Dynorphin – located in PAG
44
Q

Unconventional neurotransmitters

A

Endocanabinoids: act as neuromodulator to decrease transmission of pain (medical marijuana)

Cannibis (marijuana): alters perception, incresed sociability, induced euphoria. Possible role in mood disorders, anxiety and appetite control. Approved pain relief in MS.

Nitric oxide: gas– may actually be involved in neurodegenerative processes.

Neurology 1- M2 (22 decks)

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