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Lecture 3 Flashcards

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1
Q

What is the lizard: a case of PD?

A 
•  Loss of DA neurons in SN
•  Knowledge of DA transmission integral for Treatment development
–  L-dopa
    •  Symptom loss
    •  Doesn’t stop disease progression
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2
Q

What is resting membrane potential?

A

• Neuron at rest
– Unstimulated/inactive
• Membrane lipid bilayer
– Ions cannot easily cross
• Positively or negatively charged particles
• Unequally distributed across membrane
• Membrane polarized
– Carrying a charge
– -70mV (inside of neuron is 70 mv less than outside)
• Difference in electrical charge inside and outside cell

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3
Q

How is membrane potential recorded?

A

• Intracellular electrode
– Microelectrode
• Extracellular electrodes
• Detect difference between inside and outside of cells

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4
Q

What was the giant squid motor neurons used for?

A

• Used in early studies of resting membrane potential stability
• Hodgkin and Huxley with Eccles won Nobel prize for uncovering ionic mechanism of action potentials
• .5mm diameter (humans is 0.015 mm)
– Large diameter allowed easy electrode insertion
• Terminateonmuscle
• Similar to other multipolar neurons

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5
Q

What is the ionic distribution at rest like?

A

• Sodium (Na+) higher outside
– Membrane extremely resists passage
• Enters by random motion
– Driven inside cell by electrostatic forces and concentration gradient
• Chloride (Cl-) higher outside
– Membrane slightly resists passage
– At equilibrium
• Potassium (K+) higher inside
– Membrane moderately resists passage
– Driven inside cell by electrostatic pressure
– Driven out by concentration gradient
• Negatively charged proteins inside
– Cannot cross membrane

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6
Q

What is random motion?

A

Random motion:
Passage of ions through ion channels
down concentration gradient when neuron at rest

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7
Q

How do ions maintain resting potential?

A

Homogenizing factors
- Concentration gradient
• Tend to equally distribute
• Move from high to low concentration
– Electrostatic pressure
• Like repels like
• Opposites attract
Non-homogenizing factors
– Passive (no energy requirement)
• Random motion
• Due to Selective permeability-ion channels
– At rest:Cl-and K+ PASS READILY
– Active (hi energy requirement)
• Sodium-potassium pumps; maintain stability of RMP in spite of random motion of Na and K down concentration gradients
• Ion distribution returned to rest despite random motion

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8
Q

What are sodium potassium pumps; discovered by H&H?

A

Active transporter
– Energy consuming
Continuously transfer 3Na+ out and 2K+ in

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9
Q

What are postsynaptic potentials?

A

• Create signals in neurons
• Neurotransmitters bind to postsynaptic cell
– Cause electrical change in post synaptic cell
• Excitatory neurotransmitter:
– Depolariza1on (increase ++++)
– Membrane potential less negative
– Excitatory post synaptic potential (EPSP)
» Increase likelihood of AP
• Inhibitory neurotransmitter
– Hyper-polarization (increase—)
– Membrane poten=al more negative
– Inhibitory post synaptic potential (IPSP)
» Decrease likelihood of AP

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10
Q

What are EPSP and IPSP?

A 
•  Rapidtransmission
    –  Instantaneous rate of
transmission
      •  Duration can be variable 
        –  due to graded response
•  Graded
    –  Amplitude proportional to
      •  Stronger stimuli produce bigger IPSP or EPSP
        –  Bigger ion influx
        –  Due to increased NT release or receptor signalling
    –  Transmit decrementally 
     •  Passive spread from
synapse (dendrite or soma)
     •  Get weaker as travel (like sound through air)
 signal intensity
      –  Cant travel far (2 mm max)
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11
Q

What is an EPSP?

A

Graded response: amplitude of signal proportional to stimulus intensity
->bigger stimulation = bigger PSP
->larger +ion influx = larger EPSP
Sodium ion flow inward is responsible for the generation of an EPSP

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12
Q

What is an IPSP

A 
Graded response: amplitude
of signal proportional to
stimulus intensity
->larger -ion influx = larger IPSP
Chloride ion flow inward is usually responsible for the generation of an IPSP
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13
Q

What is the integration of PSP to generate AP?

A

• Adding or combining signals into one overall output (or inhibition of output)
– One EPSP will not suffice
– Need summation
• Net affect of synaptic activity
• Threshold of excitation at axon hillock (axon initial segment)
– Synapses closer to axon hillock have larger effect on firing due to decremental transmission of far away PSPs
• Many inhibitory inputs
• Some distal dendritic sites have
mechanisms to amplify their PSPs
• integration of inputs must result in about -65 mv at hillock for AP

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14
Q

What is spatial summation?

A
  • Occurs at Axon initial segment (AIS)
  • integration (of EPSP and IPSP) across post synaptic locations
  • local EPSPs or IPSPs occurring simultaneously combine to form larger response (or cancel out to form weaker)
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15
Q

What is temporal summation?

A
  • Integration across time on same synapse
  • Rapid succession
  • Ex. High frequency vs low frequency inputs
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16
Q

What are action potentials?

A 
•  Massive
•  Momentary
•  Reversal of membrane potential
    –  -70mV to +50 mV (in 1 msec)
• Does not degrade over space
    –  Due to voltage gated channel
•  All-or-none
   –  Equal strength throughout
   –  Occur as long as threshold of activation reached
   –  Intensity not graded, but frequency increases with more stimulation
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17
Q

How do voltage gated sodium channels generate and propagate APs?

A

• AP=fire, spike
• Threshold for excitation reached by postsynaptic integration at AIS
– Depolarized to at least -65 mv
– Opens voltage-gated ion channels
• Fast reversal of membrane potential
– -70 mvà+50 mv
– 1 msec
• All-or-none/not graded
– Occur to full extent –or– not at all
– Does not change response based off stimulus
• Just frequency

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18
Q

How are APs produced and conducted?

A

Voltage gated ion channels

- Open or close in response to membrane potential

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19
Q

What do ions do in APs?

A

Threshold of excitation
– VG Sodium channels open (rising phase)
• Rush in: electrostatic AND concentration gradient
• Increases membrane potential +50 mv
• Closes vg channel
– VG K+ channels open
• Driven out: electrostatic and concentration gradient
– Membrane repolarized; and slightly hyperpolarized (refractory period)
» K channels close gradually
» Resting potential re-established by random motion of ions and sodium potassium pump.

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20
Q

What is a refractory period?

A

• Absolute
– brief (1msec) post initiation
– Impossible to initiate new AP
in same neuron
– Sodium channels inactivated
– Spreads down axon behind AP
• Prevent backwards movements of AP
– Backwards propogating APs into soma and dendrites from axon hillock
• Limits to firing rate to 1000x per sec max
– Firing rate determined by stimulation intensity (of PSPs)
• Relative
– Follows absolute period
– Requires larger than threshold stimulus to initiate new AP
– More intense stimulation increase firing rate

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21
Q

What is axon conduction of action potentials?

A 
•  Active and passive
–  Requires energy
•  Nondecremental
–  Just as strong from beginning (axon
hillock) to end (synaptic terminal)
•  Row of voltage-gated sodium channels
–  Domino effect 
–  Tightly packed
      •  Creates waves of depolarization 
–  Spreading can occur in either
direction
     •  Anterograde: hillock -> boutons
          –  Orthodromic conduction
     •  Retrograde: boutons -> hillock 
     –  Antidromic conduction
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22
Q

What is conduction in myelinated axons?

A

• Instant conduction along myelin=faster
– Ion flow only at nodes
• Saltatory conduction
– Ap jumps node to node
– Requires less energy
– Sodium channels only on nodes
• Passive (rapid and decremental) node to node
– Diminished before next node
• enough to open next node VG- Na+ channel

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23
Q

What is the velocity of axonal conduction?

A

• Faster in large diameter
– Less friction
• Faster in myelinated
• Large & myelinated really fast
– Large motor neurons • 224 MPH (100 m/s)
– VS 1 m/sec IN UNMYELINATED
– VS 25 m/sec IN UNMYELINATED SQUID GIANT MOTOR AXONS
• 100 m/sec in cats; 60 m/ sec in humans

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24
Q

PSP vs AP

A

EPSPs/IPSPs
• Decremental over space and time
• Fast
• Passive (energy is not used)

Action Potentials
• Nondecremental
• Conducted more slowly than PSPs
• Passive and active (use ATP)

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25
Q

What are interneuron APs?

A 
•  Not well understood
•  Conduction is Passive and decremental
•  Function to integrate neural activity in brain structure
– Visual cortex
•  No axons
•  No AP
•  Small
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26
Q

What is the difference between cerebral neurons vs squid motor neurons?

A

• Hodkin-Huxley model based of squid neurons
– Not all cerebral neurons behave the same way
• More complex than model motor neurons
• Some cerebral neurons:
– Fire AP continually without
input
– Axons actively conduct graded signals and AP
– AP duration, frequency and amplitude different across neuron types
– Do not display AP
– Dendrites can conduct AP
• Comparison with motor neurons with caution

27
Q

What are synaptic contacts?

A 
•  Axodendritic
–  Axon ->dendrite
–  Most common
•  Axosomatic
–  Axon->soma
•  Axoaxonic
–  Axon -> axon
–  Mediate presynaptic inhibition or facilitation
     •  Selectively influence synapse rather than entire neuron
•  Dendrodendrtic
–  Dendrite -> dendrite
–  Reciprocal
      •  Can be transmitted in either direction
•  Dendroaxonic
–  Dendrite -> axon
•  Directed synapse
–  Site of NT release close to post synaptic
contact
–  Most common
•  Undirected synapse
–  Site of release and contact far
–  Varicosities
     •  String of beads
–  Common for monoamines (NE, DA)
–  Neuroendocrine system releases neurohormones into blood stream
28
Q

What are dendrites?

A

Shaft

Spine

29
Q

What is the chemical transmission of signals?

A 
1.  2.  3.  4.  5. 
• Neurotransmitter molecules
• Early studies on NMJ
–  Muscles large
–  Muscles only receive one synapse 
–  Acetylcholine (Ach)
1. AP reaches end of axon terminal 2. Calcium enters cell
3. Release NT into cleft (exocytosis) 
4. NT binds receptors
5. Receptors influence post synaptic neurons
•  Ion permeability (ionotropic) 
      –  Create EPSP or IPSP
•  Intracellular signalling (metabotropic) 
      –  Longer lasting
6. NT degradation/recycling
30
Q

What is small molecule neurotransmitter synthesis?

A
  • Enzymatic conversion of amino acid precursors

* Presence of enzyme dictates which type of NT are released from cell

31
Q

What are large molecule neurotransmitter synthesis?

A

Peptides

Processed by enzymes

32
Q

What is neurotransmitter synthesis?

A

• Small molecule
– Classical neurotransmiPers
– Punctateeffects
– ReleaseinpulseforeachAP
– Synthesized in cytoplasm and golgi apparatus of terminals
• monoamines: Vesicles stuffed with precursor amino acid and synthesizing enzymes enroute to terminal
– Released into cleft
• Large molecule
– Neuropeptides
– Released gradually in response to increases in AP
– Widespread effects
– Released into ECF, ventricles or bloodstream
– Neuromodulators
– Synthesized in cell body, packaged in vesicles and then transported to terminal

33
Q

What is neurotransmitter packaging?

A 
•  Secretory vesicles
–  Proteins synthesized in RER
–  Transported to golgi
–  Bud off golgi to form vesicle
–  Fast antergrade axonal transport
–  Transporter proteins actively pump NTs into vesicles
       •  Example: VAchT
•  Small clear core vesicles
–  Contain small molelcule NT
–  40-60nm DIAMETER
•  Large dense core vesicles
–  Contain neuropeptides
–  90-250nmdiameter
•  Coexistence
–  More than one type of NT synthesized and released in neuron
      •  Normally mix of small and large NT
34
Q

How are neurotransmitters transported?

A 
•  Anterograde to axon terminal
–  Motor proteins 
     •  Kinesin
       –  Uses series of attachment detachment steps
–  Microtubule highway system
    •  Colchicine and vinblastine disrupt MT and prevent transport
–  Requires energy
–  Requires calcium
–  Speed of transport is 0.5-1.5 cm/hr
35
Q

How are neurotransmitters released?

A
  1. AP in axon terminal
  2. Open voltage gated Ca++ channels
    – Clustered in active zone
  3. Increase calcium influx
  4. Activates proteins responsible for
    – Mobilizing vesicles
    • Synapsin removes vesicles from mt network
    – Fusing vesicles with synaptic membrane
    • Synaptotagmin
    • Snap25
    • Syntaxin
  5. Vesicles move to active zone
  6. Vesicles dock onto synaptic membrane
  7. Fuse with synaptic membrane and release NTs into cles
    – Exocytosis
36
Q

What is vesicle recapture?

A 
•  Local resynthesis of synaptic vesicles
•  Pit formation 
–  Kiss and run
hypothesis
      •  Direct recycling
•  Clatharin coating
–  Endocytosis
–  Cycle through endosomal compartment
–  Indirect recycling
37
Q

What are neurotransmitter receptors?

A

• Pre and post synaptic cell
• Specific for neurotransmitter
– Multiple receptor subtypes for each NT
• NT act differently in different areas of brain
• Distribution varies across CNS
– NT can only influence cells with receptors
– Ligand = molecule specific to receptor
• Example: Ach is a ligand for Ach receptor

38
Q

What are inotropic receptors?

A 
•  Ligand–gated ion channels
– NT can open or close ion channel
     •  Influx or blockade of of sodium, chloride, potassium, or calcium
•  Fast acting
•  Generate EPSP or
IPSP
•  Found post
39
Q

What are metabotropic receptors?

A 
•  7 TMD
•  G protein coupled
–  Second messenger signalling
    •  Change gene expression
    •  Modify existing proteins
    •  Open or close ion channels
      –  Indirectly induce IPSP or EPSP
•  Slow acting
•  Long lasting changes
•  More varied and diffuse effects
•  More prevalent than ionotropic
•  All neuropeptide receptors are metabotropic
•  Found pre and post synaptically
–  Presynaptic inhibition/ facilitation
40
Q

How are neurotransmitter receptors activated?

A 
•  EPSP OR IPSP (ionotropic)
–  Summated to initiate or inhibit AP generation in post synaptic cell
•  Activate second messenger systems (metabotropic)
–  1st messenger=NT
–  2ND Messenger= Calcium, DAG, IP3, cyclic AMP (cAMP)
    •  Initiate intracellular cascades
    •  Open other ion channels
    •  Long lasting changes in: 
      –  Synapse structure
      –  Gene expression
        »  Think effects of
epigenetics 
     –  Cell survival
41
Q

What are auto receptors?

A 
•  Metabotropic
•  Bind to own neuron’s NT
•  Presynaptic
•  Provide feedback
– Reduce release when NT high
– Increase release when NT low
42
Q

What is neurotransmitter reuptake?

A 
•  Transporters on cell neurons and/or glia pick up NT from synaptic cles
– In the cell:
    •  NTs are repackaged into
vesicles for future release
    •  NTs are degraded by enzymes intracellularly
     –  Excreted
        »  Monoamines
     –  Used as precursors for NT synthesis
       »  Glutamate/GABA
    –  Used as precursors for energy
production
      »  Glutamate
43
Q

What is neurotransmitter degradation?

A

• Some NTs do not have transporters for reuptake
– Enzymes degraded in cleft
• Acetylcholine
– Acetylcholinesterase
» Inhibitors: pesticides, nerve gases venoms, reversible inhibitors used for treating ad
• Some NTs are taken back up into cell but degraded in cytosol
– Dopamine
• Mao

44
Q

What is neurotransmitter recycling?

A
  • NT reuptake can provide more NT to be repackaged and released immediately
  • Some NT s can be broken down to form more of the same NT or used as a precursor to form different NT
45
Q

What do glia do in synaptic transmission?

A 
Astrocytes
–  Domains
    •  Even distribution
    •  Little overlap of astrocytes
    •  Coordinate activity of synapses in domain
    •  40K processes=high potential to regulate
–  Modulate neuronal activity 
    •  Have NT receptors
    •  Release NT
–  Tripartite synapse
    •  Presynaptic, post synaptic and
astrocyte cell
–  Uptake glutamate
    •  Reduce excitotoxicity
    •  Stimulate energy provision to neuron
        –  Support ongoing neuronal activity
46
Q

How do glial communicate via gap junctions?

A 
•  Made up of connexin 
–  Mutations and disease
•  Connect cytoplasm of 2 adjacent cells
–  Second messengers
 –  Electrical signals
•  Electrical synapse
–  Faster than chemical synapse
•  also found in interneurons
•  Function to synchronize
activities of similar cells 
–  interneurons
47
Q

What are amino acid transmitters?

A

• Small molecule
• Fast acting directed
synapses
• Byproducts of intermediary metabolism

48
Q

What are excitatory amino acid NT?

A 
•  Carry 2 negative charges
•  Dendrite major receiving area
–  Require a lot of input for excitation
•  Glutamate
–  Most prevalent in CNS
–  Ionotropic
     •  Sodium, potassium, and
calcium
–  Metabotropic
     •  Gs and Gq
•  Aspartate
•  Generate EPSP
49
Q

What are inhibitory amino acid NTs?

A 
•  Inhibitory
–  Carry one negative charge
–  Soma major receiving area
    •  Require less input for inhibition
–  GABA
    •  Synthesized from glutamate
    •  Most prevalent inhibitory NT in CNS
    •  Interneurons
    •  Ionotropic
        –  Chloride influx or potassium efflux
    •  Metabotropic 
         –  Gi/o
–  Glycine
    •  Mainly in spinal cord
   •  Ionotropic receptor
       –  Chloride ions
–  Generate IPSP
   •  Can generate EPSP in certain conditions
50
Q

What is the difference between glutamate vs gaba?

A 
•  Excitation vs inhibition
•  Yin and yang
•  Epilepsy
– Too much glutamate – Not enough GABA
•  Learning and memory 
– Wire together fire
together
– Too much GABA or not enough glutamate impairs memory
51
Q

What are monoamine neurotransmitters?

A 
•  AKA biogenic amines
•  MAO degrades
•  Catecholamines 
–  Dopamine(DA)
–  Norepinephrine(NE)
–  Epinephrine (adrenalin) (EPI) 
–  Precursortyrosine
•  Indolamines
–  Serotonin (5-HT)
–  Melatonin
–  Precursortryptophan
•  Histamines
•  Diffused effects
–  Metabotropic receptors 
–  Released by varocosities
•  Psychotropic drugs mimic or affect these systems
52
Q

What are catecholamines?

A 
•  Modulators in PNS and CNS
•  Several receptor subtypes
•  EPI only released in PNS
–  Sympathetic nervous system
•  Fight or flight
•  Increase energy
availability
•  NE and DA found in both PNS and CNS
–  Cant cross BBB
–  Stay and made in CNS/PNS
53
Q

What is catecholamine distribution in the brain

A 
• NE
- Locus coereleus
-Stress/anxiety
-Vigilance
-NE enzymes only in NE neurons
• DA restricted distribution
- Nigrostriatal system
    •  Movement and reward
- Dorsal mesostriatal pathway
   •  Movement intiation
    –  Parkinson’s disease
- Ventral nigrostriatal pathway 
    •  Positive incentive/reward
Mesolimbic cortical
    •  Projects to limbic structures
    •  Role in schizophrenia
- Periventricular
    •  Originate in hypothalamus
     –  Motivated behaviours hunger, thirst and sex
-Tuberalhypophyseal
    •  Lactation
-DA neurons do not have enzymes to further convert to NE or EPI
54
Q

What are indolamines?

A 
• Serotonin (5HT)
– Modulatory
–  Several receptor subtypes
–  Distributed in 2 clusters 
     •  Raphe nuclei
          –  Provide 80% of 5HT to forebrain 
     •  Caudal system
         –  Sensory and motor function in spinal cord
–  Appetite, sleep and aggression 
     •  Decreased 5-HT increases
aggression
    •  High 5ht decreases carbohydrate appetite
    •  Decreased 5-ht = insomnia
–  LSD
55
Q

What is indolamines (melatonin)?

A 
– Fluctuates with light cycle 
    •  Signals seasonal day length
– Regulate circadian rhythms
– Secreted in darkness
    •  TV, laptop, cellphones at
night?
– Cause drowsiness/sleep
   •  Used as sleep aid
56
Q

What is acetylcholine (ACH)?

A 
•  First identified in NMJ 
–  Botox
–  curare
•  Modulatory
–  Several receptor subtypes
     •  Different CNS and PNS distributions
     •  Nicotinic
        –  Motor
        –  Curare
     •  Muscarinic 
        –  In ANS
        –  atropine
•  Simple synthesis and
degradation
      –  Unique synaptic degradation (AchE)
      –  Easy synthesis acetate+choline (ChAT)
•  Role in learning and memory
    –  Alzheimer’s disease
    –  Dietary choline
    –  Atropine (mAchR antagonist)
57
Q

What are unconventional neurotransmitters (soluble gas)?

A 
•  Soluble gases
–  Nitric oxide (NO)
–  Carbon monoxide (CO)
–  Both synthesized in neural cytoplasm
–  Retrograde transmission
–  Rapid diffusion to ECF
   •  Cross membranes
   •  Stimulate second messenger production
–  Difficult to study 
    •  Rapid breakdown 
    •  Exist for seconds
58
Q

What are unconventional neurotransmitters (endocanninoids)?

A 
- Receptors highly
distributed 
–  Anadimide
  •  Sanskrit for “eternal bliss”
– Pain reduction
– Increase appetite
– FaPy acids cross membranes
– Retrograde transmission
59
Q

What are neuropeptides?

A

Actions depend on amino acids, sequence

Loosely grouped: pituitary, hypothalamus, brain-gut, opiod, misc

60
Q

Drugs and synaptic transmissions?

A

Agnostic - mimic efforts of the neurotransmitter
Antagonists - blocks the effect of the neurotransmitter
Alter NT activity at any point in cycle

61
Q

What is behavioural pharmacology?

A

• Influential lines of research
• Treatments for neurological or neuropathological disorders
– Anxiety
– Depression
– Schizophrenia
– Parkinson’s and Alzheimer’s disease
– Epilepsy
• Drugs target specific receptors for specific effects
• Drug discovery and endogenous agonist discovery give insight into brain mechanisms of pleasure and pain
– Opioids

62
Q

What is drug addiction?

A
  • Legal status irrelevant
  • Ease of crossing BBB
  • Habitual use of a drug despite consequences and efforts to stop
  • Physical vs psychological dependence
  • Rewarding brain stimulation and CPP
  • Mesotelencephalic dopamine system
63
Q

What are opioids?

A 
•  Endogenous
–  Endorphin and enkephalin
•  Exogenous
–  From opium poppy resin (morphine/ heroin)
•  Produce analgesia
•  Act in PAG, hypothalamus, limbic

Psych 275 (4 decks)

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