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202: Theme 1 > Synaptic Transmission and Neural Plasticity > Flashcards

Synaptic Transmission and Neural Plasticity Flashcards

1
Q

Axon Hillock

A

the beginning of the axon before the axon proper

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2
Q

What are the two types of synaptic transmission responses?

A
  • Direct excitatory neurotransmission (direct)
    • the membrane of the next cell becomes either depolarized or hyperpolarised
  • Neuromodulation (indirect)
    • alters the presynaptic cells ability to produce/release a neurotransmitter are alters the postsynaptic cell’s ability to respond to the neurotransmitter
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3
Q

Criteria for a chemical to be a neurotransmitter

A
  • synthesized in the neuron
  • present in the presynaptic terminal and released in amounts sufficient to produce a defined effect on the postsynaptic neuron or effector organ
  • when administered exogenously it mimics the action of the endogenously released transmitter
  • a specific mechanism exists for removing it from the synaptic cleft
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4
Q

Synaptic Vesicles

A
  • vesicles are anchored to the cytoskeleton by synapsin
    • Ca2+ activates Calcium calmodulin activated kinase II (CaMKII) phosphorylated synapsin
    • P-synapsin can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • voltage-gated Ca2+
  • SNARE complex at the active zone
  • SYnaptobrevin and Synaptogotagmin

go over

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5
Q

Cleavage of SNARE proteins by cordial toxins

A
  • Botulinum toxin
    • neuromuscular transmission ACh
  • Tetanus Toxin
    • interneurons at spinal cord, GABA Gly
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6
Q

Diseases that affects presynaptic terminal;

A
  • Congential myasthenic syndromes: impaired vesicle recycling
  • Latrotoxin: triggers vesicle fusion
  • Botulinum and tetanus toxins: affect snare proteins involved in vesicle formation
  • LEMS attack presynaptic Ca2+ channels
  • Cognitive disorders: impair transsynaptic signalling
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7
Q

Synaptic membrane transporters

A
  • Vesicular transporters powered by proton gradient
    • use ATPase proton pumps
    • make vesicles acidic (pH5.5)
    • 1 glutamate for 1H+ (a counter-transport mechanism)
  • Plasma membrane transporters powered by electrochemical gradient
    • Na+ higher and K+ higher inside
    • Glutamate co-transported with 2 Na+ molecules
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8
Q

Overview of the Categories of neurotransmitters

A
  • Amino acids: faster (glutamate)
    • Synthesized locally in presynaptic terminal
  • Monoamines:
    • Stored in synaptic vesicles
  • Acetylcholine:
    • Released in response to local increase in Ca2+
  • Neuropeptides: slower
    • Synthesized in the cell soma and transported to the terminal
    • Stored in secretory granules
    • Released in response to global increase in Ca2+
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9
Q

Explain the differential release of neuropeptides and small molecule co-transmitters

A
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10
Q

Fast Transmission Amino Acid transmitters

A
  • Excitatory: slightly depolarises the postsynaptic cell’s membrane
    • Glutamate (Glu) (CNS)
  • 2) Inhibitory: slightly hyperpolarises the postsynaptic cell’s membrane
    • (γ-aminobutyric acid) GABA (brain)
    • Glycine (Gly) (spinal cord and brain stem)
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11
Q

Diffuse Modulatory System: Serotonergic system

A

Function in: mood, sleep, pain, emotion, appetite

  • produced by a small set of neurons in the brain stem: Raphe nuclei
  • produced in several areas in the brain
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12
Q

the Neuronal Layers of the brain

A
  • 1-6/ A-G
    • A- Pyrimdal neuorns
    • B - Spiny Stellate neurons
    • G - Chandelier
    • Layers 3/4 have a lot of cortical input, but mainly from the thalamus (main periphery relay channel)
    • Layers 5/6 mainly take projections towards the cortical structures: they feedback to thalamus with processing information for motor functions.
  • Excitation: Glu
  • Inhibition: GABA
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13
Q

Glutamate (Glu)

A
  • Synthesied in presynatic terminals
    • from glucose in the Krebs cylce
    • from glutamine converted by glutaminase
  • loaded and stored in vesicles by vesicular glutamate transporters (VGLUTs)
  • reuptake by excitatory amino acid transporters (EAATs) in the plasma membrane of presynaptic cell and surrounding glia
  • glial cells convert Glu to glutamine and this is transported from the glia back to nerve terminals where it is converted back into Glutamate.
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14
Q

GABA (γ-aminobutyric acid)

A
  • synthesized from glutamate (Glu) in a reaction catalyzed by glutamic acid decarboxylase (GAD)
  • loaded and stored into vesicles by a vesicular GABA transporter, GAT (Gly uses the same transporter)
  • cleared from synapse by reuptake using transporters on glia and neurons including non-GABAergic neurons
  • GABA is made de novo more often than it is recycled
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15
Q

When amino acid transmitter release is not regulated

Causes

A
  • too much Glu/too little GABA: hyper-excitability| epilepsy| excitotoxicity
  • too much GABA: sedation| Coma
  • Cerebral ischemia
    • ​the metabolic events that retain the electrochemical gradient are abolished
    • reversal of the Na+ / K+ gradient
    • transporters release glutamate from cells by reverse operation
    • excitotoxic cell death (Ca2+ -> enzymes -> digestion)
  • GHB γ-hydroxybutyrate (date rape drug)
    • a GABA metabolite that can be converted back to GABA
    • Increases amount of available GABA
    • too much leads to unconsciousness and coma
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16
Q

Types of Monoamines

A
  • Catecholamines
    • Dopamine
    • Epinephrine (adrenaline)
    • Norepinephrine
  • Indolamines
    • Serotonin (5-Hydroxytryptamine, 5-HT)
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17
Q

Catecholamine synthesis

A
  • Tyrosine -> L-dopa (can cross blood-brain barrier)–> Dopamine
    • Levodopa is administered for treating Parkinson’s disease
  • Dopamine -(DBH)-> Norepinpherine NE -(PNMT)-> Epinephrine
    • ​DBH (Dopamine B-hydroxylase) only in synaptic vesicles, NE is the only transmitter synthesised within vesicles
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18
Q

Catecholamine storage

A
  • loaded into vesicles by Vesicular monoamine transporters (VMATs)
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19
Q

Catecholamine release and reuptake

  • in the cytoplasm as well
A
  • released by Ca2+ dependent exocytosis
  • binds and activates the receptor
  • reuptake of catecholamines terminates the signal
    • reuptake powered by electrochemical gradient: created by dopamine transporters (DATs) and Norepipherine transporters (NETs
  • in the cytoplasm catecholamines are:
  • reloaded back into vesicles
  • enzymatically degraded by Monoamine oxidase (MAO)
  • inactivated by Catechol-o-methyl-transferase (COMT)
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20
Q

Drugs that affect the release and reuptake of catecholamines

A
  • Amphetamine: reverses transporter so pumps out more transmitter and blocks reuptake (DA & NE)
  • Cocaine and Methylphenidate (Ritalin): block DA reuptake into terminals. More DA in synaptic cleft – extended action on the postsynaptic neuron.
  • Selegiline: MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations ( treatment of early-stage PD, depression and dementia).
  • Entacapone: COMT inhibitor (treatment of PD), doesn’t allow DA to be broken down
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21
Q

What are these abbreviations:

NETs:

DATs:

MAOs:
COMT:

SERTs

A
  • NETs: Norepinepherine transporters
  • DATs: Dopamine transporter
  • MAOs: Monoamine oxidases
  • ​COMT: Catechol-o-methyl-transferase
  • SERTs: Serotonin transporters
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22
Q

Serotonin Synthesis

A
  • Tryptophan –> 5-Hydroxtryophan–> 5-Hydrotryptamine
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23
Q

Serotonin storage, release

A
  • stored in vesicles
  • signal terminated by reuptake by Serotonin transporters (SERTs) on presynaptic membrane
  • destroyed by MAOs in the cytoplasm
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24
Q

Drugs that affect serotonin release and reuptake

A
  • Fluoxetine (Prozac): blocks reuptake of serotonin (SSRI – selective serotonin reuptake inhibitor) (treatment of depression, OCD)
  • Fenfluramine: stimulates the release of serotonin and inhibits its reuptake (has been used as an appetite suppressant in the treatment of obesity)
  • MDMA: methylenedioxymethamphetamine (ecstasy) causes NE and serotonin transporters to run backwards releasing neurotransmitter into synapse/extracellular space (assessed for therapeutic potential in PTSD)
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25
Q

Acetylcholine formation, degradation, and reuptake

A
  • Choline acetyltransferase (ChAT, CAT) converts choline+ Acetyl CoA (coenzyme A) into acetylcholine.
  • packaged into vesicles by vesicular acetylcholine transporter (VAChT).
  • rapidly degraded in the synaptic cleft by acetylcholinesterase (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
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26
Q

Drugs that affect acetylcholine degradation

A
  • AChE (Acetylcholinesterase) inhibitors
    • blocks the breakdown of ACh, prolonging its actions in the synaptic cleft
      • Neostigmine: treatment of myasthenia gravis (MG)
        • _​_prolongs the present of ACh which helps the symptoms of the disease
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27
Q

Neuropeptide release and degradation

A
  • Follow the secretory pathway and NOT released in the same manner as small molecule transmitters
  • dense-core vesicle fusion and exocytosis occurs as a result of global elevations of Ca2+ (sustained or repeated depolarization or release of Ca2+ from intracellular stores)
  • neuropeptide vesicle membrane recycled but not refilled
  • bind to and activate the receptor on the postsynaptic neurone
  • neuropeptides signalling is terminated by diffusion from site of release and degradation by proteases in the extracellular environment
  • release is slower than small-molecule release and signals may be maintained for longer
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28
Q

Nitric Oxide and Carbon Monoxide as retrograde signals

A

1) Nitric oxide made in postsynaptic neuron by Nitric oxide synthase (activated by the binding of Ca2+ and calmodulin)
2) The gas is not stored but rapidly diffuses from its site of synthesis. Diffuses between cells (into presynaptic cell - retrograde transmitter)
3) Activates guanylyl cyclase which makes the second messenger cGMP
4) Within a few seconds of being produced NO is converted to biologically inactive compound (switching off the signal)
5) Potentially useful for coordinating activities of multiple cells in a small region (tens of micrometers)

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29
Q

Endocannabinoids

A
  • small lipids which cause reduced GABA release at certain inhibitory terminals
  • e.g Cannabis sativa (the active component of marijuana)
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30
Q

Ionotropic Receptors

A

a type of neurotransmitter receptor that contains a neurotransmitter binding site and an ion channel

  • it is a type of ligand-gated channel
  • in the absence of a neurotransmitter, the ion channel component of the protein is inactive
  • can be an EPSP or an IPSP reaction that the channel stimulates
    • most inhibitory neurotransmitters bind to Cl- ionotropic channels
31
Q

Metabotropic Receptors (Metabolic receptor)

A

a neurotransmitter receptor that contains only a neurotransmitter binding site: no ion channel component

  • can be coupled with G-protein either directly or via a second messenger
  • binding triggers uncoupling of heteromeric G-protein on the intracellular surface
  • this transduces a signal across the cell membrane
32
Q

Define Selectivity

A
  • what ions are fluxed
33
Q

Define Conductance

A
  • the rate of flux helps determine the magnitude of the effect
34
Q

Glutamate Ionotropic receptors

A

they flux Na+ causing an EPSP, these are the three receptors that respond to glutamate

  • NMDA:
    • ​agonist: N-methyl D-aspartate
    • antagonist: APV (2-amino-5-phosphonovaleric acid)
  • AMPA
    • ​agonist: AMPA
    • antagonist: CNQX
  • Kainate
    • ​agonist: Kainic acid
    • antagonist: CNQX
35
Q

NMDA receptors selectivity and conductance

A
  • NMDA receptors are responsible for late-phase EPSP
  • only activated in an already depolarized membrane in the presences of glutamate and glycine
  1. Slow opening channel – permeable to Ca2+ as well as Na+ and K+
  2. requires an extracellular glycine as a cofactor to open the channel
  3. it is also gated by a membrane voltage
    • Non-NMDA receptors (AMPA, and Kainate) have to be activated in advance to produce the appropriate voltage for the NMDA receptor to be activated
  • Mg2+ ion plugs pore when the membrane is at its resting potential
  • When the membrane depolarizes Mg2+ is ejected from the channel by electrostatic repulsion which allows conductance of the other cations
36
Q

Dysregulation of NMDA receptors

A
  • Channel Blockers
    • these drugs produce symptoms that resemble hallucinations associated with Schizophrenia
      • Dizocilipine (MK801)
      • Phencyclidine, ketamine
    • Remacemide
    • Memantine
    • Mg2+
  • Drugs that enhance current flow through NMDA channels
    • Glutamate excitotoxicity
      • excessive Ca+ into the cell activated Ca-dependent enzymes that degrade proteins lipids and nucleic acids
      • this type of cell damage occurs after cardiac arrest, stroke, oxygen deficiency and repeated intense seizures (status epilepticus)
37
Q

Examples of Ionotropic Receptors

A
  • Glutamate - excitatory
  • GABA(A) - inhibitory (brain)
  • Glycine - inhibitory (spinal cord and brain stem)
  • Nicotine - excitatory at NMJ (neuromuscular junction), excitatory or modulatory in the CNS (nicotinic receptors)
  • Serotonin -excitatory or modulatory
  • ATP- excitatory
38
Q

What are the three main synaptic second-messenger systems?

what are their target actions?

A
  • Norpinpherine: Increase protein phosphorylation
  • Glutamate: Increase protein phosphorylation and activate calcium-binding proteins
  • Dopamine: Decrease protein phosphorylation
39
Q

Activation of G-proteins

A

1) in resting-state the heteromer is bound to GDP
2) on binding of a ligand to the receptor the GDP is switched for a GTP and the heteromer splits in two
3) the Ga subunit and Gbg complex divide and diffuse separately through the membrane
4) these individual entities are able to stimulate the activity of other effector proteins
5) alpha subunits have intrinsic GTP-GDP enzymatic activity allowing the signal to be transient: the break down from GTP to GDP switches off its activity
6) at this point the heteromer recomplexes and awaits activation by ligand binding to another receptor.

40
Q

Explain the G-protein-coupled effector systems

Alpha units and Beta, Gamma complexes

A
  • 20 alpha subunits
    • Gs: stimulates adenylyl cyclase: increases the activity of cAMP and Protein Kinase A
      • Stimulatory Beta receptor
    • Gi: inhibits adenylyl cyclase: inhibits cAMP and Protein kinase A
      • Inhibitory alpha-2 receptor
    • Gq: stimulates phospholipase C (other fc)
  • Beta gamma complexes (5 beta, 12 gamma)
    • activate K+ channels directly
    • the mode of action for muscarinic ACh receptors in heart and the GABA receptor
41
Q

The Gq Second Messenger cascade: PIP2

A
  • Gq activates phospholipase C (PLC)
  • converts PIP2 into IP3 and diacylglycerol (DAG)
  • DAG activates protein kinase C (PKC) and IP3 releases Ca2+ from internal stores
  • which activates Ca2+ dependent enzymes
42
Q

How are Presynaptic receptors modulated?

A
  • autoreceptors regulate release of transmitter by modulating its synthesis, storage, release or reuptake
    • e.g. phosphorylation of tyrosine hydroxylase
  • heteroreceptors (axoaxonic synapses or extrasynaptic) regulate synthesis and/or release of transmitters of other ligands receptors (not directly the neurotransmitter)
    • e.g. NE can influence the release of ACh by modulating α-adrenergic receptors
43
Q

How are Postsynaptic receptors modulated?

A

they change the firing pattern or activity

  • increase or decrease the rate of cell firing (directly by action at ligand-gated ion channels or indirectly G -protein or phosphorylation-coupled channels)
  • long term synaptic changes
44
Q

Metabotropic receptors structure and examples

A
  • metabotropic glutamate receptors
  • GABA(B) receptor
  • muscarinic acetylcholine receptors
  • dopamine receptors
  • noradrenergic and adrenergic receptors
  • serotonin receptors
  • neuropeptide receptors
45
Q

Receptor tyrosine kinases

A

an enzyme-linked receptor found in neurons

  • Transmembrane proteins with intrinsic tyrosine kinase activity activated by neurotrophin binding (e.g. NGF, BDNF)
  • on activation it autophosphorylates
    • it phosphorylates regulatory subunits
    • this starts the signal transduction cascade
46
Q

Give examples of the two types of ACh receptors

A
  • G-protein coupled receptor (metabotropic)
    • Heart tissue: mAChR -> G-protein -> K+ channels -> hyperpolarisation (m=muscularinic slower)
  • Ligand-gated channel (ionotropic)
    • Skeletal muscle: nAChR -> Na+ ion channels -> depolarisation (n= nicotinic faster)
47
Q

GABA Ionotropic Receptors

A

they flux Cl-, which causes IPSP, hyperpolarizing the postsynaptic neuron

  • prevents postsynaptic neuron from firing unless there is sufficient glutamate stimulation to overcome the hyperpolarization (the refractory period)
48
Q

Examples of Metametabotropic glutamate receptors

A
  • Group I: mGluR1+5 Gq
    • somatodendritic: largely excitatory
  • Group II: mGluR2+3 Gi
    • somatodendritic & nerve terminals: reduce neuronal excitability
  • Group III: mGluR4,6,7+8 Gi
    • Nerve terminals: reduce neuronal excitability
49
Q

Explain Hebb’s rule and cell assembly

A
  • Objects are internally represented by cortical cells that are reciprocally interconnected in a cell assembly
  • When an external stimulus is encountered the cell assembly is activated, and persistent activation strengthens the connections of the cell assembly
    • so much so that after learning even if the stimuli is only partially present, a few activated connections can cause the whole assembly to be activated and the initial stimuli is recalled i.e circle
50
Q

Explain Associative Long Term Potentiation

A

If the activity of strong synapses is sufficient to trigger an action potential in the neuron, the dendritic spike will depolarize the membrane of dendritic spines, priming NMDA receptors so that any weak synapses active at that time will become strengthened.

51
Q

What are the key rules of synaptic modification?

A
  • Neurons that fire together wire together
  • Neurons that fire out of sync lose their link
  • strengthening and weakening synaptic connections in the brain provides a means for learning and memories can be formed
52
Q

Explain Long Term Potentiation (LTP)

A
  • Temporal: Summation of inputs reaches a stimulus threshold that leads to the induction of LTP. e.g. Repetitive stimulation (HFS)
  • Associative: simultaneous stimulation of a strong and weak pathway will induce LTP at both pathways. (Spatial summation)
    • Coincidence detection: “Cells that fire together wire together”
  • Specific: LTP at one synapse is not propagated to adjacent synapses (input specific).
53
Q

What happens at the synapse to produce the LTP effect?

A
  • Ca2+ entry through the NMDA receptor leads to activation of:
    • Protein kinase C
    • Calcium calmodulin-dependent protein kinase II (CaMKII)
  • Phosphorylates existing AMPA receptors, increasing their effectiveness
  • Stimulates the insertion of new AMPA receptors into the membrane
54
Q

Explain what CaMKII and the molecular switch is

A
  • Ca2+ entry through the NMDA receptor leads to activation of
  • Calcium calmodulin-dependent protein kinase II (CaMKII)
  • CaMKII has an autocatalytic activity - becomes phosphorylated
  • When phosphorylated is constitutively active - no longer requires Ca2+
  • Maintains phosphorylation, insertion of AMPA receptors etc. after the depolarizing stimulus has receded
  • This is a molecular switch which maintains increased excitability of neuron for minutes to hours
55
Q

Explain Presynaptic events in LTP

(long term potentiation)

A
  • Postsynaptic neuron can feedback to presynaptic neuron by retrograde neurotransmitter - Nitric Oxide (NO)
  • Ca2+ through the NMDA channel activates Nitric oxide synthase
  • NO diffuses from the site of production and activates guanylyl cyclase in the presynaptic terminal
  • Guanylyl cyclase produces the second messenger cGMP
  • Signal transduction cascade leads to increased glutamate release from the synaptic button
56
Q

Explain Late Phase LTP

A
  • Late phase LTP is long-lasting LTP that can last hours, days or months
  • This requires new protein synthesis and can involve morphological changes and the establishments of new synapses
  • Ca2+ activated signal transduction cascades activate new protein synthesis from dendritically localized mRNAs
  • this filter back to the cell body to stimulate new gene transcription (CREB -mediated), protein synthesis and recruitment of new proteins to the synapse
57
Q

Long Term Depression

A
  • is caused by Low frequency stimulation (LFS: 100x 1 Hz): there is a decrease in EPSP amplitude on further stimulation at a low frequency
  • Same players involved:
    • NMDA dependant process
    • AMPA receptors are de-phosphorylated and removed from the membrane
  • Prolonged low-level rises in Ca2+ activate phosphatases rather than kinases
58
Q

What evidence is there to show that NMDA is involved with synaptic activity and learning?

A
  • NMDA receptor activity in the hippocampus essential for both LTP and spatial learning
  • AP5 - NMDA receptor antagonist
    • blocks hippocampal LTP
    • blocks learning in the Morris Water Maze
59
Q

What are the effects of Alcohol on learning and memory?

A
  • Alcohol is an NMDA receptor antagonist (as well as other sites)
  • Blackouts and amnesia caused by drinking
    • directly blocking normal LTP processes
  • Alcohol disrupts hippocampal theta rhythms and disrupts short term memory.
  • Chronic alcoholism and associated nutritional deficiency can result to Korsakoff syndrome or psychosis: loss of recent memory, and tendency to fabricate accounts of recent events (confabulation).
60
Q

What are the effects of Benzodiazepines on learning and memory?

A
  • Indirect agonist of GABAA receptors:
    • binding increases the receptor affinity for GABA
    • increase frequency of channel opening
    • anxiolytic and hypnotic drugs
  • Side effect to anxiolytic and sedative properties:
    • anterograde amnesia
61
Q

What are the effects of cholinergic and anticholinergic?

A
  • Acetylcholine projections:
  • Basal forebrain bundle:
    • Medial septum to hippocampus
    • Basal nucleus to cortex
  • Septum to hippocampus projection regulates theta waves
  • Scopolamine (muscarinic receptor antagonist)
    • suppresses theta waves and impairs spatial learning
62
Q

Explain the use of Acethycholinesterase Inhibitors in Alzheimer’s Disease

A
  • they boost cholinergic function
  • improve memory impairment
  • e.g physostigmine
63
Q

What determines gene expression in individual cells?

A
  • Inducing Factors: signalling molecules provided by other cells
    • freely diffusable, exerting their action over a long-range or tethered to the cell surface acting locally
    • They can modify gene expression, cell shape and motility. cells in different positions in the embryo are exposed to different inducing factors, can effect the final cell outcome
  • Competence: the ability of a cell to respond to inducing factors this depends on:
    • the exact set of surface receptors
    • transduction molecules
    • transcription factors expressed by the cell
64
Q

Define Neurogenesis

A
  • the process by which neurons are generated
    • 5th week – 5th month of gestation
    • Peak rate of 250,000 new neurons / minute
65
Q

What are Neural Stem Cells/ Neural precursor cells

A
  • Infinitely self –renewing
  • After terminal division and differentiation, they can give rise to the full range of cell classes within the relevant tissue,
    • e.g. inhibitory and excitatory neurons, astrocytes, oligodendrocytes.
66
Q

What are Neural Progenitor cells?

A
  • Incapable of continuing self – renewal
  • Capable to give rise to only one class of differentiated progeny,
    • e.g. an oligodendroglial progenitor cell will give rise to oligodendrocytes until its mitotic capacity is exhausted.
67
Q

What are Neurobloasts?

A
  • Postmitotic, immature nerve cells that will differentiate into a neuron
    • formed when a precursor cell is horizontally cleaved, it contains the Notch-1 protein
  • the fate of the migrating neuron will be determined by
    • age of the precursor cell
    • position in the ventricular zone
    • the environment at the time of division
68
Q

How do neuroblasts differentiate?

A
  • Pathway selection
    • e.g. retinal ganglion cell reaching the correct thalamic location.
  • Target selection
    • e.g. selecting the appropriate thalamic nucleus, LGN.
  • Address selection
    • which LGN layer.

The formation of the axon and dendrites is guided by the filopodia which guide the growth cone (consists of growth cones called lamellipodium)

  • the growth of the neuroblast is controlled by guidance cues
    • chemoattractant: netrin receptors towards areas with netrin
    • chemorepellents: robo away from slits on the midline
69
Q

Explain Trophic interactions in neuronal cell development

A
  • Gradients in the expression of guidance cues and their axonal receptors can impose topographic order,
    • final refinement of connections often requires large scale reduction of newly formed neurons and synapses.
  • The protein netrin is secreted by cells in the ventral midline of the spinal cord. Axons with the netrin receptors are attracted to the region of highest netrin concentration
  • The protein slit is secreted by midline cells. Axons that express the protein robo, the slit receptor, grow away from the region of highest slit concentration.
    • Up-regulation of robo by axons that cross the midline ensures that they keep growing away from the midline.
70
Q

Explain how synapse elimination occurs

A
  • Initially each muscle fibre receives inputs from several alpha motor neurons.
  • Over the course of development, all inputs but one are lost.
  • Postsynaptic AChR loss precedes the withdrawal of the axon branch.
  • Simply blocking a subset of receptors with α-bungarotoxin can also stimulate synapse elimination.
71
Q

Explain the “critical period” concept

A
  • This describes a variable time window for different skills/behaviours e.g. sensorimotor skills, language acquisition, visual perception, emotional functions to be developed. Successful completion of this period depends on
    • Availability of appropriate influences
    • Neural capacity to respond to them
72
Q

Explain Ocular Dominance Columns and visual deprivation

A
  • these are afferent terminals in the fourth cortical layer that form a series of alternating eye-specific domains
  • visual deprivation: there is a period of time after birth where any alterations to the stimuli available to the visual cortex will permanently affect the vision of the individual
73
Q

Potential barriers to regeneration in the cortical brain

A

In the postnatal and adult brain, significant barriers to regeneration are present.

  • Radial glia are exhausted and become a “lost highway” to any neuronal migration.
  • Cortical neurons are no longer generated and thus virtually no neurons can be found migrating into the cortex.
  • Neuronal plasticity becomes significantly attenuated, preventing the type of plasticity observed prior to developmental critical periods.
  • Interneuron progenitors and mINs disappear.
  • Parenchymal glia do not cross lineage boundaries and become reactive after injury and degeneration.
74
Q

Explain the importance of neurogenesis in the hippocampus and how that affects memory

A
  • Without neurogenesis, new events are limited by the set of sparse ‘codes’ (combinations of active neurons) provided by mature granule cells in the dentate gyrus
  • New neurons (shown in green) provide new sparse codes for encoding new information, while older memories are preserved because they are represented by older neurons

202: Theme 1 (14 decks)

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