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Neuro > Principals of neuronal function > Flashcards

Principals of neuronal function Flashcards

1
Q

What are the different stains we can use to visualise nervous tissue? What do each help visualise?

A
  • Nissl → nuclei
  • Weigert → axon tracts
  • Golgi → cell morphology
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2
Q

Why is Nissl staining useful? Why is it not?

A
  1. It distinguishes between neurons and glial cells- neurons have Nissl bodies - sites of protein translation in neurons
  2. Allows study of arrangement of neurons in dif brain regions
  3. does not show whole neuronal structure
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3
Q

What does Weigert stain?

A

Myelin

Does not sain grey matter

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4
Q

What does Golgi stain consist of?

A

Silver nitrate and potassium dichromate

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5
Q

What does Golgi staining result in?

A

Small number of neurons become entirely dark-stained as silver chromate precipitates out

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6
Q

What is immunohistochemistry?

A

Selectively identifying antigens (proteins) in cells of a tissue
Antibodies bind → enzyme or dye is activated → antigen can then been seen under a microscope

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7
Q

Describe in situ hybridisation briefly

A

Uses a labelled complementary DNA, RNA or modified nucleic acid (probe) to localise a specific DNA or RNA sequence

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8
Q

Describe fluorescence microscopy

A

Optical microscopt that uses fluoresence

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9
Q

Describe difference between SEM and TEM

A 
TEM = 2D
SEM = 3D
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10
Q

Describe CT

A

Rotating X-rays to create cross-sectional images of the body
More detail than normal X rays

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11
Q

Describe MRI

A

Uses strong magnetic fields and radio waves to produce details images
The magnetic field reactions with protons in our hydrogen atoms

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12
Q

Describe fMRI

A

Same principle as MRI scans but they measure metabolic function
Looks at changes in blood oxygenation

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13
Q

Describe EEG

A

Measures electrical activity of the brain via electrodes on the scalp

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14
Q

Look at differences between MR-T1, MR-T2 and Xray-CT on OneNote

A

OneNote

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15
Q

Draw the graph that compares MR-T1, MR-T2 and Xray-CT

A

One Note

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16
Q

Describe differences between T1 and T2 MRI

A

T1 images are used to differentate anatomical structures set on T1 values - High fat content tissues [white matter] is brighter, with water filled compartments [CSF] are dark

T2 images are used to differentate anatomical structures on T2 values - water filled compartments [CSF} are bright, whilst tissues with high fat content [white matter] are darker - this is good for demonstrating pathology, as most lesions are associated with increased water content

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17
Q

Describe PET imaging

A

Tracer inserted into body
Collects in areas with higher chemical activity → could be a sugar
Used to determine cancers, heart disease, brain disorders

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18
Q

Describe MEG scan

A

Magnetoencephalography
Recording magnetic fields
Used to map brain function and record the exact location of the source of epileptic seizures

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19
Q

What are the types of glial cell?

A
  • astrocytes, oligodendrocytes, microglia, ependymal cells
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20
Q

What are the functions of astrocytes (from spec)?

A
  • CNS development → guide developing axons
  • ion homeostasis → APQ4 regulates fluid homeostasis
  • neurotransmitter uptake → high levels of neurotransmitter transporters, clear them from synaptic space
  • local control of blood flow → astrocyte-mediated vasodilation in response to increased neural activity → glutamate induced cox-1 mediated signalling
  • blood brain barrier → induce barrier properties in epithelial cells
  • inhibitory role in CNS repair → astrocyte derrived chondroitin suphate rich ECM inhibits axon sprouting in damage
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21
Q

What do oligodendrocytes do?

A
  • function to form myelin sheath around several nerve axons
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22
Q

What do microglia do?

A

Macrophages of CNS

  • clear cellular debris
  • clearing apoptotic neurons during development
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23
Q

What do ependymal cells do?

A

Production of CSF that fills the ventricles

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24
Q

Discuss the neuron doctrine

A

The “Neuron Doctrine” was based on Cajal’s and other’s observations,
which included descriptions of synapses and their proposed function. It is
an over-simplification of how a neuron functions – activation, action
potential, transmitter release. It is now clear that in addition to synaptic
contacts there are gap junctions, which modulate cell activation,
modulatory receptors on pre-synaptic elements, and the modulatory action
of transmitters, hormones and gaseous messengers in the local
environment which affect neuronal activity

25
Q

What are the three components of the neuronal cytoskeleton?

A

Microfilaments of actin are particularly important
in dynamic structures in neurons.

Neurofilaments are the main structural proteins of
the cytoskeleton and maintain the cell shape.

Microtubules are structural and enable intracellular
transport to occur over long distances.

26
Q

What are the two forms of glial in the PNS?

A
  • Schwann cells and satellite cells
27
Q

Discuss specialised gila in other locations

A

Müller glial cells in the retina. In

the olfactory system there are specialised olfactory ensheathing cell.

28
Q

What is Wallerian degeneration?

A

a process which occurs due to a cut or crushing injury to a neuron. The axon segment which lies distally to the cell body undergoes a degeneration process within 24-36 Hours of a lesion

29
Q

Describe Wallerian degeneration

A

Initially prior to degeneration the separated distal axon unit remains electrically excitable

After injury the cytoskeleton of the distal axon degenerates and is followed by degeneration of the myelin sheath and breaking of the axon membrane - this is dependent on ubiquitin and calpain proteases and so suggests that this is an active process, and thought to be dependent on a lack of sufficient NMNAT delivery from the Soma to the axon terminal

Macrophages infiltrate the axon and myelin sheath and clear the debris from degeneration

The neurolemma remains intact as a hollow tube

The distal portion of the intact nerve fibre sends sprouts to the neurolemma tube, attracted by growth factors produced by the Schwann cells in the tubes

If it reaches the tube, the sprouts grow into it, and reinervate the tissue

If the sprouts can not reach the tube [too large gap, scar tissue forms], then surgery can aid in guiding sprouts to the tubes

30
Q

Discuss difference in regeneration between CNS and PNS

A

Regeneration is slower in the CNS than PNS - in the CNS, myelin sheaths are produced by oligodendrocytes and not by Schwann Cells. Also sprouting is inhibited by the chondroitin sulfate rich ECM of the CNS as produced by astrocytes, inhibiting CNS repair.

31
Q

Describe MS

What are the different types?

A

Immune attack of oligodendocytes myelin, causing demyelination leading to either:

  • functional recovery by partial myelination, which becomes less effective after each episode
  • no remyelination

• Decreasingly effective remyelination causes formation of a scar-like plaque/lesion around the damaged axons and are thought to be the origin of symptoms

Types:
• Progressive-relapsing: steady increase in disability with super-imposed attacks
• Secondary progressive: initial relapsing/remitting MS, suddenly beginning to worsen without periods of remission
• Primary progressive: steady increase in disability without attacks
• Relapsing-remitting: unpredictable attacks which may/may not leave permanent deficits followed by periods of remission

32
Q

Describe motor neuron disease

A

loss of neurons in the ventral horn of the spinal cord, and in the corticospinal tracts, meaning there is a mixture of upper and lower motor neuron signs

ALS is characterised by stiff muscles, twitching and weakness due to muscle atrophy’ eventually asphyxiation

Can be inherited; mutation in SOD-1 [gain of function]

Sporadic; no clear cause but the motor neurons seem to undergo apoptosis

No cure - riluzole [glutamate antagonist] can prolong life for 2-3 months

33
Q

Describe unipolar neurons

A

o One neurite projecting from the cell body (soma) in one direction

34
Q

Descibe bipolar neurons

A

o Cell body two neurites (axonal projections) going bidrectionally to dendritic trees ie. In the retina

35
Q

Describe pseudo-unipolar neurons

A

o Neurons containing one axon which splits into two branches, often found in the peripheral nervous system- one branch running to the periphery, the other to the spinal cord ie. Dorsal root ganglion neurons

36
Q

Describe multipolar neurons

A

o Neurons which usually have a single long axon, and many dendrites allowing for integration of information
 Dendritic branches can emerge from the cell body (soma) of the neuron
 Ie. Interneurons in the brain, motor neurons
 Pyramidal cells of the hippocampus, and purkinje cells of the cerebellum are both multipolar neurons

37
Q

Describe AD

A

o Loss of cholinergic fibres in the cortex and subcortical regions in a predictable sequence
 Entorhinal cortex and hippocampus accounting for initial memory loss (partic. short term memory) which is first noticed
 Entorhinal cortex is input/output of hippocampus, crucial for forming new memories
 Damage to olfactory bulbs/cortices, amygdala, cingulate gyrus, and hypothalamus can be related to changes in appetite, mood swings, and violence associated with the disease

38
Q

Comparison of PNS and CNS regeneration: plasticity

A

CNS:
- damage to CNS cant be repaired; little/no plasticity or capacity for repair
- damaged astrocytes try to rebuild the BBB they form with their processes, the astrocytic scar is inhibitory
- excess glutamate release from damaged neurons is excitotoxic to surrounding neurons
- oligodendroyctes are inhibitory for axon regeneration as a part of their normal role in maintaining organised connectivity in the brain
PNS:
- Adult PNS regeneration occurs because Schwann cells de-differentiate and upregulate production of neurotrophic factors and growth-promoting ECM

39
Q

Role of GF in neuronal survival and plasticity

A

• Glial scar and astrocytes
o CSPGs (chondroitin sulphate proteoglycans) released from hypertrophic astrocytes and are inhibitory ECM molecules ie. Aggrecan
• Myelin associated glycoproteins expressed by oligodendrocytes normally prevent collateral sprouting from axons ie. NOGO, OMgp, MAG
o When damaged they release their cell surface inhibitory proteins, blocking axon regeneration

40
Q

Discuss the possible application for cell therapy in PD/ cell therapy in general

A

• Peripheral nerve grafts can be used to bridge damaged spinal cord/optic nerve and allow CNS regeneration just to the pro-repair role of Schwann cells
• Olfactory ensheathing glial cells which enable the growth of olfactory axons from the periphery into the CNS (olfactory bulb) are under clinical trial
• Grafting embryonic cells for parkinson’s
o Embryonic substantia nigra cell transplant to the striatum has been done with varying results

41
Q

Group the chemical messengers of the CNS

A

o Amino acids (GABA, Glycine)
o Acetylcholine
o Monoamines: catecholamines (NAd, Dopamine), Indoleamines (serotonin), others (melatonin, histamine)
o Peptides: hypothalamic releasing factor (somatostatin), tachykinins (substance P), opioids (enkephalins), cholecystokinin
o Gaseous: NO, CO
o Misc: adenosine, ATP, endocannabinoids

42
Q

Criteria to establish transmitters

A

1 - location (transmitter itself, needs to be biosynthetic/have metabolic enzymes, reuptake mechanisms need to be present, needs receptors)

  1. release → in response to presynaptic depolarisation, in physiologically relevant quantities
  2. Action → direct application of the transmitter, or agonist, must evoke the same post-synaptic response
  3. Removal → reuptake or metabolic methods
43
Q

What are the glutamate receptors?

A

AMPA, NMDA and mGluR

44
Q

Discuss AMPA

A
  • four binding sites
  • channel opening upon binding of two glutamate ligands
  • allows Na influx
  • GluR2 blocks Ca entry to prevent Ca second messenger signalling
45
Q

Discuss NMDA

A
  • non-specific cation (Na/Ca) channel
  • slower than AMPA
  • blocked by Mg (voltage-dependent)
  • able to elicit LTP and LTD
46
Q

Describe mGluR

A

mGluR1 and 5 are q (increase NMDA receptor activity and risk of excitotoxicity)
others are Gi coupled (decrease)

47
Q

Synthesis of GABA

A

from glutamate by Glutamic acid decarboxylase [GAD] - active vitamin B6 is a required cofactor

48
Q

Discuss GABA receptors

A

GABA(A)
- ionotropic, linked to Cl- channels (inhibitory)
GABA(B) - Gi coupled - caused opening of K+ channels to hyperpolarise the neuron

49
Q

Action of benzodiazepines

A

GABA(A) agonist - increase inhibition and reduce anxiety

50
Q

Discuss degradation of GABA

A

Reuptake of GABA is either done at the presynaptic neuron by GAT1 or in neighboruing glial cells by GAT3 after which it is recycled - in glial cells GABA forms glutamate and then reforms glutamine [glutamine synthase]

51
Q

Describe action of baclofen

A

Baclofen - treatment of spacitity [GABAb agonist]

52
Q

Describe barbituates

A

barbituates enhance transmission by GABAaR agonist action → for epilepsy

53
Q

Drug that inhibits GABA breakdown

A

Valproate inhibits GABA metabolism → anticonvulsant

54
Q

Describe glycine

A
  • Inhibitory NT
  • Ionotropic choride current
  • Causes IPSPs
  • Required co-agonist along with glutamate for NMDA receptors
55
Q

Major sites of production of monoamine NTs

A

locus coeruleus (NA) substantia nigra pars
compacta/ventral tegmental area (DA), reticular formation, nucleus raphe
(5HT)

56
Q

How many 5-T receptors are there?

A 
14
o	3A, 3B, 3C are ion channels
o	1A, 1B, 1D, 1E, 1F all Gi coupled
o	2A/2B/2C all Gq coupled
o	4/6/7/5A/5B all Gs coupled
57
Q

Discuss dopamine receptors

A

G coupled
D1 & D5 → Gs
D2, D3, D4 → Gi

58
Q

What does ChAT do?

A

Choline acetyltransferase

used to synthesize ACj from choline and acetyl-CoA in the presynaptic terminal

Neuro (23 decks)

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