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BPK306 > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

what are the types of neuroglia?

A
  • astrocytes - form BBB
  • microglia - immune function
  • ependymal cells
  • oligodendria (CNS)
  • Schwann cells (PNS)
  • satellite cells
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2
Q

how do neuroglia differ from neurons?

A
  • do not form synapses
  • have only one type of projection
  • are able to divide (glial cell precursors can differentiate)
  • less electrically excitable
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3
Q

what does the peripheral nervous system consist of?

A
  • sensory afferents
  • somatic motor efferents (skeletal)
  • autonomic efferents (cardiac, smooth)
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4
Q

what is grey matter? what is white matter?

A
  • grey: inner part of spinal cord, contains neuronal cell bodies and dendrites
  • white: outer part of spinal cord, contains axons of descending and ascending fibres
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5
Q

what is the dorsal column medial leminiscus?

A
  • ascending tract (sensory)
  • carries sensory input on fine touch, vibration, and proprioception ot the brain
  • located on dorsal side of SC
  • sacral, lumbar, thoracic, cervical (medial to lateral)
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6
Q

what is the spinothalamic pathway?

A
  • ascending tract (sensory)
  • carries sensory input on temperature, crude touch, and pain to the brain
  • divided into lateral (from medial to lateral: cervical -> sacral) and anterior
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7
Q

what are the corticospinal tracts?

A
  • descending pathways (motor)
  • carry motor signals from the brain to the skeletal muscles to control movement
  • pyramidal and extrapyramidal
  • pyramidal divided into lateral (from medial to lateral: cervical -> sacral) and anterior
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8
Q

what are the functions of the CNS?

A
  • gather and integrate info from PNS
  • process and perceive info from PNS
  • organize reflex and autonomic responses
  • planning and executing voluntary movements
  • higher functions like cognition, learning, and memory
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9
Q

what is the function of the cerebrum?

A

performs high-order functions, composed of specialized lobes where integration is devoted

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10
Q

what does the frontal lobe do?

A

control skeletal (voluntary) muscle movements
- coordinates information from other association areas
- controls some behaviours (PFC)

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11
Q

what does the temporal lobe do?

A

contains auditory cortex + auditory association area
- hearing

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12
Q

what does the occipital lobe do?

A

contains visual cortex + visual association area
- vision

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13
Q

what does the parietal lobe do?

A

contains primary somatosensory cortex + sensory association area
- sensory information from skin, musculoskeletal system, viscera, and taste buds

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14
Q

what is the purpose of association areas?

A

neural pathways extend from sensory areas to association areas, which integrate stimuli into perception (input goes to primary cortices, interpreted in association areas)

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15
Q

what is BA1-3? what is BA4?

A
  • BA1-3 = sensory cortex
  • BA4 = motor cortex
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16
Q

how is the cerebral cortex organized?

A

6-layered architecture
- superficial layers have connections with other cortical areas
- intermediate layers receive input from subcortical areas
- deep layers project to subcortical areas
- thickness of each layer varies around the cortex

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17
Q

what are cortical columns?

A

6-layered functional networks
- make up the basic processing module for the cortex
- different functions for each layer (ex. input vs output)
- size of each layer varies around the cortex (ex. sensory cortex will have bigger input layers)

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18
Q

what are cortical-subcortical loops?

A

information loops between the cortex and grey matter structures (thalamus and basal ganglia)
- thalamus: relay centre for sensory and motor info
- basal ganglia: movement processing

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19
Q

what structures make up the basal ganglia?

A
  • putamen
  • globus pallidus
  • subthalamic nucleus
  • caudate
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20
Q

what are examples of cortical-subcortical loops?

A
  • motor circuit (motor coordination): sensorimotor and premotor cortex -> thalamus -> BG ->
  • limbic circuit (emotion): limbic and paralimbic cortex, hippocampus, and amygdala -> thalamus -> BG ->
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21
Q

where do motor fibres crossover (i.e. where does the corticobulbar tract turn into the lateral corticospinal tract?)

A

medullary pyramids (decussation of pyramids)

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22
Q

how are autonomic fibres organized?

A

motor fibres are accompanied by sensory fibres (nerves are mixed)

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23
Q

what is a physiological example of mixed nerves?

A

with inflammation in the GI tract (ex. appendicitis), GI motility will decrease and patient will feel visceral pain (referred pain) that is poorly localized
- referred: pain felt in one location may be caused by damage in a different location

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24
Q

does afferent information reach consciousness?

A

no, ANS operates on a subcortical level
- involved in homeostatic regulation (heart rate, GI motility, etc.)

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25
Q

what neurotransmitters are involved in the ANS?

A
  • glutamate (most common)
  • ANGII
  • CCK
  • oxytocin
  • somatostatin
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26
Q

how do autonomic reflex arcs differ from somatic?

A

ANS contains 2-neuron efferents
- presynaptic cell bodies in CNS, postsynaptic cell bodies in ganglia

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27
Q

what cranial nerves are part of the parasympathetic NS?

A
  • III: oculomotor
  • VII: facial
  • IX: glossopharyngeal
  • X: vagus
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28
Q

what are autonomic afferents called?
what type of fibres are preganglionic efferents? what type of fibres are postganglionic efferents? what are their conduction velocities?

A
  • general visceral afferents (GVAs)
  • preganglionic: type B fibres (3-15 m/s)
  • postganglionic: type C fibres (0.5-2 m/s)
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29
Q

where are the preganglionic and postganglionic cell bodies in the sympathetic NS? what neurotransmitters do they use?

A
  • preganglionic: thoracolumbar spinal cord; ACh
  • postganglionic: peripheral ganglia (close to SC, far from target); NE
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30
Q

where are the preganglionic and postganglionic cell bodies in the parasympathetic NS? what neurotransmitters do they use?

A
  • preganglionic: craniosacral spinal cord; ACh
  • postganglionic: peripheral ganglia (near to or within the wall of the target organ); ACh
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31
Q

where do preganglionic efferent cells originate and how do they exit the spinal cord?

A
  • concentrated in the lateral horn of SC
  • exit SC via ventral root and enter the paravertebral ganglia at the same level
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32
Q

what happens to preganglionic efferents after the enter the paravertebral ganglia (chain of ganglia beside the SC)?

A
  • some synapse there
  • some give off collaterals that travel rostrally or caudally
  • some pass through the ganglia and enter a splanchnic nerve to enter the prevertebral ganglia (within abdominal cavity)
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33
Q

what is a splanchnic nerve?

A

mixed nerve (motor and sensory) that innervate the viscera
- smooth muscles, glands, etc.

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34
Q

where are the cell bodies of presynaptic parasympathetic neurons situated?

A
  • cranial nerves III, VII, IX, and X (brainstem)
  • sacral spinal cord (S2-S4)
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35
Q

what is unique about the smooth muscle of blood vessels?

A

have only sympathetic innervation

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36
Q

what happens to ciliary muscle in response to sympathetic vs parasympathetic input?

A

SNS: a-adrenergic (NE)
- pupil dilation (mydriasis), enhances far vision
PNS: M3-muscarinic (ACh)
- pupillary constriction (miosis), enhances near vision

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37
Q

what happens to the heart in response to sympathetic vs parasympathetic input?

A

SNS: B1-adrenergic (NE)
- SA node and ventricles; increases HR and contractility
PNS: M2-muscarinic (ACh)
- decreased HR and contractility

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38
Q

what happens to the stomach and small intestine in response to sympathetic vs parasympathetic input?

A

SNS: a- and B2-adrenergic (NE)
- decreased motility, sphincter contraction, reduced secretions
PNS: M1-, M2-, and M3-muscarinic (ACh)
- increased motility, relaxation of sphincters, increased secretions

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39
Q

what happens to the lungs in response to sympathetic vs parasympathetic input?

A

SNS: B2-adrenergic (NE)
- bronchodilation, increased ventilation
PNS: M3-muscarinic (ACh)
- bronchoconstriction

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40
Q

what happens to the abdominal arterioles in response to sympathetic vs parasympathetic input?

A

SNS: a- and B2-adrenergic (NE)
- vasoconstriction; diversion of blood from the GI tract to muscles
PNS: M3-muscarinic (ACh)
- vasodilation

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41
Q

what happens to the salivary and lacrimal glands with parasympathetic stimulation? what happens to the bladder?

A

M3-muscarinic (ACh)
- increased secretion
M2- and M3-muscarinic (ACh)
- contraction, sphincter relaxation

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42
Q

how is the ANS controlled by the CNS? what regions regulate autonomic function?

A
  • firing of ANS preganglionic cells is determined by pathways that synapse onto them
  • hypothalamus, preoptic and septal regions, lateral hypothalamus
  • important for temperature regulation, food/water intake
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43
Q

what does cooling do to the body? what does heating do to the body?

A
  • cooling: causes shivering, piloerection (goosebumps), increase in thyroid activity
  • heating: reduces thyroid activity, sweating, and vasodilation
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44
Q

what happens when there are lesions to the heat loss centre (preoptic area/anterior hypothalamus)?

A

prevents sweating and cutaneous vasodilation, leads to hyperthermia (overheating)

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45
Q

what happens when there are lesions to the heat conservation centre (posterior hypothalamus)?

A

hypothermia

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46
Q

what is activated when blood glucose levels drop?

A

glucoreceptors in the hypothalamus

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47
Q

what happens when there are lesions to the lateral hypothalamus?

A

suppresses appetite/food intake (aphagia), potentially causing starvation and death

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48
Q

what happens when there are lesions to the ventromedial area (satiety centre)?

A

hyperphagia, potentially causing obesity

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49
Q

what causes Argyll Robertson Pupil?

A

caused by syphilis, which is caused by treponema pallidum (acts on the parasympathetic fibres of CN3

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50
Q

what are the stages of syphilis that eventually leads to ARP?

A
  • primary: single sore; days-weeks
  • secondary: rash over the body, hands, and feet; months
  • tertiary: neurological, cardiovascular ARP; years-decades
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51
Q

what is the physiology behind ARP?

A

pupil fails to respond to light but accommodation reflex is normal
- optic fibres that project to the pretectal area of the midbrain are damaged (possibly due to bacteria in subarachnoid space) -> pretectal area projects to EN nucleus that gives rise to parasympathetic innervation of the eye that controls the pupillary reflex

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52
Q

what is the sympathetic input for micturition?

A

tonic
- pontine micturition centre (supraspinal) sends sympathetic preganglionic nerves from the lumbar spinal cord that synapse on postganglionic nerve -> hypogastric nerve
- input from the hypogastric nerve inhibits detrusor (muscle lining wall of bladder) through B-adrenergic receptors and excites the internal sphincter through a-adrenergic receptors

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53
Q

what is the parasympathetic input for micturition?

A
  • pelvic nerve contains visceral afferent innervation of the detrusor and sends it to the pontine micturition centre
  • pontine micturition centre sends descending commands to the sacral spinal cord via the reticulospinal pathway
  • pelvic nerve travels from sacral SC to excite the detrusor muscle and inhibit the internal sphincter
  • pudendal nerve travels from sacral SC to excite the external sphincter (striated muscle) through voluntary contraction
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54
Q

how are biological membranes like a circuit?

A
  • capacitor: plates correspond to inner and outer faces of the membrane
  • variable resistance (inverse of conductance; g): corresponds to gated ion channels shown with a switch
  • electromotive forces: separation of charged ions across the cell membrane, set up by Na+/K+-ATPase
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55
Q

what kind of properties do molecules need to have in order to cross the membrane without a channel?

A
  • small
  • lipophilic
  • uncharged
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56
Q

how are ion channels structured?

A

transmembrane proteins with a single pore
- some are multimers of homomeric or heteromeric subunits (HCN, Kv)
- some are monomers with repeating TM subunits

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57
Q

how are Nav and Cav structured?

A

pores are formed by monomers with 4 repeating 6-TM spanning regions

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58
Q

what are properties of selective ion channel structure?

A
  • TM protein segments arranged around a central pore
  • selectivity filter that regulates which ions can permeate the pore
  • gate that can be opened or closed (some have more than one gate)
  • voltage-gated channels have a voltage sensor
  • ligand-gated channels have an intracellular or extracellular ligand binding site
  • some have binding sites for intracellular proteins or second messengers
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59
Q

what are the phases of gating of the Nav channel?

A

involves 2 gates: activation and inactivation (ball and chain)
- depolarization to threshold opens the activation gate
- inactivation gate then closes, halting ion flow
- inactivation cannot be opened until the membrane repolarizes

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60
Q

what are the primary mechanisms that establish the RMP?

A
  • Na+/K+-ATPase
  • K+ leak channels
  • resting permeability to Na+ and Cl- (not much)
  • RMP ~ -70 mV
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61
Q

what are the concentrations and permeability of K+?

A
  • ECF: 5 mM
  • ICF: 150 mM
  • P: 1
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62
Q

what are the concentrations and permeability of Na+?

A
  • ECF: 145 mM
  • ICF: 15 mM
  • P: 0.03
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63
Q

what are the concentrations and permeability of Cl-?

A
  • ECF: 100 mM
  • ICF: 25 mM
  • P: 0.1
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64
Q

what are the concentrations and permeability of Ca2+?

A
  • ECF: 1 mM
  • ICF: 10^-7 mM
  • P: 0
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65
Q

what is the electrochemical driving force of an ion?

A

the difference between the membrane potential and the eqm potential of a given ion (Vm-Eion)

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66
Q

for a positive ion, what happens when Vm-Eion>0?

A

ion flows outward

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67
Q

for a positive ion, what happens when Vm-Eion<0?

A

ion flows inward

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68
Q

for a positive ion, what happens when Vm-Eion=0?

A

ion flow stops

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69
Q

what is the Nernst equation?

A

Eion=61/z log ([ion]out/[ion]in)
- predicts the equilibrium potential of a given ion

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70
Q

what is the GHK equation?

A

what is it hoe?
- predicts membrane potential using multiple ions

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71
Q

what is Ohm’s Law?

A

V=IR; V=I/g; I=gV
- resistance is the inverse of conductance
- a stimulus (change in current) will cause a resulting change in the membrane potential (voltage)

72
Q

what can a stimulus (current) be a result of?

A
  • input from another neuron (at synapses)
  • can be caused by passive (graded) potential or active (action) potential
  • can be spontaneous (ex. in pacemaker cells)
  • electrophysiological studies
73
Q

what 3 passive properties are important in neurons? what do they determine

A

determine how far a passive (graded) potential generated in a dendrite will travel, and whether a passive potential will result in an AP at the axon hillock
- membrane capacitance
- membrane (input) resistance
- intracellular longitudinal (axial) resistance along axons and dendrites

74
Q

what do Rm and Cm determine? what does Rm also determine?

A
  • Rm and Cm determine the shape and magnitude of a voltage response
  • Rm also predicts how likely a small applied current is to generate an appreciable voltage response
75
Q

how is the instantaneous current response not observed in voltage response?

A

voltage responses evoked by depolarizing and hyperpolarizing responses are rounded

76
Q

why is voltage change not instantaneous like current change?

A
  • capacitance makes voltage change lag
  • in order for membrane depolarization to occur, injected charges need to cause rearrangement of charges at the membrane -> the higher the capacitance of the membrane, the longer this will take (capacitance is inverse of voltage)
77
Q

what is the length constant?

A
  • length constant = the distance from the site of current injection where the voltage response is 1/e of its original amplitude
  • length constant = sqrt (Rm/Ra)
  • the higher the ratio of Rm to Ra, the lower the loss of current and the greater the length constant
78
Q

how does increasing diameter affect Rm, Ra, and the length constant?

A
  • decreases Rm (more ion channels)
  • decreases Ra much more
  • increased length constant
79
Q

how are changes in Vm measured?

A

using an internal electrode and an extracellular reference electrode

80
Q

when do slower Kv channels open in an AP?

A

-20 mV

81
Q

what happens to Nav channels at 30 mV?

A

they become inactivated

82
Q

what properties ensure that AP propagation is unidirectional?

A
  • Nav inactivation
  • increased Pk
83
Q

where does synaptic integration occur? what properties does this location have?

A

axon hillock
- high density of Nav channels -> lowest threshold for spike initiation

84
Q

what is temporal summation? what is spatial summation?

A
  • temporal: successive stimulations at the same location (same input source)
  • spatial: successive stimulations at different locations (different input sources)
85
Q

what is the shunting effect?

A

when summation doesn’t produce a greatly additive effect
- could be due to other factors (ex. cell resistance) reducing the expected summation

86
Q

what is an excitatory postsynaptic potential (EPSP)?

A

transient depolarization of postsynaptic neuron due to increased conductance of the postsynaptic membrane to Na+/K+ in response to NT binding
- at RMP, driving force for Na+ to enter the cell is greater than for K+ to leave, resulting in depolarization

87
Q

what is an inhibitory postsynaptic potential (IPSP)?

A

transient hyperpolarization of postsynaptic neuron due to (most often) increased Cl- conductance of postsynaptic membrane in response to NT binding
- Cl- enters the cell at RMP causing hyperpolarization

88
Q

what is saltatory conduction?

A

when an AP jumps from node to node due to myelination

89
Q

in what axons is conduction the fastest?

A

large, myelinated axons
- greater diameter reduces axial resistance

90
Q

how do active and passive potentials change with distance?

A
  • active: AP magnitude and duration is constant; delay between stimulus and response increases with distance
  • passive: graded potential magnitude decreases with distance
91
Q

why are APs regenerated at Nodes of Ranvier?

A
  • membrane conductance is high
  • membrane resistance is low (due to channels and no myelin)
  • Nav and Kv density is high
92
Q

why do passive potentials propagate rapidly between nodes?

A
  • membrane resistance is high (no channels, lots of myelin)
  • membrane capacitance is low (capacitance is difference in charge between plates; if plates are farther apart due to myelin, capacitance decreases)
93
Q

how do you improve conduction in axons?

A
  • increase diameter of axon (decreases axial resistance -> increases conduction velocity)
  • myelinate the axon (increases membrane resistance)
94
Q

what makes myelin in the CNS? PNS?

A
  • CNS: oligodendrocytes
  • PNS: Schwann cells
95
Q

what is multiple sclerosis? what is a conduction block? what is a frequency-related block?

A

a disease of myelination in the CNS
- immune attack causes demyelination
- conduction block: Nav channel density gets too low, terminating the AP
- frequency-related block: conduction still occurring but decreases in frequency at each node

96
Q

what is cross-talk between demyelinated axons?

A

AP in one axon terminates and continues in another axon

97
Q

what events lead up to synaptic transmission?

A
  • input received from dendrites is passively propagated to the hillock
  • input can be excitatory or inhibitory, summation occurs at hillock
  • if summed signal is subthreshold = no AP
  • if summed signal is suprathreshold = AP occurs and propagates down axon
98
Q

what are the different types of NTs?

A
  • small molecule (glutamate (primary excitatory NT), GABA, ACh)
  • gaseous (NO)
  • amines (DA, NE, 5-HT)
99
Q

what determines the action of a NT?

A

the receptor it binds to

100
Q

where does ACh act? what receptors does it act on?

A
  • PNS: at NMJ and autonomic ganglia
  • CNS: basal ganglia and SC
    receptors:
  • nAChRs @ NMJ
  • MAChRs at autonomic ganglia
101
Q

what are the inhibitory NTs?

A
  • GABA: inhibitory NT in the brain
  • glycine: inhibitory NT in SC
102
Q

what is DA used for? what about 5-HT?

A

DA: motivation, motor function, reward and pleasure
- 5-HT: mood, appetite, sleep

103
Q

how do ionotropic receptors act? what responses do they produce? what are some examples?

A

action:
1) NT binds
2) conformational change results in channel (pore) opening
3) ions flow across membrane
- fast EPSPs and IPSPs
examples:
- CNS: ionotropic glutamate receptors (NMDA, AMPA, iGluR in retina), GABAa, GABAc
- NMJ: nAChRs

104
Q

how do metabotropic receptors act? what responses do they produce? what are some examples?

A

action:
1) NT binds
2) G protein activated
3) G protein subunits or intracellular messengers modulate ion channels
4) ion channel opens
5) ions flow across membrane
- slower responses
examples:
- CNS: metabotropic glutamate receptors (mGluR), GABAb
- PNS: MAChRs

105
Q

what is the reversal potential of an EPSP?

A

the potential at which the net direction of ion flux reverses
- when the Na+ influx exactly offsets the K+ efflux (0 net current/ion flow)

106
Q

what is happens when Eion is reached?

A

when the electrical gradient and concentration gradient of an ion are balanced, causing no net movement of THAT ION across the membrane

107
Q

how can you experimentally determine the reversal potential for an EPSP?

A

ex) a dendrite held at a varying voltages (voltage clamp) while applying a fixed EPSC to elicit a constant EPSP
- single channel current recording using patch clamp
- ex) at -102mV, an EPSP will display a greater Na+ influx and K+ will also move inward b/c the Vm is more (-) than Ek
- ex) at -32mV, an EPSP will display K+ efflux and weaker Na+ influx since it is closer to ENa than -102mV (also farther away from Ek so greater drive for K+ to move)

108
Q

what is an excitatory postsynaptic current (EPSC)?

A

currents that are applied to elicit an EPSP
- active (ionotropic channels opening and closing)

109
Q

how are extracellular signals converted into intracellular events?

A

signal transduction: the transmission of an extracellular stimulus to an intracellular signal via specific membrane receptors

110
Q

what are properties of ligand-gated channels?

A
  • can be directly or indirectly gated
  • often non-specific (permeable to Na+ and K+, sometimes Ca2+)
  • heteromeric, vary in subunit composition (generally, 5 subunits, each with 4-TM spanning helices)
111
Q

what is an example of direct gating?

A

NT binding to the ionotropic receptor
- nAChR directly binding ACh

112
Q

what is an example of indirect gating?

A

NT downstream binding to an ion channel by directly binding a GPCR
- MAChR binding ACh, G protein subunit activates K+ channel

113
Q

what is the structure of metabotropic receptors?

A

7 TM spanning helices, extracellular ligand binding site, intracellular G protein binding site
- helices surround central aqueous pocket containing ligand binding site

114
Q

what is the process of G protein activation?

A
  • ligand binding to the GPCR leads to activation of the G protein by switching it from GDP bound (inactive) to GTP bound (active)
  • a subunit dissociates from By subunit, both can go on to activate intracellular effector molecules
  • effector activation leads to second messenger molecules (cAMP, Ca2+) that have other cellular effects (opening/closing ion channels, regulating gene expression)
115
Q

what is presynaptic modulation?

A

presynaptic neuron second messengers can modulate the activity of K+ and Ca2+ channels + NT release to regulate the efficacy of NT release -> affects the size of the postsynaptic potential

116
Q

what is postsynaptic modulation?

A

postsynaptic neuron second messengers can directly alter the amplitude of postsynaptic potentials by modulating ionotropic receptors

117
Q

what is the Gs pathway?

A
  • E/NE binds to B1-adrenergic receptor
  • activates alpha(s) subunit, which activates adenylyl cyclase (AC)
  • AC converts ATP to cAMP
  • cAMP activates protein kinase A (PKA)
  • net effect = upregulated activity of voltage-gated HCN channels, speeding up heart rate
118
Q

what is the Gi pathway?

A

opposite of Gs, inhibits AC
- slows down heart rate

119
Q

what is the Gt pathway?

A
  • light photoactivates rhodopsin, causing the dissociation of alpha(t) (transducin) from By
  • transducin activates phosphodiesterase (PDE)
  • PDE breaks down cGMP to GMP, decreasing cGMP levels
  • decreased cGMP levels closes CNG channels that are normally open in the dark, hyperpolarizing the cell and reducing glutamate release
120
Q

what is the Gq pathway?

A
  • ACh binds to M1-muscarinic receptors in smooth muscle surrounding the bronchi, causing the dissociation of alpha(q) from By
  • alpha(q) activates phospholipase C (PLC)
  • PLC converts PIP2 (in the membrane) to IP3, acting on IP3 receptors on the ER membrane
  • causes Ca2+ release from ER, causing smooth muscle contraction and bronchoconstriction
  • PLC also converts PIP2 -> DAG
  • DAG activates protein kinase C (PKC)
121
Q

what equipment is used in electrophysiological measurements?

A
  • intracellular electrode: applies current/voltage commands
  • extracellular electrode: reference
122
Q

what does in vivo mean? what does in vitro mean?

A
  • in vivo: as a whole animal
  • in vitro: specific neurons, cells, etc.
123
Q

what are voltage clamps? what are they used for?

A

the experimenter specifies a voltage and measures the resulting current; useful for:
- study single channels or one specific type of channel
- investigate which ions the channel is permeable to or the speed of opening and closing
- testing if a particular chemical or substance alters the channel

124
Q

what are current clamps? what are they used for?

A

the experimenter injects current and measures the resulting changes in membrane potential (voltage, usually APS); useful for:
- study excitable cells like neurons
- find out which ions are important for APs
- test if a drug blocks APs

125
Q

what are patch clamps? what are they used for?

A

form a tight (high-resistance) seal between a glass micropipette containing an electrode and the plasma membrane of a cell
- allows experimenter to control the extracellular and intracellular composition

126
Q

what are the types of patch clamp configurations?

A
  • cell-attached recording: tight contact between pipette and membrane
  • inside-out recording: single channel recording, can modify intracellular/cytoplasmic domain
  • whole-cell recording: cytoplasm is continuous with pipette interior
  • outside-out recording: extracellular domain is accessible (can test the actions of NTs, etc.)
127
Q

how can current be measured?

A
  • through individual channels (single channel/microscopic current)
  • through numerous channels (macroscopic current)
  • average of microscopic currents display the macroscopic current*
128
Q

what is the convention for current recordings?

A

positive current entering the cell presents as downward deflections

129
Q

what are the advantages and disadvantages of in vivo?

A

advantages:
- real-time recording in live animals
- high physiological relevance
disadvantages:
- technically difficult
- little to no control of intracellular or extracellular fluids

130
Q

what are the advantages and disadvantages of in vitro?

A

advantages:
- isolated tissues or cells are easier to work with
- control over solutions
disadvantages:
- less physiologically relevant
- molecular techniques required

131
Q

what are the advantages and disadvantages of heterologous expression?

A

advantages:
- higher expression levels result in larger currents
- control over solution composition
- ability to modify channel structure
disadvantages:
- endogenous channels may interfere with recordings
- less physiological relevance

132
Q

what is defined by the slope of the I-V curve? what does an I-V curve look like in the absence of a concentration gradient?

A
  • conductance (y)
  • linear (m=y)
133
Q

what is Hebb’s rule? what does Hebbian plasticity entail?

A

neurons that fire together, wire together
- learning and memory can occur due to the changes in strength of connections between neurons; can lead to:
- LTP
- LTD

134
Q

what is homeostatic plasticity?

A

moves neurons back to their original state (set point/baseline) after modification -> in terms of firing (ex. temporarily increased input/firing returning back to baseline)
- ex. after potentiation

135
Q

what is potentiation (facilitation)?

A

with higher frequency/increased stimulation, greater passive potentials are elicited (ex. EPSP will change in size based on frequency of input)
- no summation

136
Q

what is the trisynaptic circuit of the hippocampus?

A

circuit with high degree of potentiation
- preforant path (from entorhinal cortex) synapses onto granule cell in dentate gyrus -> granule cell synapses onto CA3 pyramidal cell -> Schaffer collaterals synapse on CA1 pyramidal cells

137
Q

what are Schaffer collaterals?

A

axons that travel from CA3 to CA1 (axons of CA3 pyramidal neurons)
- synapse on CA1 most studied area of LTP

138
Q

what is long-term potentiation (LTP)?

A

a process whereby synaptic activity increases future postsynaptic potentials

139
Q

what is the favoured mechanism of LTP?

A

AMPAR and NMDAR (glutamate receptors permeable to Na+ and K+; NMDAR additionally permeable to Ca2+)
- at RMP, NMDAR are blocked by Mg2+
- Ca2+ influx through NMDAR activates intracellular CaMKII pathway
- causes insertion of AMPAR on postsynaptic membrane from vesicles

140
Q

what are the properties of AMPARs?

A
  • permeable to Na+ and K+
  • tetrameric (GluA1-4)
  • central Arg provides specificity
  • inward current at -mV, outward current at +mV
  • without GluA2, inwardly rectifying
141
Q

what are the properties of NMDARs?

A
  • blocked by Mg2+ at RMP
  • depolarization dispels Mg2+
  • permeable to Na+, K+, and Ca2+
142
Q

what are the postsynaptic events that cause LTP?

A

high activation:
- high amounts of glutamate binds to AMPARs on postsynaptic membrane, depolarizing the membrane
- adjacent NMDARs become depolarized, removing Mg2+ block and bind glutamate, allowing Ca2+ influx
- activates CaMKII pathway, phosphorylating AMPARs and causing exocytosis of AMPARs from vesicles
- net result: greater expression of AMPARs on postsynaptic membrane

143
Q

what are the postsynaptic events that cause LTD?

A

weak activation:
- low amounts of glutamate bind AMPARs on postsynaptic membrane, depolarizing the membrane
- adjacent NMDARs become depolarized, removing Mg2+ block and bind glutamate, allowing Ca2+ influx
- activates PP2B (calcineurin) and PP1 (protein phosphatase 1) pathway, causing dephosphorylation of AMPARs and causing endocytosis of AMPARs into vesicles
- net result: lower expression of AMPARs on postsynaptic membrane

144
Q

what is the hippocampus? what does bilateral loss of the hippocampi result in?

A
  • medial temporal lobe structure with well characterized regions and connections critical for long-term memories
  • loss will produce anterograde amnesia, or inability to form new memories
145
Q

what are the 4 major structures that form the hippocampal LTP circuit?

A

1) CA1: major output goes to layer V of entorhinal cortex (EC)
2) CA3: receives input from dentate gyrus (DG) and EC
3) DG: projects to CA3 and receives input from EC
4) EC: interface between hippocampus and cortex

146
Q

where is LTP observed in the hippocampal circuit? what principles are present?

A

repeated stimulation of EC cells that project to DG leads to increased EPSPs in DG overtime
- only the activated set of synapses will be potentiated (input specificity)
- enough presynaptic axons must fire coincidentally to activate the postsynaptic cell (cooperativity)

147
Q

how does LTP present in dendritic spines?

A

enhanced receptors, more visible spines, changed configuration

148
Q

how does fear learning move from local to distributed? what does this explain?

A
  • 1 day after learning: most associations involve hippocampus
  • 36 days after learning: connections involve cerebral cortex, thalamus
  • explains why loss of hippocampus prevents new memories but old memories are preserved
149
Q

how does brain plasticity contribute to recovery after surgery?

A

following traumatic injury, functional brain responses can be “remapped” through new groups of neurons being recruited (new connections are made and strengthened to compensate for those lost)

150
Q

how are children brain connections different than teens/adults?

A
  • children: connections are stronger between neurons that are anatomically close but functionally unrelated
  • teens/adults: connections are stronger between neurons that are functionally related but distant
151
Q

what does outward current look like on an IV plot?

A

positive

152
Q

what are the early and late stages of LTP?

A
  • early: insertion of receptors from vesicle stores
  • late: modification of gene expression and structural changes
153
Q

are LTD and LTP dictated by presynaptic or postsynaptic mechanisms?

A

postsynaptic

154
Q

what are “silent” synapses?

A

synapses that contain only NMDARs
- can be woken up by LTP protocols that cause insertion of AMPARs on the membrane

155
Q

what is the mechanism of presynaptic LTP?

A

repetitive synaptic activity leads to entry of presynaptic Ca2+ -> AC pathway -> increased cAMP -> protein kinase A (PKA) activation -> Rab3a and RIM1 (vesciular related proteins) -> exocytosis of more NT release

156
Q

what is the mechanism of NMDAR LTD?

A

Ca2+ entry through NMDAR channels -> protein phosphatases calcineurin and protein phosphatase 1 (PP1) activate -> dephosphorylates AMPARs and triggers endocytosis of AMPARs
- happens spontaneously (no way of knowing when)

157
Q

what is the mechanism of mGluR LTD?

A

mGluR triggers AMPAR postsynaptic internalization, a process that appears to require protein synthesis

158
Q

what is the mechanism of endocannabinoid (eCB) LTD?

A

mGluR activation -> phospholipase C (PLC) and/or intracellular Ca2+ initiates the synthesis of eCB
- eCB travels in a retrograde manner to bind to presynaptic cannabinoid 1 receptors (CB1R) that depress NT release

159
Q

how is LTP maintained (what late events occur)?

A

structural changes that maintain plasticity
- AMPARs are anchored by scaffolding protein groups including PSD95, cadherins and catenins
- involves changes in expression of levels of structural proteins at postsynaptic density (PSD)

160
Q

what is the function of:
a) PSD95?
b) cadherins?
c) catenins?

A

a) PSD95: anchors NMDARs to cytoskeleton
b) cadherins: mediate adhesion through interactions across the synaptic membrane and associate with AMPARs
c) catenins: couple AMPARs to cytoskeleton

161
Q

how does LTP and LTD occur with changes in structural proteins?

A
  • LTP: cadherins are increasingly associated with synaptic membrane
  • LTD: internalization of cadherins is required for removal of AMPARs
162
Q

when is information stored?

A

when synapses that connect neurons become more (LTP) or less (LTD) able to fire in response to a particular stimulus

163
Q

how are memories stored into STM?

A

at first in the hippocampus, where synapses between excitatory neurons start to form new circuits within seconds of the events to be remembered and increases in the strength of even a small number of synapses create a new circuit that stores a new memory (STM)

164
Q

how does forgetting occur?

A

when release of NT does not produce EPSPs sufficient to reach threshold, the synapse becomes weaker and the circuit may disappear entirely

165
Q

what is the experimental evidence that links LTP to learning and memory?

A
  • in absence of LTP, learning and memory is substantially impaired
  • LTP increased during fear conditioning
  • memories can be inactivated and reactivated with LTD and LTP
166
Q

what are hippocampal place cells? why are they significant?

A
  • place cells: pyramidal neurons within the hippocampus
  • single unit recordings from hippocampus show that specific place cells fire only when an animal is in a particular location
  • through simultaneous exposure, place cells can fire in response to associated stimuli (foods, light, touch), providing a link to learning and memory
167
Q

what are Purkinje cells? what kind of input do they receive?

A
  • large GABAergic neurons that project to deep cerebellar nuclei (important for motor learning)
    2 types of excitatory input:
  • powerful synaptic contact from a single climbing fibre (from inferior olive nucleus)
  • synaptic input from ~150k parallel fibres, from the tiny granule cells of the cerebellum itself
168
Q

when do parallel fibre synapses change their strength?

A

only if they are active at the same time as the climbing fibre
- EPSPs generated by the parallel fibres became smaller when both the parallel fibres and the climbing fibres were coactivated at low frequencies

169
Q

what does the climbing fibre represent?

A

error signal (modifies motor movement)
- feedback mechanism

170
Q

how is the climbing fibre and parallel fibres related to LTD?

A

parallel fibre EPSP amplitude decreases with climbing fibre stimulation
- parallel fibre activates motor movement, climbing fibre activated when movement is wrong, so LTD is used to unlearn that configuration of movement

171
Q

what molecular events of the parallel fibre onto the Purkinje cell causes LTD?

A

glutamate released from parallel fibre binds mGluR on Purkinje cell dendritic spine -> activates PLC -> converts PIP2 to IP3 and DAG (IP3 causes Ca2+ release from ER which activates PKC; DAG directly activates PKC) -> PKC phosphorylates substrate proteins -> internalization of AMPARs

172
Q

what molecular events of the climbing fibre onto the Purkinje cell causes LTD?

A

climbing fibre depolarizes Purkinje cell dendritic spine causing Ca2+ influx -> increased intracellular Ca2+ induces Ca2+ release from ER -> activates PKC -> PKC phosphorylates substrate proteins -> internalization of AMPARs

173
Q

how is Alzheimer’s Disease related to synaptic plasticity?

A
  • in AD, LTP is blocked and LTD is triggered (believed to underlie cognitive decline)
  • associated with loss of plasticity
  • AB oligomers bind to NMDARs/AMDARs causing their internalization; leads to thinning and loss of synapses (causing memory problems)
174
Q

how is addiction related to synaptic plasticity?

A
  • drugs of abuse (ex. cocaine) alter synaptic plasticity in the brain’s reward centre, leading to changes in behaviour
  • associated with excessive plasticity
175
Q

what are the molecular events relating plasticity and addiction?

A
  • drugs of abuse modulate synaptic function and plasticity in the Ventral Tegmental Area (large part of reward system)
  • cocaine, amph, ecstasy target DA transport, directly increasing DA
  • other drugs target GABAergic neurons , inhibiting their activity and indirectly increasing DA
  • others elicit LTP by increasing the AMPAR/NMDAR ratio at glutamatergic neurons (through mGluR)
  • increase DA in VTA and projection areas
176
Q

how are NMDARs affecting GABAergic neurons?

A

NMDAR on glutamatergic neurons cause Ca2+ influx and activate nitric oxide synthase (NOS) -> diffuses to GABAergic neurons and inhibits GC pathway, decreasing levels of cGMP

177
Q

how is cocaine use related to structural proteins?

A
  • normally, GluA1/2 AMPARs are present in synapses, making them impermeable to Ca2+
  • cocaine use inserts cadherins which insert GluA1 homomers at synapse from vesicles (GluA1 is Ca2+ permeable)

BPK306 (4 decks)

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