2.2 Neural Components and Networks Flashcards
What are the 2 types of cell in the NS?
State 4 functions of each
1) Neuroglia:
- maintain ionic state
- structure, scaffolding, support
- aid recovery/restructure
- nourishment and protection
2) Neurones: Functional units of the nervous system
- React to chemical and sensory stimuli
- Conduction of impulses
- Emit specific chemical regulators
Are Neuroglia or Neurons more abundant?
Neuroglia (3:1)
What are the 4 types of Neuroglia in the CNS?
1) Astrocytes
2) Oligodendrocytes
3) Microglia
4) Ependymal cells
State the 2 types of neuroglia found in the PNS + the function of each
1) Schwann cells: myelination
2) Satellite cells: like astrocytes for the PNS, sympathetic and parasympathetic systems
Give 4 specific functions of Neuroglia
1) Surround neurones and hold them in place (support)
2) Supply nutrients and O2 to neurones
3) They insulate one neurone from another
4) Destroy pathogens and remove dead neurones
What the most abundant type of Neuroglia
Astrocytes
How do Astrocytes communicate with each other?
Star shaped ➞ projections link neurones to signal each other (also link blood supply).
They utilise ATP for signalling + have gap junctions which allow communication with one and other (passing of AP is different to neurons)
What are the 2 main types of Astrocytes?
Fibrous astrocytes: found in the white matter
Protoplasmic astrocytes: found in the gray matter
List 4 functions of an Astrocyte
1) Maintain EC environment for neurons by removing excess K+
2) Help form the BBB
3) Re-cycle NT’s released during synaptic transmission
4) Regulate vasoconstriction and dilation using substances like Arachadonic acid
What is the function of an Oligodendrocyte and why is this important?
Myelinate axons to provide insulation
Important as it increases efficiency of signal propagation down axon.
What are microglia, where are they found and what is their function?
These are macrophage-like cells found in all regions of the brain and spinal cord
Act as scavengers, modulate inflammation and impt in cell turnover and death (multiple when brain in damaged)
Where are Ependymal cells located and what is their function?
They line the spinal cord and ventricular system of the brain
Responsible for the creation and secretion of CSF + have sinner which beat to help circulate CSF
What is the function of Schwann cells?
Provide myelination to axons in the PNS + have phagocytic activity to clear cellular debris allowing for axonal regrowth in the PNS
(similar to oligodendrocytes)
Where are satellite cells located and what is their function?
Small cells that surround neurones in the sensory (SNS and PNS) ganglia.
They help to regulate the external chemical environment and are very sensitive to injury and inflammation (may contribute to some pathological states eg. chronic pain)
What are the receptive regions of a neurone and what occurs here?
Dendrites ➞ where incoming signals from other neurones synapse, creating an AP within that neurone.
Where do inputs from dendrites arrive?
What specifically occurs at this site?
The ‘axon hillock’ ➞ where multiple inputs result in summation of signals. If this summation reaches a specific threshold then an AP will be generated
What are the 2 types of summation?
Explain each
1) Spatial: multiple pre-synaptic neurones release enough NT to exceed the threshold of the postsynaptic neurone
2) Temporal: when one presynaptic neurone releases neurotransmitter many times over a period of time.
Gaps in the myelin of neurons are known as _________, the signal passes through these gaps by _________.
nodes of ranvier, saltatory conduction
What is the end of the axon known as and what does it contain?
What occurs here and how does it differ between the CNS and PNS?
Axon terminal which have vesicles containing NT’s
When the AP reaches the terminals it causes the release of these NT into the synaptic cleft to be passed onto the next cell.
CNS is neuron-neuron vs the PNS which usually occurs at the NMJ
What ions are responsible for the resting membrane potential and what pump aids this?
What creates the electrochemical (EC) difference?
High [K+] INSIDE and High [Na+] OUSIDE established by the Na+/K+ ATPase (3 Na+ OUT and 2 K+ IN)
The EC difference is due to some K+ leaking out of the cell, taking its + charge with it.
How is an AP initated?
1) stimulus triggers slight rise in charge intracellularly causing it to become slightly less negative.
2) voltage-gated Na+ channels open allowing Na+ to move into the cell
3) this results in depolarisation, if threshold is reached an AP is generated.
Na+ channels are ‘fast channels’, what does this mean?
State 2 reasons why this is important?
They open AND inactivate (refractory) rapidly after being activated
Important as it prevents another AP from being generated and ensures the AP only propagates in the forward direction.
Explain the 5 phases of an AP, incl which ions are responsible for each
What are Synapses and what are the 2 types of connections?
Junctions that allow information to be transferred from one neuron to the next. Connection can be:
- Electrical: direct transfer of ions
- Chemical (most common): release of a NT
(Rarely physical)
What is the neuron before and neuron after the synaps called and state the function of each
What is the space between these?
Pre-synaptic neuron: sends messege can be excitatory or inhibitory
Post-synaptic neuron (effector): carries the message either excitatory or inhibitory
Between is the Synaptic cleft: fluid filled extracellular space
Compare and exitatory vs inhibitory signal on the MP
How many iputs can a post-synaptic neuron respond to?
Excitatory ➞ increases MP, making an AP more likely to occur.
Inhibitory ➞ causes hyper-polarisation of the cell, making MP more negative and an AP less likely to occur.
There can be multiple inputs into a post-synaptic neurons (from 1 to 100,000)
Explain what occurs at a chemical synapse
1) AP travels down pre-synaptic neurone to axon terminal
2) depolarisation occurs ➞ VGCCs open
3) Ca 2+ influx cause vesicles to fuse with pre-synaptic membrane
4) fusion causes NT is release into synaptic cleft via exocytosis
5) NT binds receptors on post-synaptic membrane
6) ion channels open ➞ excitatory or inhibitory response
7) NT is taken up by glial uptake or enzymatic degredation
What is an electrical synapse and where are they most abundant?
Electrical synapses = gap junctions
Involves the direct transfer of ions through a mechanical and/or electrical link between the two cells.
Often found in neural systems b/c these require the fastest possible response (eg. defensive reflexes)
Give 3 comparisons between an electrical (ES) vs chemical (CS) synapse
1) ES are more rare than CS as there is a lot less flexibility
2) ES are much faster than CS b/c space between pre and post synaptic neurone is much smaller.
3) ES do NOT have any ‘gain’ whereas EC do
Gain means that increasing NT binding can amplify the signal. In an ES post-synaptic neurone can only receive a signal that is the same or smaller than that of the pre-synaptic neurone.
What are the 2 broad chemical catagories of NT’s
State which is faster and incl examples
1) small molecule NT’s: generally fast signals
* ACh, GABA, dopamine, adrenaline+NA, serotonin and histamine
2) neuropeptides: generally slower
* Endorphins (bind opioid receptor)
Give 2 broad catagories of NT’s and NT channels
NT can be ➞ excitatory (depolarise) or inhibitory (hyper-polarise)
NT channels can be ➞ Fast (ionotrophic- integral ion channel) or slow (metabotrophic- GPCR)
List 3 instances where ACh is used as a NT?
1) NMJ
2) Pre/post-synaptic ganglion of the ANS
3) Post-synaptic membrane of the PNS
(Brain also contains a number of cholinergic areas)
How does the ACh receptor differ in the pre-synaptic (ANS) post-synaptic (NMJ) differ?
ANS: pre-synaptic neurone is ionotrophic in the form of a nicotinic receptor
NMJ: post synaptic neurone/effector cell is metabotrophic in the form of a muscurinic receptor
How do Alzheimers drugs work?
The use of choliesterase inhibitors delays breakdown of ACh.
Early breakdown of ACh in the cleft is thought to be partly responsible for early degeneration seen in Alzheimers disease.
Note: cannot prevet/reverse effects but some can delay onset or progression.
What is the most prevalent NT in the brain and is it excitatory or inhibitory?
Give 2 functions it is involved in and 2 receptor classes it binds
Glutamate - excitatory.
Involved in cognitive functions (ie. learning and memory) and very important in synaptic plasticity
Receptor classes: AMPA receptors and NMDA receptors (both inotropic Ca2+ channels)
What is Excitotoxicity and explain why it is dangerous?
Clinically when may this be seen?
This is damage/death to nerve cells due to pathologically high levels of glutamate. Can be due to:
- excessive glutamate release
- excessive uptake of glutamate
Excess glutamate causes excessive stimulation of NMDA and AMPA receptors causing them to remain open. This allows excess Ca2+ entry into cells ➞ neuronal damage and eventually cell death.
Can be seen in brain injury, Ischemia (stroke) Autism, ASL and Alzheimers
What is the most predominant inhibitory NT
How does it inhibit AP’s and what is the clinical relevance of this for drugs?
GABA ➞ its receptors are ions channels that allow either Cl- flow INTO cell or K+ OUT of cell. Both result in hyper-polarisation which makes the cell less likely to depolarise thus reduces neuronal excitability
This is often the target of anti-epileptic drugs
Give 6 excitatory NT’s
1) Glutamate
2) ACh
3) Catecholamines (epinephrine, norepinephrine, dopamine)
4) Serotonin (acts on the 5HT)
5) Histamine
6) ATP
List 2 Inhibitory NT’s
GABA: gamma-Aminobutyric acid
Glycine
List 3 NT’s that can be excitatory AND Inhibitory
1) Neuropeptides
2) Endocannabinoids
3) Nitric Oxide
What receptors does serotonin act on?
List 4 functions of this NT
Acts on the 5HT receptors
Functions:
- modulating cognition
- reward pathways
- influence on memory and learning
- vomiting
- vasoconstriction
What is motor neuron disease? (MND)
State how it is diagnosed and treated?
MND is an umbrella term for a group of progressive disorders which lead to loss of motor neurones
Diagnosis:
- Normal nerve conduction studies
- MRI ➞ brain may show cortical atrophy
Treatment: supportive only (most patients die from Lung dysfunction)
What signs would be seen with MND?
Signs: UMN, LMN or combined signs
- UMN: hyper-reflexia, tightness, spasticity and muscle spasms
- LMN: muscle atrophy and fasciculations
Each MND affects patients differently. All cause movement related symptoms but varry in patterns of muscle weakness
What does ALS stand for and what gene is linked to the inherrited form of this disease
Amyotrophic lateral sclerosis Linked to mutations in the super-oxide-dismutase gene
Give 3 examples of ‘supportive’ treatment
feeding tubes, giving O2 and physiotherapy
What is Multiple Sclerosis and what is though to be the cause?
MS is a disease of demyelination of axons in the CNS. Axons loose their myelin sheath ➞ ability to send signals down axons is impaired (impaired saltatory condition)
The cause is unclear but though to due to an autoimmune component or failure to produce myelin producing cells
NOTE: it is only the myelin sheath that is attacked, the axon itself is preserved
How is MS diagnosed?
“Two or more, separate, episodes of CNS demyelination”
These can either occur on seperate days and includes sensory and/or motor symptoms eg. numbness, cold, pins and needles
OR a diagnosis can be made if patient develops other signs eg. optic neuritis
What is a classic early first sign of MS?
Patient can’t see the colour red
List one thing that may be seen on a CT of a patient with MS
List another diagnostic test that can be used and identify what would be indicative of MS
CT: plaques in white matter of brain or spinal cord (more common in per-ventricular/corpus callosum/optic tracts)
Other: Electrophoresis of CSF ➞ MS may show oligoclonal bands (bands of IgG that are raised in MS, marker of inflammation)
What are the 3 types of MS and what characterises each?
1) Relapsing and remitting: clearly defined attacks of new or increasing neurologic symptoms followed by periods of partial or complete recovery (remission)
2) 1o progressive: worsening neurologic function from onset of symptoms
3) 2o progressive: follows initial relapsing-remitting course which eventually transitions to progressive worsening
What is Guillain-Barre Syndrome + how is it characterised?
Is this condition life threatening and what is its prognosis?
Disease of de-myelination of the PNS, predominantly affecting the motor system (‘peripheral neuropathy’)
Characterised by classic ascending paralysis (starts at legs and moves up) with a range of severity (mild weakness to complete paralysis)
Can become life threating if it spreads into thorax and diaphragm because it will hinder ability to breathe
Recovery is spontaneous usually after a few weeks and some patients will have no progression at all.
How would you manage Guillain-Barre Syndrome?
Management is supportive:
- Plasma exchange
- IV immunoglobulin
- Mortality rate 5%
- 20% have long term disability
List 2 potential triggers for Guillain-Barre Syndrome
1) Prior infection eg. gastroenteritis or a resp tract infection
2) It is also commonly linked with campylobacter
What is Myasthenia Gravis?
Autoimmune disease caused by auto-antibodies against the ACh receptors are produced.
These Interfere with neuronal transmission between motor neurons and skeletal muscle.
Give 4 classic signs/symptoms of Myasthenia Gravis
Main = Muscle fatiguability
Others Incl:
- Drooping eye lids
- Intermittent double vision
- Issues chewing foods
- Speech dysarthria
How would you diagnose and treat Myasthenia Gravis?
Diagnosis: clinical suspicion, autoantibodies, electromyography, rdrophonium test
Treatment
- Cholinesterase inhibitors
- Immunosuppression
- Thymectomy (b/c of association with Thymic tumours)
What NT is low in depression and anxiety?
How is it treated?
Serotonin–strongly associated with mood
Treatment: Improved outcome with multiple treatments
- SSRIs and SNRIs (selective NA reuptake inhibitors)
- counselling + other cognitive therapies
Give a condition associated with abnormal levels of the following NT:
- Dopamine
- ACh
- Dopamine & noradrenaline
- GABA
- Parkinson’s disease and Schizophrenia
- Alzheimer’s disease
- ADHD
- Alcohol addiction
