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Neuroanatomy > Basic Neuroscience > Flashcards

Basic Neuroscience Flashcards

1
Q

In H&E, what does Haemotoxylin stain and what colour?

A

Nucleic Acids (nucleolus) blue

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2
Q

In H&E what does Eosin stain and what colour?

A

Proteins red

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3
Q

In a chemical synapse, what does depolarisation of synaptic terminal cause?

A

Opening VGCCs, triggering NT release

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4
Q

How do ions flow between electrical synapses?

A

through connexins directly opposite to each other

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5
Q

Which kind of synapses are often concentrated on dendritic spines?

A

Excitatory- often glutamate

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6
Q

Which diseases have been linked to reduced dendritic spine density?

A

AD and SZ

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7
Q

What are Betz cells?

A

Upper motor neurons found in motor cortex, large, excitatory (glut), long projections, pyramidal cells

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8
Q

What disease are Betz cells vulnerable to

A

MND

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9
Q

What are medium spiny neurons?

A

small striatal inhibitory (GABA) interneurons

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10
Q

what disease are medium spiny neurons vulnerable to?

A

HD

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11
Q

2 functions of oligodendrocytes

A

myelinating and metabolic support

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12
Q

Can one oligodendrocyte sheath several neurons?

A

Yes

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13
Q

What electrochemically allows tight binding between myelin and neurons

A

positively charged MBP proteins - bind to negative neurons

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14
Q

What do microglia look like in resting state?

A

highly ramified with surveying motile processes

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15
Q

what do microglia look like upon activation

A

small, dense, amoeboid

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16
Q

What are the 2 types of microglia?

A

M1 and M2

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17
Q

What is M1 microglia?

A

Pro-inflammatory ‘bad’ cytokine production

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18
Q

What is M2 microglia?

A

Neuroprotective ‘good’ cytokine production

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19
Q

How are microglia involved in synaptic plasticity

A

phagocytic dendritic pruning

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20
Q

Which are the most abundant glial cell?

A

Astrocytes

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21
Q

what’s a key marker used to detect astrocytes?

A

GFAP (glial fibrillary acidic protein)

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22
Q

how do astrocytes contribute to BBB

A

their end-feet

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23
Q

Are A1 astrocytes proinflammatory or neuroprotective?

A

proinflammatory

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24
Q

are A2 astrocytes proinflammatory or neuroprotective?

A

neuroprotective

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25
Q

Name 3 specialised Glia

A

Radial Glia, Bergmann Glia, Muller Cells

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26
Q

Define Nuclei in CNS

A

group of cell bodies

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27
Q

Define tracts in CNS

A

group of axons

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28
Q

Define Ganglia in PNS

A

group of cell odies and supporting cells

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29
Q

Define Nerves in PNS

A

axon bundles

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30
Q

name 4 contributors to the BBB

A

endothelial tight cell junctions, basement membrane with few fenestrations, astrocyte end feet and pericytes

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31
Q

What lack normal BBB?

A

circumventricular organs

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32
Q

Name 2 circumventricular organs:

A

Posterior Pituitary Area Postrema, Pineal Body

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33
Q

Name 2 routes for CSF reabsorption

A

Arachnoid granulations, meningeal lymphatics, perineural spaces

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34
Q

Describe ependymal cells

A

Epithelial-like, lines ventricles and spinal cord, CSF production/flow, ciliated

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35
Q

Describe Choroid Plexus

A

frond-like projections in ventricles, modified ependymal cells, highly vascularised and clustered, CSF production, CSF-blood barrier

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36
Q

Which ion gradient is the primary determinant of resting membrane potential?

A

K+

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37
Q

Which other 2 ions (other than K+) have an effect on resting membrane potential

A

Na+ and Cl-

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38
Q

What causes depolarisation simply?

A

influx of Na+

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39
Q

What causes repolarisation simply?

A

closure of Na+ channels and opening of K+ VG channels

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40
Q

What causes hyperpolarisation simply?

A

K+ VG channels staying open after resting potential reached

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41
Q

Which ion channel does TTX block?

A

Na+

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42
Q

Which ion channels does TEA block?

A

K+

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43
Q

enough EPSP causes

A

generation of AP

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44
Q

what’s the most common cause of an EPSP generating AP

A

influx of Na+ ions from positive NT glutamate

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45
Q

Does a larger stimulus produce a larger AP?

A

no

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46
Q

Does a larger stimulus produce more APs?

A

Yes

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47
Q

can a second stimulus in the absolute refractory period trigger another AP?

A

No

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48
Q

can a second stimulus in the relative refractory period trigger another AP?

A

yes, however, it may need to be larger as the cell is in a hyperpolarised state

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49
Q

What is the advantage of refractory period?

A

it favours unidirectional propogration

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50
Q

What do uniporters do?

A

one substance in one direction

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51
Q

what do symporters do?

A

2 substances, 1 direction

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52
Q

what do antiporters to

A

2 substances in opposite directions

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53
Q

give 2 examples of uniporters

A

Na+, K+. Cl-, Ca2+ channels

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54
Q

give 2 examples of symporters

A

Na/Cl-/K+ cotransporter
K+/Cl- cotransporter
Na+/Neurotransmitter co-transporter e.g. DAT

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55
Q

Give 2 types of antiporters

A

ATPase pumps and ion exchangers

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56
Q

Which active process contributes towards maintaining electrochemical gradient in neuron

A

Na+/K+ ATPase

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57
Q

what ratio in/out for Na+/K+ ATPase

A

3 Na+ out and 2 K+ in

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58
Q

describe the structure of Na+/K+ ATPase

A

10 alpha TM helices, mainly cytoplasmic
Single beta helix- mainly extracellular
N, P and A domains

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59
Q

What 2 toxins inhibit Na+/K+ ATPase?

A

Digoxin an Ouabain

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60
Q

What are the 2 types of Ca2+ ATPases?

A

PMCA and SERCA

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61
Q

what are Ca2+ ATPases structurally similar to?

A

Na+/K+ ATPases

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62
Q

what 3 important structures do VGSC contain?

A

voltage sensor (charged helix)
selectivity filter (pore)
gating mechanisms (on-off)

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63
Q

what are the 2 main types of drugs which target Na+ VGSCs?

A

Antiepileptics e.g. lamotrigine and Anaesthetics e.g. lidocaine

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64
Q

What’s the mechanism of the opening and closing of VGSCs?

A

charged helix voltage sensor detects membrane depolarisation and changes shape to allow Na+ influx, it is rapidly inactivated by channel-inactivating segment (plug) during hyperpolarisation

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65
Q

Which ion channel is a key target of toxins?

A

VGSCs

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66
Q

Name 2 disorders that mutations of VGSC genes are linked to

A

epilepsy, migraine, ASD, ataxia, pain insensitivity, extreme pain disorder

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67
Q

What are VG potassium channels structurally similar to?

A

VGSCs

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68
Q

Describe the structure of VGPCs

A

4 alpha subunits with 6 TM helices and regulatory Beta subunits

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69
Q

Name 1 disorder linked with VGPC gene mutations

A

epilepsy and ataxia

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70
Q

name 2 disorders linked to Calcium channel gene mutations

A

ataxia, migraine, childhood absence epilepsy

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71
Q

What aspects of an ion channel can channelopathies effect? name 2

A

channel assembly/ function, permeability, gating, inactivation

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72
Q

what’s a dominant negative mutation

A

where a mutation in one subunit impacts all other subunits

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73
Q

Name 3 different Ionotropic receptors/ ligand-gated ion channels

A

NMDA/AMPA/Kainate
nAChR
5-HT
GlyR
GABAb

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74
Q

What is an ionotropic receptor

A

where the receptor is an ion channel itself

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75
Q

what are transient receptor potential (TRP) channels?

A

cation channels, gated by a number of factors, linked to pain, migraine and itch, found in PNS and CNS

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76
Q

Name 2 differences between electrical and chemical synaptic transmission

A

fewer electrical synapses
faster transmission of electrical
narrower synapses of electrical
electrical less tightly regulated

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77
Q

Which aspect of electrical transmission has genetic disease relevance?

A

Conexins

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78
Q

What disorder is linked to GJB1 connexin gene mutation?

A

Charcot-Marie Tooth neuropathy

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79
Q

What disorder is linked to GJC2 connexin gene mutation

A

Lewy Dystrophy or spastic Paraplegia

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80
Q

Name the 3 criteria which define NTs

A
  • present in presynaptic neuron
  • released in response to presynaptic neuron depolarisation with Ca2+ dependant release
  • Specific receptors present on postsynaptic cell
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81
Q

What are the 2 main classes of NT?

A

Small Molecule and Peptide NTs

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82
Q

What are the 2 types of neurotransmitter production/transport?

A

Slow-Axonal and Fast-Axonal

83
Q

What kind of NTs travel by slow-axonal transport?

A

small

84
Q

describe fast-axonal transport of NTs

A

they travel in vesicles down microtubule tracks

85
Q

describe the 2 types of vesicles and what they hold

A

Small clear, hold small NTs suchas Gly, Glu, GABA ACh and ATP
Dense-core, hold serotonin, histamine, catecholamines, neuropeptides

86
Q

What coats synaptic vesicles

A

proteins

87
Q

What are SNAPs

A

Synaptic Associated Proteins

88
Q

How does exocytosis occur in NT vesicles, with reference to SNAREs

A

SNAP receptors on vesicles interact with SNAREs and other proteins on pre-synaptic terminal causing pore to open. Afterwards SNARE complexes disassemble and vesicles are recycled

89
Q

Which 2 toxins target SNARE proteins?

A

botulinum (botox) and tetanus (these toxins are proteases which cleave SNAREs)

90
Q

What are the 3 main types of synaptic membrane vesicle recyling?

A

Clathrin mediated endocytosis
ultrafast endocytosis
Kiss-and-run endocytosis

91
Q

How does Clathrin-mediated endocytosis occur?

A

Pits form in synaptic terminal after exocytosis and clathrin forms a network over budding membranes, which narrow and bud off

92
Q

What is ultrafast endocytosis?

A

Where larger membrane sacs are formed at distal sites, away from vesicle release

93
Q

What is a tri-partite synapse?

A

One where pre- and post-synaptic terminals and glial cells (astrocytes) reuptake ions/NTs

94
Q

As well as components of tri-partite synapse, what else removes NTs from synapse?

A

enzymes- break them down

95
Q

What are the 2 key types of NT receptor?

A

ionotropic and metabotropic

96
Q

which type of NT receptor tends to act faster with shorter term effects?

A

Ionotropic

97
Q

What structure are most metabotropic receptors

A

GPCRs

98
Q

How many subunits tend to make up a GPCR?

A

3

99
Q

What is summation

A

The sum of inhibitory and excitatory inputs- which summate in whether or not an AP is produced

100
Q

Is glutamate a small or large NT?

A

Small

101
Q

Are GABA and Glycine big or small NTs

A

small

102
Q

Is Glutamate charged?

A

yes

103
Q

are GABA and glycine charged?

A

No

104
Q

What is GABAs main role?

A

Main brain inhibitory NT

105
Q

How is GABA sythesised?

A

from glutamate by glutamic acid decarboxylase (GAD)

106
Q

What loads GABA into synaptic vesicles?

A

vesicular inhibitory amino acid transporter (VIAAT)

107
Q

What clears GABA from the synapse?

A

GABA transporter (GAT)
(an Na+ dependent co-transporter)

108
Q

What are the 2 main types of GABA receptor?

A

GABAa and GABAb

109
Q

Describe GABAa

A

ionotropic
chloride channel
2 alpha, 2 beta, 1 gamma subunit

110
Q

Describe GABAb

A

metabotropic
hyperpolarise by driving K+ out of cell and inhibiting Ca2+ influx
G-protein signalling

111
Q

What do agonists of GABAa generally do

A

Sedate/ CNS depressants

112
Q

Name 3 classes of GABAa agonists

A

anxiolytics, anti-convulsants, anaesthetics, barbiturates, benzos

113
Q

What do Barbiturates do at the GABAa receptor?

A

activate it

114
Q

What do Benzos do at the GABAa receptor?

A

enhance

115
Q

What do antagonists of GABAa receptors do?

A

used for Benzo ODs and epilepsy models

116
Q

What are GABAb agonists used for?

A

spasticity (MND and MS)

117
Q

what are GABA reuptake inhibitors used for?

A

focal seizures

118
Q

What are GABA analogues (agonists) used for?

A

seizures/ neuropathic pain e.g. gabapentin

119
Q

Is GABA inhibitory or excitatory in early brain development?

A

excitatory

120
Q

Describe GABA’s excitatory function in early brain development

A

immature brain has high levels of NKCC1 (sodium potassium chloride channel 1) where GABA causes efflux of Cl- – depolarising

121
Q

Why is it important for GABA to be excitatory in early development?

A

brain is growing and growth and connections need to be stimulated

122
Q

What’s different about GABA in mature brain?

A

higher KCC2 channels and low Cl-, where Cl- influx due to GABA causes inhibition

123
Q

What is Glycine’s overall role?

A

Main inhibitory NT in spinal cord and brainstem

124
Q

What loads Glycine into vesicles?

A

VIAAT

125
Q

What clears Glycine from synapses?

A

GlyT (Glycine transporter)

126
Q

What causes Hyperplexia?

A

Mutations in GlyT

127
Q

What is hyperlexia?

A

exaggerated startle

128
Q

Why does an increase in Glycine in Hyperlexia cause excitatory symptoms?

A

Desensitisation of post-synaptic membrane

129
Q

What is Hyperlexia managed with?

A

Clonazepam (Benzo)

130
Q

What kind of receptor are Glycine receptors?

A

Ionotropic Chloride Channels

131
Q

What’s the structure of Glycine receptors?

A

5 subunits
3 alpha and 2 beta each with 4 TM domains clustered by gephryn

132
Q

What kind of NT class is ATP?

A

Purine

133
Q

Are Purines Excitatory of Inhibitory?

A

Excitatory

134
Q

Where is ATP found as an NT?

A

CNS and PNS

135
Q

Is adenosine a NT?

A

No it’s a neuromodulator

136
Q

What class of receptor responds to purines?

A

Both ionotropic and metabotropic

137
Q

What, structurally makes an NT an Amine?

A

Ring structure

138
Q

give examples of biogenic amine NTs

A

Catecholamines (Dopamine, Noradrenaline, Adrenaline)
Histamine
Serotonin

139
Q

Describe the biosynthesis of Catecholamines

A

L-tyrosine–> L-Dopa –> Dopamine –> Noradrenaline –> Adrenaline

140
Q

What loads catecholamine NTs in vesicles?

A

monoamine transporter (VMAT)

141
Q

What catabolises catecholamines? (2)

A

MAO (monoamine oxidase) and COMT (catech-O-methyltransferase)

142
Q

What are the 3 pathways of Dopaminergic neurons?

A

nigrostriatal
mesolimbic
mesocortical

143
Q

Describe the nigrostriatal dopaminergic pathway

A

From SN to Striatum
involved in movement

144
Q

Describe the mesolimbic dopaminergic pathway

A

from midbrain ventral tegmentum to limbic system
involved in reward

145
Q

Describe the mesocortical dopaminergic pathway

A

from midbrain ventral tegmentum to cortex
involved in cognition, emotion
(affected in SZ)

146
Q

What removes dopamine from synapses?

A

DAT (dopamine transporter) (Na+ dependent co-transporter)

147
Q

What drugs target DAT?

A

Cocaine and Amphetamines

148
Q

What disease are MAO and COMT inhibitors used in?

A

PD

149
Q

What class of receptors are dopamine receptors?

A

Metabotropic

150
Q

What are the 2 classes of dopaminergic receptors?

A

D1-like Gs
D2-like Gi

151
Q

What’s the differences between D1-like Gs and D2-like Gi receptors?

A

D1- stimulatory- increase cAMP levels
D2- inhibitory- reduce cAMP levels

152
Q

Why do antipsychotics have so many side-affects?

A

they lack specificity so act on a number of receptors

153
Q

What functions is Noradrenaline involved with?

A

Sleep, Wakefulness and attention

154
Q

Where’s the main source of NA?

A

Locus Coeruleus

155
Q

Does NA have many of few connections through the brain?

A

Many

156
Q

Is adrenaline abundant in CNS?

A

No

157
Q

Where is adrenaline produced in CNS?

A

clusters of neurons in the medulla

158
Q

What class of receptors detect adrenergic NTs?

A

metabotropic

159
Q

What is the neural role of Histamine?

A

Wakefulness, Appetite, memory

160
Q

What class of receptors detect Histamine?

A

Metabotropic

161
Q

What o antihistamines that cross BBB do?

A

act as sedatives e.g. promethazine blocks H1 and makes people sleepy

162
Q

Where in the brain is histamine produced?

A

Tuberomammillary nucleus in the posterior hypothalamus

163
Q

Name 3 functions of Serotonin

A

Mood, sleep, wakefulness, appetite, nausea

164
Q

What clears Serotonin from synapses?

A

SERT (serotonin transporter)

165
Q

What drugs target SERT?

A

SSRIs

166
Q

What class of receptors are serotonin receptors?

A

All metabotropic except 5=HT3

167
Q

Is Serotonin inhibitory or excitatory?

A

either- depends on cAMP regulation

168
Q

Can multiple neuroactive peptides be released from a single vesicle?

A

yes

169
Q

what class of receptors detect peptide NTs?

A

metaboptropic

170
Q

Name 3 classes of peptide NTs

A

brain/gut peptides e.g. substance p, orexins
opioid peptides e.g. endorphins
pituitary peptides e.g. ACTH

171
Q

Overall, what is synaptic plasticity?

A

increases or decreases in synaptic strength in response to synaptic activity

172
Q

What is short-term plasticity?

A

Plasticity which lasts milliseconds to seconds, temporary and is related to NT release

173
Q

What is synaptic faciliation?

A

When paired stimuli are given close together and the second PSP is greater than first due to increased Ca2+ has there has not been full closure of Calcium channel

174
Q

As the interval between stimulations decreases, does synaptic facilitation increase or decrease?

A

decrease (calcium normalises between stims)

175
Q

What is synaptic depression?

A

Where a train of stimulation, causes post-synaptic potential to decrease after each stimulus

176
Q

Why does synaptic depression occur?

A

There’s a finite supply of vesicles which reduce over repeated stimulation (if there’s a gap in stimulation, it will recover as vesicle levels restore)- hence is short-term plasticity

177
Q

What is long-term plasticity the basis of?

A

learning and memory

178
Q

What are the 2 main forms of long-term plasticity?

A

Long-term potentiation- LTP
Long-term depression- LTD

179
Q

Briefly describe the trisynaptic circuit in mice

A

inputs from entorhinal cortex, synapses onto dendate gyrus, projection to CA3 neurons, from here schaffer’s collaterals synapse to CA1 neurons

180
Q

Which aspect of the trisynaptic circuit in mice is studied in LTPresearch?

A

schaffer’s collaterals to CA1 synapses

181
Q

How is LTP studied?

A

Tetanic stimulation causing a greater induced response over time

182
Q

What are the 4 properties of LTP?

A

-co-operative- crucial number of fibres must be simultaneously activated
- input-specific- synapse must be activated during induction
Associative- induction at concurrently active synapses
Hebb’s Law- Spike-timing dependant plasticity

183
Q

What is the mechanism underlying LTP?

A

It is NMDA receptor dependent, where high frequency stimulation causes prolonged depolarisation and alleviation of the Mg2+ block in NMDA receptors, increased Ca2+ activates kinase which causes the insertion of additional AMPA receptors from IC pool, synapses can now carry greater current

184
Q

How has LTP been exhibited to remodel dendritic spines?

A

Glutamate uncaging studies indicated LTP being associated with the fast growth of new and already existing spines

185
Q

Describe late-phase LTP and gene expression

A

Induction of LTP activates cell signalling pathways sending signals to the nucleus changing gene expression and activating CREB pathway to increase expression of plasticity. the earliest genes expressed are transcription genes themselves (e.g. c-fos) which go on to induce transcription of further proteins linked to plasticity

186
Q

How is LTD induced?

A

prolonged low-frequency stimulation

187
Q

What is the mechanism of hippocampal LTD?

A

a small and slow increase in calcium influx is triggered by the LFS, this activates phosphatase and leads to dephosphorylation of stargazin and endocytosis of AMPAR

188
Q

Describe cerebellar LTD

A

When climbing and parallel fibres are simultaneously activated, LTD is seen in purkinje cells

189
Q

What diseases does mutation in the SCN1A cause (VGSC)?

A

epilepsy, migraine, autism

190
Q

what diseases does mutation in SCN2A cause (VGSC)?

A

epilepsy, ataxia, autism

191
Q

what diseases does mutation in SCN3A cause (VGSC)?

A

epilepsy

192
Q

what diseases does mutation in SCN9A cause (VGSC)?

A

either extreme pain or pain insensitivity (depending on up or down regulation)

193
Q

What disease is linked to KCNA1 gene mutations in VGPCs?

A

episodic ataxia type 1

194
Q

What disease is linked to KCNQ2, 3 and MA1 gene mutations in VGPCs?

A

epilepsy

195
Q

describe the structure of voltage-gated calcium channels

A

a pore forming alpha-1 subunit and variation in other combinations of alpha, beta, gamma etc.

196
Q

what does a mutation in CACNA1A gene cause (VGCC)

A

episodic ataxia type 2 and spinocerebellar ataxia type 6

197
Q

what does a mutation in CACNA1B gene cause (VGCC)

A

myoclonus-dystonia syndrome

198
Q

what does a mutation in CACNA1C gene cause (VGCC)

A

x-linked congenital stationary night blindness

199
Q

what does a mutation in CACNA1H gene cause (VGCC)

A

childhood absence epilepsy

200
Q

which class of drugs act on adrenergic receptors

A

beta-blockers e.g. propranalol

201
Q

Name the drowsy antihistamine that crosses the BBB

A

Promethazine

202
Q

Name a serotonin receptor agonist

A

sumatriptan (migraines), anxiolytics, LSD,

203
Q

name a serotonin receptor antagonist

A

atypical antipsychotics, ondansetron (anti-emetic), SSRIs/ other antidepressants, clomipramine, fenfluramine, MAOI antidepressants

Neuroanatomy (5 decks)

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