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PSYC2020 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Glial Cells

A

Glia support neurons
Often quoted as outnumbering neurons but probably about the same
Glia = ‘glue’ – but don’t hold neurons together
Numerous types and many function
Divisions – microglia and macroglia
Microglia – brain’s immune system
Macroglia
Myelination (Schwann cells in PNS, oligodendrocytes in CNS
Structural/functional support of neurons (astrocytes)

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2
Q

Glial Cells - Myelination

Schwann Cells

A 
Axon myelination in the PNS
Multiple cells along a single axon
Cell turns around the axon several times wrapping it in membrane
Can guide axon regeneration after damage
Nerves can regrow
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3
Q

Glial Cells - Myelination

Oligodendrocytes

A 
Axon myelination in the CNS
Single cells provides several segments, often multiple axons
Cell extensions wrap around the axon
No axon regeneration after damage
No regrowth in the CNS
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4
Q

Glial Cells

Astrocytes

A

Star shaped – ‘astro’
Surround neurons and contact brain’s vasculature
‘Blood-brain barrier’ (seal off capillaries)
Support – nutrition, growth factors, clear waste, physical matrix to separate neurons
Activity - modulate neural activity, maintain efficient signalling (K+ and neurotransmitter uptake), maintain axon function

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5
Q

Glial Cells

Microglia

A

Brain’s immune system
Response to injury or disease – multiply, release antigens, phagocytosis
Rapidly activate to stop pathogens
Anti-inflammatory response, eg after stroke
Eliminate excess neurotransmitters

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6
Q

Glial Cell Dysfunction - MS

A

Acute, inflammatory autoimmune disease
Brain, spinal cord, optic nerves
36.6 / 100,000
Female : male 2.3 : 1
Increased prevalence with increasing south latitude in Australia (7 times more in Hobart than Queensland)
No cure but treatments to manage symptoms and slow progression – immune supress, anti-inflammatories
Visual - blurred and double vision, nystagmus, ‘flashes’
Motor - weakness of muscles, slurred speech, muscle wastage, poor posture, tics
Sensory - numbness, tingling, pain
Coordination and balance
Cognitive - short- and long-term memory, forgetfulness, slowed recall

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7
Q

Glial Cell Dysfunction - Tumours

A

Frontal lobe astrocytoma
Temporal lobe glioblastoma multiforme
Gliomas are most common (40-50% of all brain tumours)
Relatively fast growing, arising from any type of glial cells, hence gliomas, astrocytomas, and oligodendrogliomas.

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8
Q

Neuron Morphology and Structure

A 
Typical Neuron
Dendrites
Cell body (soma)
Axon
Axon terminals
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9
Q

Neuron - Basic Cell Structures

A

Ribosomes (the speckles) and endoplasmic reticulum to generate proteins: neurotransmitters
Golgi complex to package neurotransmitter into vesicles
Microtubules to transport vesicles and proteins along the axon
Synaptic vesicles contain neurotransmitter for release
Mitochondria for energy

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10
Q

Neuron – Signalling Specialisations

A 
Specialised secretory cell
Targeted and long distance
Irritability – responds to being stimulated
Collect Information
Integrate Information
Transmit Information
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11
Q

Neuron – Signalling Specialisations

Dendrites

A 
Collect information from other connected neurons (synapse)
Chemical messengers (neurotransmitters) bind to receptors and cause electrical changes 
Electrical changes spread from the dendrite and into the soma
Electrical changes weaken with distance and over time
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12
Q 
Neuron – Signalling Specialisations
Cell body (soma)
A

Integrates information from all of the inputs (synapses)
Electrical changes from all inputs spread to the soma and add together
Critical point – the junction between the soma and the axon (axon hillock)
If electrical changes beyond the axon hillock reaches a critical value, then the neuron will fire

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13
Q

Neuron – Signalling Specialisations

Axon

A

Transmits the signal away from the soma
Signal is transmitted electrically by action potential
Myelin protects the axon and promotes fast transmission of the signal
Action potentials occur at Nodes of Ranvier

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14
Q

Neuron – Signalling Specialisations

Axon terminals

A

Transmits the signal to other neurons
Signal is transmitted chemically by neurotransmitters
Terminal buttons store neurotransmitter in vesicles
Action potential triggers release into the synapse

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15
Q

Sensory Neuron

A

Unipolar (pseudo-unipolar)
Afferent neuron – into the CNS
Messages from receptors to the brain or spinal cord

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16
Q

Motor Neuron

A

Multipolar
Efferent neuron – out of the CNS
Messages from the brain or spinal cord to the muscles /organs

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17
Q

Interneuron

A

Multipolar
Relays message from sensory neuron to motor neuron in the spinal cord
Local connections in the brain

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18
Q

Neuron Dysfunction - Dementia

A

Dementia is caused by neurodegeneration – the damage and death of the brain’s neurons

Australian statistics
Second leading cause of death (leading in females)
In 2018, estimated 425,416 Australians living with dementia
Age most important risk factor – 3 in 10 people over the age of 85 and almost 1 in 10 people over 65 have dementia
Other risk factors – CV health, diabetes, cholesterol, family history, head injury
Main types – Alzheimer’s disease (AD), frontotemporal dementia (FTD), vascular dementia (VD), dementia with Lewy bodies (DLB)

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19
Q

Alzheimer’s Disease

A

Cerebral atrophy
External surface of the brain with widened sulci and narrowed gyri
Commences in medial temporal lobe – hippocampus and entorhinal cortex
Early memory loss and spatial navigation impairment
Later progresses to broader cortex and subcortical
Motor difficulties, impairments in executive planning and decision making
Cortical loss and thinning of gyri
Shrunken hippocampus
Enlarged ventricles
Plaques and Tangles
Abnormal protein aggregates associated – amyloid beta and tau
Aβ – extracellular plaques
Synapse toxicity ???
Tau – intracellular tangles; twisted ropes within swollen cell body
Axon toxicity ???
Maybe causative, maybe not
Latest – Herpes virus ???

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20
Q

Neuronal Communication

A

3 Phases

Collection and integration of information

Transmission of information along the axon

Transmission of information from the axon terminals

21
Q

Membrane Potentials

A 
Transport
Diffusion
Outside
Inside
Important Ions:
Na+
K+
Cl-
Protein-
Resting Potential
-70mV
“POLARISED”
Local change
Less polarisation (closer to zero) 
“DEPOLARISED”
Spreads (decremental)
Decays (time)
Local change
More polarisation (away from zero) 
“HYPERPOLARISED”
Spreads (decremental)
Decays (time)
22
Q

Neuronal Communication

Collection and integration of information

A

Local polarisation change at the dendrites (and soma)

Depolarisation – excitatory post-synaptic potential

Hyperpolarisation – inhibitory post-synaptic potential

Neurotransmitter binds and an associated ion channel opens or closes, causing a Post-Synaptic Potential (PSP)

EPSP – inside gets more positive (usually Na+ flows in)

IPSP – inside gets more negative (either K+ flows out or Cl- flows in)

Fast acting

AXON HILLOCK
Effect of many local EPSPs and IPSPs spread (decremental) and decay
Axon hillock – portion of the soma adjacent to the axon
If membrane potential just beyond the hillock reaches a threshold (-55mV)
Triggers ACTION POTENTIAL

23
Q

Neuronal Communication

Transmission of information along the axon

A

Action Potential

Dendrites and soma – decremental conduction
Axon – Action Potential (AP) – active ‘firing’ of the neuron
Local depol / repol
Active so FAST
Triggered by depolarization
Key – Voltage Gated Ion Channels
Voltage Gated Ion Channels

Open and close depending on the local membrane potential

Voltage gated sodium channels – allow Na+ to rush in - Depolarisation

Voltage gated potassium channels – allow K+ to rush out – Repolarization

24
Q

Three Phases of the AP

A

rising phase
repolarisation
hyperpolarisation

25
Q

Transmission Along the Axon

A

AP is non-decremental – it does NOT decay or diminish
Travels down the axon rather than passive spreading
Regenerate so travel for long distances without signal loss

26
Q

Saltatory Conduction

A

Passive conduction (fast and decremental) along each myelin segment to next node of Ranvier
New action potential generated at each node
Fast conduction along myelin segments results in faster conduction than in unmyelinated axons
Conduction in Myelinated Axons: Saltatory Conduction

27
Q

Neuronal Communication
Transmission of information from the axon terminals
The Synapse

A 
Presynaptic terminal
Vesicles containing NT
Incoming AP triggers voltage gated calcium channels
Ca2+ influx triggers NT release
Receptors for NT re-uptake

Junction / cleft / gap
NT ‘float’ briefly after release

Post-synaptic terminal
Receptors for the NTs
Most common types of synapses
Axodendritic (axon terminal buttons on dendrites)
Axosomatic (axon terminal buttons on soma / cell body)

But also
Dendritic spines (axon terminal buttons on spines of dendrites)
Dendrodendritic – dendrite to dendrite, and often bidirectional transmission
Axo-axonic – (can mediate presynaptic facilitation and inhibition of that button on the post-synaptic neurone)

28
Q

The Synapse - Other Types

A

‘String of beads’
Non-directed
Diffuse release from varicosities
Neurohormones and modulatory neurotransmitters

Gap Junction
Electrical synapse

29
Q

Neurotransmitters

A

2 basic types of neurotransmitter molecules (and 2 types of vesicles)

Small
Large

One neuron can produce and release two (or more) neurotransmitters

> 100 identified

30
Q

Neurotransmitters

types

A

Small molecules
glutamate, gaba, acetylcholine, norepinephrine
Large molecules
Also endorphins, enkephalins, some hormones
substance P

31
Q

Neurotransmitters

Small molecules

A

Synthesized in cytoplasm of the terminal button
Packaged in vesicles by the Golgi complex
Vesicles stored in clusters next to pre-synaptic membrane, waiting for the trigger to be released

32
Q

Small Molecules - Classes

A

Amino acids
Monoamines
Acetylcholine (ACh)
Soluble gases

33
Q

Amino acids

A 
Building blocks of proteins
Fast-acting synapses in the CNS
Glutamate –excitatory
GABA – inhibitory 
Aspartate and glycine
34
Q

Monoamines

A 
Synthesized from amino acid
Diffuse effects (branched, string of beads synapses)
Catecholamines (synthesized from tyrosine): dopamine, norepinephrine, epinephrine
Indolamines (synthesized from tryptophan): serotonin
35
Q

Acetylcholine (ACh)

A

Acetyl group + choline
Neuromuscular junction
Autonomic NS

36
Q

Soluble gases

A

Nitric oxide, carbon monoxide

Retrograde transmission – feedback from post-synaptic to pre-synaptic

37
Q

Neurotransmitters

Large molecules

A

Neuropeptides – short proteins (3-36 amino acids)
Assembled in the cell body by ER/ribosome
Packaged by Golgi complex
Transported to the axon terminal via microtubules
Example – endorphins - “Endogenous opioids”
Produce analgesia
Receptors were identified before the natural ligand was

38
Q

Release of Neurotransmitter

Exocytosis

A

undocked synaptic vesicle
cluster of protein molecules in membrane of synaptic vesicle
docked synaptic vesicle
cluster of protein in presynaptic membrane
entry of calcium opens fusion pore
fusion pore widens, membrane of synaptic vesicle fuses with presynaptic membrane
molecules of neurotransmitter begins to leave terminal button
presynaptic membrane

39
Q

Receptor Activation

A

Released neurotransmitter molecules produce signals in postsynaptic neurons by binding to receptors

Receptors are specific for a given neurotransmitter

Can also be different receptors for the same neurotransmitter

40
Q

Receptor Activation

A

2 Types of Receptor

Ionotropic receptors
Associated with ligand-activated ion channels

Metabotropic receptors
Associated with signal proteins and G proteins

41
Q

Ionotropic Receptors

A

Neurotransmitter binds and an associated ion channel opens or closes, causing a Post-Synaptic Potential (PSP)

EPSP – inside gets more positive (usually Na+ flows in)

IPSP – inside gets more negative (either K+ flows out or Cl- flows in)

Fast acting

42
Q

Metabotropic Receptors

A

G-protein coupled

Effects slower, longer-lasting, more diffuse, and more varied
Neurotransmitter binds.
G protein subunit breaks away.
Ion channel opened/closed OR a 2nd messenger is synthesized.
2nd messengers may have a wide variety of effects

43
Q

NT Inactivation

A

As long as the neurotransmitter is in the synapse, it is active – activity must somehow be turned off
Reuptake, Enzymatic Degradation, and Recycling
NT can be taken up by pre-synaptic receptors
‘Destroyed’ in the gap, before they get to the post-synaptic receptors.
Taken up by post-synaptic receptors

44
Q

7 steps in neurotransmitter action

A
  1. neurotransmitter molecules are synthesised from procursers under the influence of enzymes
  2. neurotransmitter molecules are stored in vesicles
  3. neurotransmitter molecules that leak from their vesicles are destroyed by enzymes
  4. action potentials cause vesicles to fuse with the presynaptic membrane and release their neurotransmitter molecules into the synapse
  5. released neurotransmitter molecules bind with autoreceptors and inhibit subsequent neurotransmitter release
  6. released neurotransmitter molecules bind to postsynaptic receptors
  7. released neurotransmitter molecules are deactivated by either reuptake or enzymatic degradation
45
Q

Neuropharmacology

A

A drug may act to alter neurotransmitter activity at any point in its “life cycle”

While still in the neuron (pre-synaptically)
Influence production
Influence release
At the synapse ‘ junction’ 
Influence destruction
Influence up-take 
Influence re-uptake
Agonists – facilitate/enhance
Antagonists - inhibit
Agonists – facilitate/enhance
Cocaine - catecholamine agonist
blocks reuptake (DAT) preventing the activity of the neurotransmitter from being “turned off”

Benzodiazepines - GABA agonists
binds to the GABA molecule and increases thebinding of GABA

Physostigmine - ACh agonist
inhibits acetylcholinesterase, which breaks down ACh
Antagonists - inhibit

Atropine – ACh antagonist
Binds and blocks ACh muscarinic receptors
Many of these metabotropic receptors are in the brain
High doses disrupt memory

Curare – ACh antagonist
Bind and blocks ACh nicotinic receptors, the ionotropic receptors at the neuromuscular junction
Causes paralysis
Treated with physostigmine

46
Q

Agonistic drug effects

A

L-Dopa increases synthesis of dopamine
black widow spider venom- increase release of ACh
Nicotine stimulates ACh receptors
Amphetamine- block reuptake of dopamine

47
Q

Antagonistic drug effects

A

PCPA inhibits the synthesis of serotonin
Reserpine prevents storage of monoamines in vesicles
Botulinum toxin blocks release of ACh Apomorphine stimulates dopamine autoreceptors; inhibits release of dopamine
Curare blocks postsynaptic ACh receptors

48
Q

Communication Dysfunction

A

Myasthenia Gravis
Autoimmune disease (20 per 100,000 US)
Action potentials in nerves are normal
Arises from a problem with synapses on muscles
Immune system destroys acetylcholine (ACh) receptors at neuromuscular junction
Symptoms
Extreme fatigability
Fluctuating muscle weakness (proximal>distal)
Problems chewing (dysphagia) and talking (dysarthria)
Respiratory weakness
Treated with acetyl-cholinesterase (AChE) inhibitors – these increase and prolong the effects of ACh on the postsynaptic membrane
Physostigmine – de-activates acetylcholinesterase (AChE) = Ach agonist
Also treated with immunosuppressive drugs, or by removal of thymus gland

49
Q

Key Learnings

A

Glia – more than just structure – myelination, immunity, structural support, functional support, modulate neural activity
Glial dysfunction – tumours and MS
Neurons – specialised secretory cells - signalling – collect and integrate info and transmit it
Neuronal dysfunction – dementia (AD)
Neuronal communication – membrane potentials – resting potentials, EPSPs, IPSPs, APs
Synapse – pre-synaptic, cleft, post-synaptic, some different types
Neurotransmitter – small and large, different classes, excitatory/inhibitory, fast acting/diffuse, synthesis, release, receptors
Neuropharmacology – agonists and antagonists
Communication dysfunction - MG

PSYC2020 (14 decks)

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