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Brain and Behavior > Exam 1 Deck 1 > Flashcards

Exam 1 Deck 1 Flashcards

1
Q

How many specialized cell types are there in the brain?

A

Four. Five if you count ependymal cells.

Neurons

Astrocytes

Oligodendroglia

Microglia

(Ependymal Cells)

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2
Q

What is the embryonic origin of neurons?

A

Ectoderm

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3
Q

What are the functional unit of the CNS?

A

neurons

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4
Q

Do neurons regenerate?

A

CNS neurons do not regenerate much (limited examples)

PNS neurons regenerate to a much greater degree.

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5
Q

What is the function of glial cells?

A

They buffer and control the communication that comes into the neurons.

Maintain the microenvironment around the neuron.

Include:

Astrocytes

Oligodendroglia

Microglia

Ependymal Cells

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6
Q

What are some functions of astrocytes?

A

Provide structure

Metabolic support

Maintain ion balance

Supply glutamate

Maintain BBB

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7
Q

Which glial cells supply glutamate to neurons?

A

Astrocytes

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8
Q

Which glial cells maintain the chemical mileu around neurons and provide support for the neuron?

A

Astrocytes

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9
Q

Which glial cells provide the myelin sheath for axons in CNS?

A

Oligodendroglia (oligodendrocytes)

They provide the sheath of multiple CNS axons

(analagous to Schwann cells in PNS)

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10
Q

What is the embryonic origin of astrocytes?

A

Ectoderm

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11
Q

What is the embryologic origin of oligodendroglia

A

Ectoderm

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12
Q

What is the embryological origin of microglia?

A

Mesoderm

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13
Q

What is the main function of microglia?

A

Act as resident macrophages of brain and spinal cord

Activated in the case of damage and phagocytose foreign matter and apoptotic neurons

Make cytokines and neurotoxins

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14
Q

Which glial cells are responsible for macrophage function in the spinal cord and brain?

A

microglia

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15
Q

Which cells help maintain the blood-brain barrier (BBB)?

A

Endothelial cells lining the capillary wall (have TIGHT JUNCTIONS unlike other capillary endothelial cells)

Astrocytes with their foot processes

Basement membrane of capillaries

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16
Q

What does the blood brai barrier do?

A

Prevents the passage of large molecules from blood into interstitial fluid of CNS

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17
Q

What is the point of the blood-CSF barrier?

A

Prevents large molecules from passing from blood to CSF

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18
Q

How is the blood-CSF barrier maintained?

A

By tight junctions between epithelial cells of the choroid plexus

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19
Q

What does the choroid plexus do?

A

Lines the ventricles and produces CSF

Tight junctions between cells help maintain the blood-CSF barrier

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20
Q

How long can a neuron last (on average) in an anoxic environment?

A

5-7 minutes

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21
Q

Which cells are most sensitive to anoxia?

A

Neurons (specifically the cell body, or soma)

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22
Q

Which cells are least sensitive to anoxia?

A

Blood vessels

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23
Q

What is the order of sensitivity of anoxia (most to least)?

A

Nerve cells (soma then axon)

Myelin and oligodendroglial cells

Astrocytes

Microglia

Blood vessels

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24
Q

What are two responses of brain neurons to injury?

A

Eosinophilic degeneration

Axonal reaction

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25
Q

What occurs durin eosinophilic degeneration?

A

Perikaryal cytoplasm becomes eosinophilic (pink) due to mitochondrial condensation

Nucleus becomes pyknotic (dark and shrunken)

Irreversible

4-6 hours after injury?

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26
Q

Which brain neuron response to injury is reversible?

A

Axonal Reaction

Eosinophilic degeneration is irreversible

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27
Q

Which brain neuron response to injury is irreversible?

A

Eosinophilic degeneration

Axonal reaction is reversible

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28
Q

What occurs during the axonal reaction of brain neuron injury?

A

Secondary nerve cell change, following damage ot axon

Swelling and rounding of cell body

Central fragmentation and the disappearance of Nissl substance (central chromatolysis)

Migration of nucleus to periphery.

Reversible if axonal integrity is restored.

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29
Q

What is unique about the brain in the response to injury that involves scarring?

A

NOT fibrous (no fibroblasts nor collagen deposition)

Instead, a glial scar forms comprised of reactive astrocytes.

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30
Q

What are the steps in the formation of a glial scar?

A

Astrocytosis - proliferation of astrocytes

Formation of reactive astrocytes - swelling of cytoplasm, fine processes are visible (star-like)

Gliosis - laying down of the scar (glial fibers coalesce made of glial fibrillary acidic protein, GFAP)

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31
Q

What occurs during astrocytosis?

A

Proliferation of astrocytes

Step 1 in the process of glial scar formation

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32
Q

What are reactive astrocytes?

A

Swollen, eosinophilic astrocytes with fine processes that contain glial fibers (looks star-like)

Step 2 in formation of glial scars

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33
Q

What occurs durin Gliosis?

A

Glial fibers coalesce and form the glial scar

Scar is made of glial fibrillary acidic protein (GFAP)

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34
Q

What is GFAP?

A

Glial fibrillary acidic protein

Makes up glial scars when coalesced

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35
Q

What makes up a glial scar?

A

Coalesced glial fibers made up of GFAP

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36
Q

What is the role of microglial cells in the brain response to injury?

A

Proliferate and accumulate within 5 days

Encircle degenerating neurons and form clusters around necrotic brain tissue (microglial nodules)

Activated microglial cells differentiate into macrophages (same function as in rest of body)

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37
Q

What are microglial nodules?

A

Clusters of microglia that encircle degenerating neurons and necrotic brain tissue

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38
Q

What is vasogenic edema?

A

Failure of tight junctions and astrocytic processes of BBB

Allows fluid and protein into cerebral parenchymal extracellular space

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39
Q

Which type of brain edema is responsive to steroids and osmotic therapy?

A

Vasogenic edema

Caused by failure of tight junctions and astrocytic processes of BBB

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40
Q

What is cytotoxic edema?

A

Derangement in cellular metabolism causes failure of ATP-dependent transport (Na, Ca)

Intracellular retention of Na, water follows

Astrocytes, capillary endothelial cells, neurons all SWELL

BBB in tact

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41
Q

Which type of brain edema is not responsive to steroids or osmotic agents?

A

Cytotoxic edema

BBB intact - caused by cellular metabolic failure (retention of Na, water follows)

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42
Q

When do you see vasogenic edema?

A

Tumors

Brain abscesses

Trauma

Inflammation

Hypertension

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43
Q

When do you see cytotoxic edema?

A

Ischemia

Hypoxia

Asphyxia

Intoxication

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44
Q

What is the Monroe-Kellie Doctrine?

A

Idea that the skull has a fixed volume and must accomodate variable volumes of brain, blood and CSF

Blood and CSF can be shunted to an extent, but beyond it, changes in either volume will result in increase in intracranial pressure

Cerebral Perfusion Pressure : CPP

Mean Arterial Pressure : MAP

Intracranial Pressure : ICP

CPP = MAP - ICP

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45
Q

What are symptoms of increased intracranial pressure?

A

Headache

Nausea

Vomiting

Bradychardia

Hypertension

Loss of consciousness

Papilledema

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46
Q

What is neuronal plasticity?

A

The change or adaptation of neuronal function and structure with activity/experience

The brain may not gain or lose many neurons, but as signals are transmitted, the neurons change over time. So the same stimulus is essentially acting on a ‘different’ neuron the second time.

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47
Q

Which type of signaling is portrayed in a “Classical” synapse?

A

Axo-dendritic synapse (Glutamatergic excitatory)

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48
Q

What type of synapse is glutamate involved in?

A

Axo-spinous (Axo-dendritic)

Classical

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49
Q

What type of synapse is GABA and the monoamines involved in?

A

Axo-dendritic

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50
Q

How are most signals between neurons transmitted?

A

Chemically via neurotransmitters and neuromodulators

Only a very small percentage are transmitted via electric signals where the two neurons share ion channels.

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51
Q

What are the seven steps of synaptic transmission?

A
  1. Nerve impulse (action potential) invades presynaptic nerve terminal.
  2. Activation of Ca2+ channels and entry of Ca2+ into nerve terminal.
  3. Ca2+ triggers neurotransmitter release via exocytosis.
  4. Released neurotransmitter activates pre- and postsynaptic receptors.
  5. Receptor activation regulates channels to yield postsynaptic currents.
  6. Released neurotransmitter is removed from synapse.
  7. Vesicles involved in exocytosis are recaptured by endocytosis.
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52
Q

What are the steps in vesicular transport and recycling?

A

Docking to the active zone

Priming in an ATP-mediated manner

Fusion mediated by increased intracellular calcium levels

Clathrin-mediated endocytosis

Recycling and vesicular neurotransmitter transport (acidified on the inside to aid in travel towards synaptic cleft)

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53
Q

Why are vesicles acidified on the inside?

A

To aid in moving down the length of the axon of a neuron (charge)

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54
Q

What mediates vesicular endocytosis of vesicles in neurons?

A

Clathrin

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55
Q

What types of changes occur in the post-synaptic neuron that are responsible for plasticity?

A

Activation of second messengers causes transient adaptations, but the plasticity is introduced when these messengers affect transcription factors

This alters target gene expression which can alter the long-term function of neurons

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56
Q

What are the amino acid neurotransmitters?

A

Glutamate

GABA (gamma- aminobutyric acid)

Glycine

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57
Q

What are the monoamine neurotransmitters?

A

dopamine

norepinephrine (noradrenalin)

epinephrine (adrenalin)

serotonin

melatonin (only in pineal gland)

acetylcholine

histamine

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58
Q

What are the nucleoside neurotransmitters

A

adenosine

ATP

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59
Q

What are the lipid-derived neurotransmitters?

A

Anandamine

2-AG

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60
Q

What is a gas neurotransmitter?

A

Nitric Oxide (NO)

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61
Q

What type of neurotransmitter is Glutamate?

A

Amino Acid

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62
Q

What type of neurotransmitter is GABA?

A

Amino Acid

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63
Q

What type of neurotransmitter is Glycine?

A

Amino Acid

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64
Q

What type of neurotransmitter is dopamine?

A

monoamine

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65
Q

What type of neurotransmitter is norepinephrine?

A

monoamine

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66
Q

What type of neurotransmitter is epinephrine?

A

monoamine

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67
Q

What type of neurotransmitter is serotonin?

A

monoamine

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68
Q

What type of neurotransmitter is melatonin?

A

monoamine

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69
Q

What type of neurotransmitter is acetylcholine?

A

monoamine

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70
Q

What type of neurotransmitter is histamine?

A

monoamine

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71
Q

What type of neurotransmitter is adenosine?

A

nucleoside

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72
Q

What type of neurotransmitter is ATP?

A

nucleoside

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73
Q

What type of neurotransmitter is anandamide?

A

lipid-derived

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74
Q

What type of neurotransmitter is 2-AG?

A

lipid-derived

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75
Q

What type of neurotransmitter is Nitric Oxide?

A

gas

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76
Q

What types of receptors are referred to as ionotropic?

A

Ligand-gated channels

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77
Q

What kind of receptors are referred to as metabotropic?

A

G protein-coupled receptors (GPCRs)

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78
Q

Which neurotransmitter is the major excitatory neurotransmitter in the brain?

A

Glutamate

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79
Q

What does glutamate signal through?

A

Ligand gated Na (and sometimes Ca) channels - AMPA, NMDA, Kainate (rapid neurotransmission)

GPCRs - mGluR1-8 (autoreceptor, modulatory)

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80
Q

Where is glutamate found?

A

ubiquitous

Only a small fraction is packaged into vesicles to act as a neurotransmitter

(krebs cycle and metabolism use glutamate)

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81
Q

What role do astrocytes play in glutamatergic neurotransmission?

A

Regulatory, sequester glutamate and modify it to glutamine via glutamine synthetase

Help provide a glutamate-glutamine shunt to buffer glutamate levels, protecting neurons from excitotoxicity which can lead to death.

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82
Q

What are the catecholamines?

A

Dopamine

Norepinephrine

Epinephrine

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83
Q

What are the indolamines?

A

Serotonin

Melatonin

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84
Q

How do ionotropic receptors work?

A

Neurotransmitter binds to site on multi-subunit ion channel.

Binding opens the channel, allowing ion flow in or out of neuron.

This creates a rapid postsynaptic current.

Glutamate, ACh, serotonin, and nucleosides activate Na (and Ca) channels - excitatory

GABA, glycine activate Cl channels - inhibitory

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85
Q

How do metabotropic receptors work?

A

Neurotransmitter binds to site on single polypeptide protein.

Binding triggers conformational change in G proteins.

Released subunites then either directly or indirectly regulate ion channels

Gi -> activate K channels or inhibit Ca channels.

Also have second messengers.

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86
Q

How do neurotrophic factors transmit signals?

A

Bind to plasma receptors that leads (directly or indirectly) to protein tyrosine kinase activation.

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87
Q

How do steroid hormones work in neurotransmission?

A

Hormones diffuse passively into cytoplasm, where they bind to the steroid receptor

This can translocate to nucleus and act on DNA as a transcription factor.

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88
Q

What are autoreceptors?

A

They are receptors expressed on nerve terminals that respond to the neurotransmitter released by those terminals.

They are linked to Gi, such that activation inhibits the nerve terminal, blocking further neurotransmitter release.

NEGATIVE FEEDBACK

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89
Q

How do neurons prevent a continual release of neurotransmitter from their axonic terminal?

A

Autoreceptors provide negative feedback that inhibits neurotransmitter release

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90
Q

What packages glutamate into vesicles?

A

Vesicular glutamate transporters (VGluT)

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91
Q

What is the major inhibitory neurotransmitter in the brain and spinal cord?

A

GABA

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92
Q

What big-picture role does GABA play in the body?

A

Regulates the level of consciousness

Too much : sleep, coma or dead

Too little: seizures, dead

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93
Q

What does GABA signal through?

A

ionotropic receptors (Cl): GABA-A => fast inhibitory signaling

metabotropic receptors: GABA-B, GABA-C => slower modulatory inhibiting signaling

autoreceptors (GABA-B)

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94
Q

What are the autoreceptors for glutamate?

A

metabotropic (mGluR)

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95
Q

What are the autoreceptors for GABA?

A

GABA-B (metabotropic)

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96
Q

How is GABA synthesized?

A

Glutamate to GABA in a single step via Glutamic Acid Decarboxylase (GAD)

Degraded by GABA transaminase

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97
Q

How is GABA degraded?

A

GABA transaminase

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98
Q

What sort of drugs act on glutamatergic synapses?

A

psychotomimetic (psychosis inducing) drugs

e.g. phencyclidine and ketamine act on NMDA as antagonists

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99
Q

What sorts of drugs act on GABAergic synapses?

A

anticonvulsant drugs and sedative-hypnotics

anticonvulsants promote GABAergic transmission (increase GABA synthesis or blocking reuptake)

sedative-hypnotics promote GABA-A receptor function (benzodiazepines, barbituates)

Drugs that block GABA-A receptors induce seizures

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100
Q

Where does glycine act primarily?

A

Spinal cord

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101
Q

What is the function of glycine?

A

Major inhibitory neurotransmitter in the spinal cord

Along with GABA

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102
Q

What effect do blockers of glycine receptors have?

A

Convulsants (induce seizures)

e.g. strychnine

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103
Q

What is the receptor for glycine signaling?

A

Trychnine-sensitive glycine receptor (ionotropic)

This gates Cl

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104
Q

What is the effect of strychnine?

A

Induces seizures.

Blocks the strychnine-sensitive glycine receptor (which would normally be inhibitory)

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105
Q

What is the secondary role of glycine in neurotransmission?

A

Acting as a co-agonist for the NMDA glutamate receptor.

Binds to a novel site on the receptor (not responsive to strychnine), and enhances the activity of glutamate on the receptor.

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106
Q

What are all catecholamines derived from?

A

Tyrosine

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107
Q

Tyrosine is an important precursor to which neurotransmitters?

A

Catecholamines

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108
Q

In general, what type of effect to monoamines exert ?

A

Modulatory - widespread projections and most neurons are responsive to them, even though few cells signal through them. They can be seen as increasing or decreasing the gain on the effect of other signals

In contrast, glutamate and GABA act in a more point-to-point fashion that exert more binary responses

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109
Q

Broadly speaking, what is the target of most drugs that act on the nervous system?

A

Monoamine neurotransmitter systems

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110
Q

What is the rate limiting enzyme in the series of reactions that produces catecholamines from tyrosine?

A

Tyrosine hydroxylase (TH)

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111
Q

What is the rate-limiting substrate in the series of reactions that produces catecholamines from tyrosine?

A

L-DOPA (Dihydroxyphenylalanine)

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112
Q

What is the reaction that directly generates dopamine?

A

DOPA decarboxylase (also known as aromatic amino acid decarboxylase) converts L-DOPA to dopamine.

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113
Q

What is the precursor to dopamine?

A

L-DOPA.

DOPA decarboxylase (also known as aromatic amino acid decarboxylase) converts L-DOPA to dopamine.

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114
Q

What is the reaction that produces norepinephrine?

A

Dopamine beta-hydroxylase (DBH) converts dopamine to norepinephrine

occurs in noradrenergic neurons

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115
Q

What is the precursor to norepinephrine?

A

dopamine

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116
Q

What is the reaction that produces epinephrine?

A

phenylethanolamine-N-methytransferase (PNMT) converts norepinephrine to epinephrine

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117
Q

what is the precursor to epinephrine?

A

norepinephrine

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118
Q

What enzymes degrade the catecholamines?

A

monoamine oxidases (MAOs) and catechol-O-methyltransferase (COMT)

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119
Q

What is the function of monoamine oxidases (MAOs) and catechol-O-methyltransferase (COMT)?

A

Degrade catecholamines.

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120
Q

What packages catecholamines into vesicles for transport?

A

VMAT (vesicular monoamine transporter)

Packages dopamine, norepinephrine, epinephrine

Also does serotonin

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121
Q

What are the three nuclei of dopaminergic neurons in the brain?

A

Substantia nigra (SN)

Ventral tegmental area (VTA)

Arcuate nucleus

SN and VTA are in the midbrain, arcuate nucleus is in the hypothalamus

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122
Q

Where is the ventral tegmental area located and what does it contain?

A

midbrain

dopaminergic neuron nucleus

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123
Q

Where is the substantia nigra located and what does it contain?

A

Midbrain

Dopaminergic neuron nucleus

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124
Q

Where is the arcuate nucleus located and what does it contain?

A

hypothalamus

Dopaminergic neuron nucleus

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125
Q

Where do the substantia nigra dopamine neurons innervate (project to)?

A

The neostriatum (caudate-putamen).

This forms the nigrostriatal dopamien pathway.

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126
Q

What is the nigrostriatal dopamine pathway?

A

Between substantia nigra and striatum

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127
Q

Where do the ventral tegmental area dopamine neurons innervate (project to)?

A

Many regions in the forebrain (including nucleus accumbens, hippocampus, amygdala, and prefrontal cortex)

Crucial for reward, motivation, emotional memory, and executive planning

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128
Q

What is the mesocorticolimbic dopaminergic neuron pathway?

A

Projections from the Ventral tegmental area to various areas in the forebrain

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129
Q

Where do the arcuate nucleus dopamine neurons innervate (project to)?

A

Anterior pituitary

Inhibits prolactin secretion

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130
Q

What is the tuberoinfundibular dopaminergic neuron pathway?

A

From the arcuate nucleus to anterior pituitary

Dopamine inhibits prolactin secretion at the anterior pituitary

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131
Q

What type of receptors are dopamine receptors?

A

GPCRs

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132
Q

Which dopamine receptors are coupled to Gs?

A

D1 and D5 (D1 class)

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133
Q

Which dopamine receptors are coupled to Gi?

A

D2, D3, D4 (D2 class)

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134
Q

Which dopamine receptors serve as autoreceptors?

A

D2 class (D2, D3, D4)

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135
Q

Which neurons are lost in Parkinson’s Disease?

A

subsgtantia nigra dopamine neurons

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136
Q

What is a mainstay of treatment for Parkinsons and why?

A

L-DOPA (dopamine precursor), since it promotes dopamine synthesis

D-2 dopamine receptor agonists (D-2 also found post-synaptically)

Parkinson’s is caused by a selective loss of substantia nigra dopamine neurons

Muscarinic cholinergic antagonists are used to treat Parkinson’s disease, based on the role of cholinergic interneurons in regulating striatal function

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137
Q

Where to psychostimulant drugs work?

A

Dopaminergic synapses by maintaining high levels of dopamine in the synapse

Cocaine inhibits the dopamine transport (blocks reuptake)

Amphetamine ‘reverses’ it (causing release of dopamine from the transporter)

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138
Q

Where do most antipsychotic drugs work?

A

At dopaminergic synapses, blocking the D2 Receptors (either antagonists or partial agonists)

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139
Q

Which types of drugs block D2 receptors (antagonists or partial agonists)?

A

Antipsychotics

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140
Q

What is the main nucleus of noradrenergic (norepinephrine) neurons in the brain?

A

Locus Ceruleus in the pons

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141
Q

Where is the locus ceruleus located?

A

the pons

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142
Q

What is the locus ceruleus?

A

The main noradrenergic (norepinephrine) nucleus in the brain

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143
Q

Where do the noradrenergic neurons from the locus ceruleus project to?

A

Most of the forebrain

Therefore, most neurons in the forebrain are responsive to noradrenergic signals, even though only very few neurons produce norepinephrine (noradrenaline)

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144
Q

How does norepinephrine (noradrenergic) signaling occur?

A

Atypical

Released and travels long distances to exert its effect on many neurons

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145
Q

What does noradrenergic signaling control?

A

Vigilance and attention

Cenral control over ANS

Responses to stress and emotional behavior

Post-ganglionic sympathetic signaling

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146
Q

What type of receptors are noradrenergic receptors?

A

All are GPCRs

Beta (Gs)

Alpha-1 (Gq)

Alpha-2 (Gi) : autoreceptor

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147
Q

What type of drugs act on norepinephrine receptors?

A

Many drugs for cardiovascular disease and upper respiratory function

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148
Q

What type of receptors do many cardiovascular disease and upper respiratory funciton drugs target?

A

Noradrenergic receptors

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149
Q

What type of drugs inhibit norepinephrine reuptake?

A

Antidepressants

Used to treat chronic pain and ADHD

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150
Q

How are MAO inhibitors used?

A

Antidepressants

Block the breakdown of monoamines (norepinephrine)

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151
Q

What amino acid are serotonin and melatonin derived from?

A

Tryptophan

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152
Q

What is 5HT?

A

5-hydroxytryptamine

Serotonin

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153
Q

What is the other name for serotonin?

A

5HT (5-hydroxytryptamine)

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154
Q

What is the rate-limiting enzyme in the production of serotonin?

A

Tryptophan hydroxylase (TPH)

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155
Q

What is the rate-limiting substrate in the production of serotonin?

A

5-hydroxytryptophan

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156
Q

What enzyme converts 5-hydroxytryptophan to 5-hydroxytryptamine (serotonin)

A

aromatic amino acid decarboxylase (AADC)

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157
Q

How is melatonin synthesized?

A

From Tryptophan, through Serotonin, via an intermediate

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158
Q

How are serotonin and melatonin degraded?

A

monoamine oxidase (MAO)

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159
Q

What enzyme packages serotonin and melatonin into synaptic vesicles?

A

VMAT (Vesicular monoamine transporter)

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160
Q

Where are the serotinergic neuron nuclei located?

A

Brainstem

Most important is the dorsal raphe nucleus

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161
Q

Which is the most important serotonergic nucleus in the brain?

A

The dorsal raphe nucleus

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162
Q

What is the dorsal raphe nucleus?

A

Most important serotonergic nucleus in the brain

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163
Q

Where does the dorsal raphe nucleus project to?

A

All over the brain and spinal cord

Exert broad modulatory effects

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164
Q

What responses do serotonergic neurons regulate?

A

Stress responses and emotional behavior

Eating and weight control

Cicadian rhythms and sleep-wake cycles

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165
Q

How many serotonin receptors are there?

A

14

5HT-3 is the only ionotropic (Ligand-gated)

The rest (5HT-1, 5HT-2, 5HT-4-7) are metabotropic (GPCR)

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166
Q

Which serotonin receptors are metabotropic?

A

5HT-1 (Gi)

5HT-2 (Gq)

5HT-4-7(Gs)

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167
Q

Which serotonin receptors are ionotropic (ligand gated)?

A

5HT-3

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168
Q

Which serotonin receptors function as autoreceptors?

A

5HT-1 (coupled to Gi)

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169
Q

How do most antidepressant drugs work?

A

Inhibit serotonin reuptake (SSRIs and SNRIs)

Also MAO inhibitors

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170
Q

What function do drugs that inhibit serotonin reuptake have?

A

Antidepressants

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171
Q

Where do new antipsychotic drugs and hallucinogenic drugs act?

A

5HT-2A receptors

antipsychotics block (they also act on D2 receptors)

hallucinogens are partial agonists

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172
Q

What drugs act on the 5HT-2A receptors?

A

New antipsychotics (which also act on D2 receptors) act as antagonists (block)

Hallucinogens act as partial agonists

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173
Q

What are 5HT-2C receptors involved in?

A

Feeding responses

Agonists decrease feeding

Antagonists promote feeding and can result in obesity

(at hypothalamus)

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174
Q

Where do new anti-migrane drugs (triptans) work?

A

5HT-1D as agonists

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175
Q

What are triptans?

A

New anti-migrane drugs that act as 5HT-1D agonists

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176
Q

How is acetylcholine synthesized?

A

From choline in a single step via choline acetyltransferase

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177
Q

What enzyme makes acetylcholine from choline + Acetyl CoA?

A

Choline acetyltransferase

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178
Q

What enzyme breaks down acetylcholine?

A

Acetylcholinesterase

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179
Q

What enzyme packages acetylcholine into vesicles?

A

Vesicular acetylcholine transporter

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180
Q

Where is acetylcholinesterase located?

A

In the synapse

Breakes down ACh into Choline, which can be transported into neurons for recycling

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181
Q

Where are cholinergic neurons located in the brain?

A

Forebrain nuclei - medial septal nuclei + Nucleus basalis of Meynert

Brainstem nuclei - dorsolateral tegmentum in the pons

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182
Q

What is the medial septal nucleus?

A

One of the two forebrain cholinergic neuron nuclei

Also the nucleus basalis of Meynert

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183
Q

What is the nucleus basalis of Meynert?

A

Forebrain cholinergic neuron nucleus

Along with the medial septal nucleus

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184
Q

What is the dorsolateral tegmentum?

A

Brainstem cholinergic neuron nucleus, located in the pons

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185
Q

Where do the forebrain cholinergic neuron nuclei project to?

A

Hippocampus and other forebrain structures

Important for learning, memory and cognition

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186
Q

Where do the brainstem cholinergic neuron nuclei project to?

A

Widely - important for sleep-wake cycles

(this is the dorsolateral tegmentum)

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187
Q

Where are cholinergic interneurons located?

A

Striatum

Important role in modulating striatal-dependent motor function

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188
Q

Which type of neurons modulate striatal-dependent motor function?

A

cholinergic interneurons

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189
Q

What is the role of acetylcholine outside of the brain?

A

ANS: All preganglionic sympathetic and parasympathetic, and most postganglionic parasympathetic

Somatic motor system: NMJ is cholinergic (with nicotinic receptors)

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190
Q

What receptors does acetylcholine act on?

A

Nicotinic (ligand-gated; ionotropic)

Muscarinic (GPCR; metabotropic) : autoreceptors

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191
Q

What are nicotinic receptors?

A

ligand-gated (ionotropic) acetylcholine receptors

Nicotinic receptors flux Na+ and Ca2+, thereby mediating excitatory postsynaptic currents

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192
Q

What type of currents do nicotinic receptors mediate?

A

Nicotinic receptors flux Na+ and Ca2+, thereby mediating excitatory postsynaptic currents

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193
Q

What does nicotine do?

A

Strong partial agonist at central cholinergic receptors

Actiavtes VTA (ventral tegmental area) dopamine neurons to promote reward

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194
Q

Why are muscarinic cholinergic antagonists are used to treat Parkinson’s disease?

A

Because cholinergic interneurons in regulating striatal function

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195
Q

What are acetylcholinesterase inhibitors used to treat?

A

Dementia due to their role in hippocampal circuits

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196
Q

What is the mechanism of the cardiovascular and related side effects (constipation, dry mouth, blurred vision) of many drugs?

A

Muscarinic receptor antagonism

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197
Q

How does botulinum toxin (botox) work?

A

Blocks ACh release

198
Q

How does curare work?

A

blocks neuromuscular junctions NMJs

nicotinic receptor antagonist - causes paralysis

199
Q

How is histamine synthesized?

A

In a single step from histidine, via histidine decarboxylase

200
Q

Where are histaminergic neurons located?

A

In the tuberomammillary nucleus in the hypothalamus

201
Q

Where is the tuberomammillary nucleus located?

A

Hypothalamus

202
Q

What is the tuberomammillary nucleus?

A

Nucleus of histaminergic neurons in the hypothalamus

203
Q

Where does the tuberomammillary nucleus project to?

A

Widespread throughout the brain

204
Q

What is the primary effect of histamine in the brain?

A

To regulate alertness and sleep-wake cycles (sedation)

205
Q

What type of receptors does histamine act on?

A

Metabotropic (GPCRS)

H1 is the most important in the brain (antihistamines)

H2 inhibits stomach acid

H3 is an autoreceptor

206
Q

What is the H1 receptor involved in?

A

Histaminergic neurotransmission in the brain (and elsewhere)

Major player in the brain

207
Q

What is the H2 receptor involved in?

A

Stomach acid secretion in the stomach

208
Q

What is the H3 receptor involved in?

A

Autoreceptor for histamine in the brain.

209
Q

What is a major difference between peptide neurotransmitters and small molecule neurotransmitters?

A

Peptides must be synthesized in the cell body and transported to terminals.

They are also degraded enzymatically once released, which is irreversible

As a result, they represent an energetically expensive process

210
Q

What types of receptors do peptide neurotransmitters act on?

A

GPCRs - metabotropic

211
Q

What is the general scheme of peptide neurotransmitter synthesis?

A

Prepropeptide gene - encodes prepropeptide mRNA - produces prepropeptide in the ER - proteolytically processed into propetide - further processed into mature peptide

212
Q

What is POMC

A

Proopiomelanocortin - a small peptide that can be proteolytically cleaved into a variety of different neurotransmitter signals

213
Q

What are some functions of peptide neurotransmitters?

A

Hypothalamic releasing and inhibitory factors (CRH, TRH, GnRH, GHRH, somatostatin)

Feedign and gut-brain peptides (Neuropeptide Y, alpha-MSH, cholecystokinin, glucagon-related peptide, vasoactive intestinal polypeptide)

Tachykinins (e.g. substance P) - involved in nociception (pain control)

214
Q

What is meant by co-transmission?

A

The notion that neurons that signal through peptides also signal through small molecules such as glutamate or monoamines

215
Q

What is another name for orexin?

A

hypocretin

216
Q

What is hypocretin?

217
Q

What type of neurotransmitter is orexin?

218
Q

Where are orexinergic neurons located?

A

In the lateral hypothalamus

219
Q

Where do orexinergic neurons from the lateral hypothalamus project to?

A

Widespread in the brain

220
Q

What type of receptors are orexin receptors?

A

GPCR - metabotropic

221
Q

What are the orexin receptors?

A

OX1 and OX2 (metabotropic GPCR)

222
Q

What is the role of orexin?

A

Promotes wakefulness

Orexinergic neurons project strongly to the histaminergic tuberomammillary nucleus and to the brainstem cholinergic nuclei, both critical for control over sleep vs. wakefulness

223
Q

Where do orexonergic neurons project strongly?

A

Orexinergic neurons project strongly to the histaminergic tuberomammillary nucleus and to the brainstem cholinergic nuclei, both critical for control over sleep vs. wakefulness

224
Q

What occurs in human narcolepsy?

A

Death of orexinergic neurons (autoimmune?)

Characterized by intrusive REM sleep during wakefulness

225
Q

What occurs when there is death of orexinergic neurons?

A

One thing that may occur is narcolepsy

226
Q

Apart from wakefulness, what are other functions that orexin modulates?

A

alertness

mood

reward

motivation

likely via strong projections to monoaminergic nuclei

227
Q

What are the three main types of opioid peptides?

A

Enkephalines (preproenkephalin)

Endorphins (prePOMC: preproopiomelanocortin)

Dynorphin (preprodynorphin)

228
Q

What type of neurotransmitter are the enkephalins?

A

opioid peptide

229
Q

What type of neurotransmitter are the endorphins?

A

opioid peptide

230
Q

What type of neurotransmitter is dynorphin?

A

opioid peptide

231
Q

Where is enkephalin synthesized?

A

Brain and spinal cord

232
Q

Where is dynorphins synthesized?

A

brain and spinal cord

233
Q

Where are endorphins synthesized?

A

hypothalamus

234
Q

Where do enkephalins act on?

A

mu and delta opioid receptors

Promote reward, positive mood, analgesia, sedation

235
Q

Where do endorphins act on?

A

mu and delta opioid receptors

promote reward, positive mood, analgesia, sedation

236
Q

Where do dynorphins act on?

A

kappa opioid receptors

promote analgesia and sedation,

Induce negative mood state

237
Q

Which opioid peptides induce a negative mood state?

A

Dynorphins

238
Q

Which opioid receptors induce a positive mood state?

A

Enkephalins and endorphins

239
Q

What receptors do opiate drugs generally act on?

A

mu opioid receptors as agonists

No difference between prescribed and illicit opiates, just pharmacokinetics

240
Q

What role do nucleosides play as neurotransmitters?

A

Modulatory

Likely to be ubiquitous

241
Q

Which nucleoside neurotransmitter is packaged in most vesicles?

242
Q

What type of receptors do nucleosides signal through?

A

Both ligand-gated (ionotropic) and GPCRs (metabotropic)

243
Q

What is the role of adenosine?

A

Regulation of sleep

Adenosine accumulates during wakefulness to promote sleep

Sleep redues adenosine levels

244
Q

What is the effect of sleep on adenosine levels?

A

Reduces them

Adenosine accumulates during wakefulness and promotes sleep

245
Q

What is an example of an adenosine receptor antagonist?

A

Caffeine

Promotes wakefulness

246
Q

What type of drug is caffeine?

A

Adenosine receptor antagonist

Promotes wakefulness

247
Q

What are lipid-derived neurotransmitters derived from?

A

arachidonic acid

Anandamide and 2-arachidonoylglycerol (2-AG)

known as endocannabinoids

248
Q

What are the endocannabinoids?

A

anandamide and 2-AG

249
Q

What are the receptors for the endocannabinoids?

A

Cannabinoid receptors CB1 and CB2 (GPCRs)

250
Q

What are the effects of cannabinoid drugs mediated through?

A

Activation of CB1 receptors

251
Q

What is marijuana?

A

Cannabinoid drug that activates CB1 receptors

252
Q

What is the effect of endocannabinoids?

A

Regulate perception, appetite, nociception, reward, and level of consciousness

253
Q

How do endocannabinoids transmit signal?

A

Endocannabinoids are synthesized postsynaptically in response to Ca2+ influx, and are then released (presumably by passive diffusion) into the synapse where they act on CB1 receptors located on nearby nerve terminals to regulate neurotransmitter release

Retrograde

254
Q

Which neurotransmitters function in a retrograde manner?

A

Endocannabinoids

Nitric Oxide

Endocannabinoids are synthesized postsynaptically in response to Ca2+ influx, and are then released (presumably by passive diffusion) into the synapse where they act on CB1 receptors located on nearby nerve terminals to regulate neurotransmitter release

NO is synthesized by nitric oxide synthase (activated by Ca2+)

255
Q

What triggers endocannabinoid synthesis and release?

A

Endocannabinoids are synthesized postsynaptically in response to Ca2+ influx, and are then released (presumably by passive diffusion) into the synapse where they act on CB1 receptors located on nearby nerve terminals to regulate neurotransmitter release

256
Q

What triggers Nitric Oxide synthesis and release?

A

Synthesized post-synaptically in response to Ca2+ influx by nitric oxide synthase, a Ca2+ activated enzyme

Then it diffuses into the synapse, where it enters nerve terminals passively

257
Q

What is the effect of Nitric Oxide?

A

Once diffused into nerve cells (retrograde), it activates many enzymes, such as guanylyl cyclase, which synthesizes cyclic GMP (cGMP), modulating the release of neurotransmitters by these neurons

258
Q

What is the main role of Nitric Oxide?

A

Neuromodulatory in the brain like endocannabinoids

Excitatory feedback

259
Q

What is the resting potential of a neuron?

260
Q

What ion mostly determines a neuron’s membrane potential?

261
Q

What ions contribute to the resting potential of a neuron?

A

K+ (most important) E = -75mV

Na: E = +40mV

Cl: E = -80mV

262
Q

At rest, which ion channels are mostly open and closed?

A

Open: K+ channels

Closed: Na+ and Cl- channels

263
Q

What is the ionic basis of an action potential?

A

Depolarization induces the opening of Na+ channels (faster) and K+ channels (slower)

This induces further depolarization until the Na+ channels close and inactivate (refractory period)

K+ channels then bring the potential back down again

264
Q

Where do local analgesics act?

A

Block voltage-gated Na+ channels

265
Q

How is tonic (pacemaker) action potential firing mediated?

A

Often mediated by the presence of HCN channels, which are activated (gated) by cyclic AMP

266
Q

What is the axon hillock?

A

Triggering point of an action potential (base of the axon)

267
Q

Why do action potentials only travel in one direction?

A

Refractory period prevents activation again

268
Q

What types of ion channels are located at the nerve terminals?

A

Voltage-gated Ca2+ channels

Open when nerve terminal is depolarized, which allows entry of calcium, and the release of neurotransmitters

269
Q

Why do muscle units reliably contract in response to every presynaptic action potential?

A

1) there is a very high probability of acetylcholine release in response to each action potential
2) the muscle endplate—through extensive folding—provides a large surface area of nicotinic acetylcholine receptors.

270
Q

What is Myasthenia Gravis?

A

autoimmune disorder caused by auto-antibodies directed against the nicotinic cholinergic receptor or another postsynaptic protein

Characterized by muscle weakness, often around the eye (ptosis, blurred vision)

Test by treating with cholinesterase inhibitor to releive symptoms

271
Q

How can you diagnose Myasthenia Gravis?

A

Treatment with cholinesterase inhibitor - instant releif of symptoms

272
Q

What is Eaton-Lambert syndrome?

A

Condition similar to Myasthenia Gravis caused by autoantibodies to presynaptic terminal (often voltage-gated Ca2+ channels)

Muscle weakness of limbs

273
Q

What is the difference between Myasthenia Gravis and Eaton-Lambert syndrome?

A

MG affects postsynaptic terminal (autoantibodies to nAChR) while EL affects the pre-synaptic terminal

274
Q

What is the activity of the Na+/K+ ATPase (Na+/K+ Pump)?

A

Pumps 3 Na+ out of the cell and 2 K+ into the cell

restores the ionic gradient and the resting potential in the neuron

Electrogenic

275
Q

What is the action of cardiac glycosides?

A

Inhibit the Na+/K+ pump and increase strength of cardiac muscle contraction

e.g. ouabain, digitalis

276
Q

What are some cardiac glycosides?

A

ouabain

digitalis

Inhibit the Na+/K+pump and increase strength of cardiac muscle contraction

277
Q

What is the action of ouabain, digitalis?

A

Inhibit Na+/K+ pump and increase strength of cardiac muscle contraction

278
Q

What is the relationship between speed of electrical conduction (speed of action potential propagation) and axon caliber?

A

Directly proportional - myelination makes it so that you don’t need HUGE axons for fast transmission

279
Q

What is the difference in conductance between myelinated and non-myelinated axons?

A

Myelinated axons are wrapped in myelin sheath which greatly increases speed of action potential propagation

Non-myelinated are slow, since the propagation is continuous and every segment must be depolarized to threshold

280
Q

What is present at Nodes of Ranvier?

A

NO myelin

Nodes are enriched in voltage-gated Na+ channels bordered by regions rich in K+ channels.

281
Q

Which cell types form myelin sheaths?

A

Oligodendrocytes

282
Q

What type of conduction is enabled by myelin?

A

saltatory - jumping from one node of Ranvier to the next

283
Q

Which disease is caused by autoimmune destruction of myelin sheaths?

A

Multiple Sclerosis (MS)

Any part of the CNS can be affected - highly variable symptoms

Can lead to the destruction of underlying axon (excitotoxicity)

284
Q

What is MS?

A

Multiple Sclerosis

Autoimmune destruction of myelin sheaths

Affects any part of the CNS - highly variable symptoms

Can lead to the destruction of underlying axon - excitotoxicity

285
Q

How is pain perceived?

A

In two waves:

Aδ fibers are larger and heavily myelinated - conduct quickly

C fibers are smaller and not myelinated - conduct slower

286
Q

What are Aδ fibers?

A

Pain sensation (nociception) fibers that transmit quickly - thick and heavily myelinated

287
Q

What are C fibers

A

Pain sensation (nociception) fibers that transmit signals slowly - thin and non-myelinated

288
Q

Can a single synaptic potential initiate an action potential?

A

No

an action potential might require dozens or hundreds of synaptic potentials that summate in time or space

289
Q

What is an EPSP or EPSC?

A

Excitatory postsynaptic potential or excitatory postsynaptic current

Need to be summed in space or time in order to trigger an action potential

290
Q

What are large EPSP (EPSC)’s mediated by?

A

glutamate

more specifically, by glutamate acting on ionotropic glutamate receptors (mostly AMPA receptors)

291
Q

What are large, fast IPSP (IPSC)’s mediated by?

A

GABA (and glycine in spinal cord)

mainly by acting on ionotropic GABA receptors (GABA-A receptors) (glycine acts on ionotropic glycine receptors)

292
Q

What determines whether or not a neuron will display an action potential?

A

Dozens (hundreds) of EPSPs and IPSPs summate at a single neuron to determine whether that neuron will display an action potential

293
Q

What is the difference between metabotropic and ionotropic (GPCR and ligand-gated) channel signaling with respect to EPSP’s and IPSPs?

A

Most G protein-coupled receptors give rise to smaller and slower EPSPs or IPSPs. This is why the neurotransmitters that mediate these responses are sometimes referred to as neuromodulators. These neuromodulatory actions modulate the ability of ionotropic receptors to trigger an action potential

294
Q

What is an EEG?

A

Electroencephalogram

Surface electrodes detect potentials from surface areas of brain

Can show potentials that originate from synchronous activity at populations of synapses

Big oscillations are not normal - show seizure activity

295
Q

What is post-tetanic potentiation (PTP)?

A

An example of short-term plasticity

Response to a signle stimulus is enhanced after a tetanus (period of high frequency stimulation)

296
Q

What is tetanus?

A

A period of high frequency stimulation

297
Q

What is paired-pulse facilitation (PPF)?

A

When a single stimulus occurs soon after an earlier one, a larger postsynaptic potential is produced (Excess Ca2+ is still in the terminal)

298
Q

What are two short-term forms of neural plasticity

A

Post-tetanic potentiation (PTP)

Paired-pulse facilitation (PPF)

299
Q

How is short-term potentiation acheived?

A

By the buildup of Ca2+ in a pre-synaptic terminal or the depletion of vesicles

300
Q

What is NMDAR-dependent LTP?

A

NMDA receptor dependent long-term potentiation

Can be brought about by tetanus which induces high levels of Ca2+ into post-synaptic spines. This activates CaMKII, which phosphorylates AMPA receptors and drives their insertion to the synapse

Also accompanied by changes in gene expression

Other non NMDAR-dependent mechanisms also present

301
Q

What is NMDAR dependent LTD?

A

NMDA receptor dependent long-term depression

Can be brought about by low-frequency stimulation which induces low Ca2+ entry, and activates Calcineurin, which removes AMPA receptors from the synaptic terminal.

Also accompanied by changes in gene expression

Other forms exist too

302
Q

What changes occur in plasticity?

A

Both in function and in morphology

E.g. neuronal spine morphology changes over time.

303
Q

How can you distinguish between an axon and a dendrite?

A

Axons keep their diameter throughout their length

Dendrites thin out as you get further away from the soma

304
Q

How do axons and dendrites differ in their microtubule arrangement?

A

In axons, MTs are aligned

In dendrites, MTs are not

305
Q

Bipolar neurons are important in what functions?

A

Sensory

Vision, audition, balance

306
Q

Where are unipolar neurons important?

A

Dorsal Root Ganglia

307
Q

What is a bouton?

A

The swelling at an axon terminal

308
Q

What is a telodendron?

A

The entire array of terminals for one axonal process

309
Q

What are multipolar neurons?

A

Prototypical neurons

They have 3-5 primary dendrites emanating from the cell body, and an axon emerging from the axon hillock. They are found throughout the CNS.

310
Q

What are bipolar neurons?

A

Have a single process, with the cell body located directly along the course of that process. The distal extension is the dendrite, and the proximal part of the process (directed toward the CNS) is the axon.

Primarily involved in sensation

311
Q

What are unipolar neurons?

A

Have a single process that extends proximally and distally from a short segment of the process that connects it to the cell body.

Although both parts of the process of a unipolar neurons are properly called “neurites”, the distal and proximal parts of the process are often referred to as the dendrite and the axon, respectively.

312
Q

What are pyramidal cells?

A

Pyramidal cells vary in size, but have a stereotypical shape: a pear- shaped soma, several dendrites (called basal dendrites) emerging from the base of the soma, a large and highly branched dendrite emerging from the apex of the soma (called the apical dendrite), and an axon that issues from the base of the cell body.

Most have spiny dendrites

Involved in signal processing and integration

313
Q

What are granule cells?

A

Granule cells are smaller, and are often star-shaped (stellate) because the dendritic tree radiates out in all directions from the soma.

Granule cells provide much of the local (regional) information processing.

314
Q

What are projection cells?

A

Neurons with long axons are projection cells

315
Q

What are interneurons?

A

Neurons with short axons are called interneurons or local circuit neurons

Many are inhibitory

316
Q

What are amacrine cells?

A

Axon-less neurons are called amacrine cells

Found mostly in the retina and olfactory bulb (rare)

317
Q

What is special about en passant synpases?

A

They occur partway along the axon as it extends

318
Q

Describe a motor end plate (neuromuscular junction, NMJ).

A

Consists of enlarged terminal containing synaptic vesicles, junctional folds, an enlarged synaptic cleft, and the muscle sole plate. It is covered by oligodendrocyte cytoplasm and basal lamina.

319
Q

Where are fibrous astrocytes found?

A

White matter

320
Q

What type of astrocytes are found in white matter?

321
Q

Where are protoplasmic astrocytes found?

A

Gray matter

322
Q

What type of astrocytes are found in gray matter?

A

Protoplasmic

323
Q

What are the two components of the brain?

A

Cerebrum

Brainstem

324
Q

What are the three components of the brainstem?

A

Medulla oblongata

Midbrain

Pons/Cerebellum

325
Q

Where do the rostral-caudal, anterior-posterior, dorsal-ventral, superior-inferior axes refer to?

326
Q

What is the axial/horizontal plane?

327
Q

What is the coronal/frontal plane?

328
Q

What is the (para/mid)saggital plane?

329
Q

What are the eight bones of the cranium?

A

Frontal

Parietal (2)

Occipital

Temporal (2)

Sphenoid

Ethmoid

330
Q

What are the four sutures of the cranium?

A

Coronal

Lamboid

Saggital

Temporal/parietal (squamosal)

331
Q

What are the three main compartments in the base of the skull?

A

Anterior Fossa

Middle Fossa

Posterior Fossa

332
Q

Which bones does the coronal suture join?

A

Frontal + 2 parietal

333
Q

What bones does the lamboid suture join?

A

2 Parietal + occipital

334
Q

What bones does the sagittal suture join?

A

The two parietal bones

335
Q

What bones does the temporal/parietal (squamosal) suture join?

A

The temporal and parietal bones

336
Q

Where does the spinal cord pass through the skull?

A

Foramen magnum

337
Q

How many vertebrae are there?

A

~30

7 Cervical

12 Thoracic

5 Lumbar

5 Sacral

1 Fused coccygeal (or 4 independent - giving you 33 total)

338
Q

How many pairs of spinal nerves are there?

A

31

8 cervical

12 thoracic

5 lumbar

5 sacral

1 coccygeal

339
Q

Where does the cauda equina start?

A

L1/L2 - important for lumbar punctures

340
Q

What are the three layers of the meninges?

A

Pia mater

Arachnoid mater

Dura mater

(From closest to outermost)

341
Q

What are the four dural folds (reflections)?

A

falx cerebri (between the two cerebral hemispheres)

tentorium cerebelli (overlying the cerebellum)

falx cerebelli (between the two cerebellar hemispheres)

diaphragma sellae (forming a roof over the pituitary fossa, perforated by the pituitary stalk)

342
Q

What is the falx cerebri?

A

A dural fold that seperates the two hemispheres of the brain

343
Q

What is the tentorium cerebelli

A

Dural fold that overlies the cerebellum

344
Q

What is the diaphragma sellae?

A

Dural fold that overlies the pituitary

345
Q

What is the falx cerebelli?

A

A dural fold that separates the hemispheres of the cerebellum

346
Q

How many layers of dura are there in the cerebrum?

A

2

outer lines the skull and serves as the periosteum (rich in vasculature)
inner follows the arachnoid in most places except in the sinuses

347
Q

What is a dural sinus?

A

Area where the outer and inner layer of the dura are not connected (allows for venous blood and other structures to course through (particularly in the cavernous sinus

348
Q

What is the superior longitudinal sinus?

A

Prominent dural sinus present at the sagittal midline, at the junction of the dural cap and the falx cerebri

349
Q

What is the coccygeal ligament comprised of?

A

Dura

Runs from the end of the spinal cord and attaches at the coccyx

350
Q

What are subarachnoid cisterns?

A

Areas in the brainstem, spinal cord and brain where the space between the pia mater and the arachnoid mater is particularly large and is filled with CSF

Quadrigeminal cistern

Interpeduncular cistern

Pontine cistern

Cisterna Magna

Lumbar cistern

351
Q

What is significant about the lumbar cistern?

A

It is a great place to extract CSF since the conus medullaris terminates rostral to it

352
Q

Where are arachnoid villi (granulations) most common?

A

along the interhemispheric fissure, associated with the superior longitudinal sinus

353
Q

What are arachnoid trabecula?

A

Parts of the arachnoid mater that extend down and connect to the pia mater - forming columns that give the subarachnoid space it’s shape

354
Q

How many layers does the pia have?

A

2

The inner one, the intima pia, adheres to the underlying nervous tissue and forms the outer wall of perivascular spaces where blood vessels enter and exit the CNS. It is avascular.

The more superficial layer, the epipia, is continuous with the arachnoid trabeculae. It is well developed in the spinal cord, but not in brain. It anchors the spinal cord to the vertebrae

355
Q

What is the intima pia?

A

The inner layer of the pia mater, that reliably follows the spinal cord

356
Q

What is the epipia?

A

The outer layer of the pia mater that anchors the spinal cord to the vertebrae via dentate ligaments

357
Q

What is a dentate ligament?

A

Outer layer of pia mater (epipia) that extends out and anchors the spinal cord laterally to the vertebrae

358
Q

What is the filum terminale compsed of?

359
Q

What are differences in the meninges between the cerebrum and the spinal cord?

A
  1. In the cerebrum, there are two distinct layers of dura. In the spinal cord, while there are trace cellular elements of a periosteal (outer) dura, for all intents and functional purposes there is only one dural layer.
  2. The cerebrum has essentially a single pial layer whereas the spinal cord has two distinct pial layers.
  3. The blood vessels of the spinal cord are in the epipial layer. Cerebral blood vessels lie on the surface of the intima pia, within the subarachnoid space.
  4. Although arachnoid villi have been described in the spinal region, they are far less common than in the cerebrum.
360
Q

Identify the central sulcus

361
Q

Identify the lateral sulcus (Sylvian fissure)

362
Q

Identify the frontal lobe

363
Q

Identify the temporal lobe

364
Q

Identify the parietal lobe.

365
Q

Identify the occipital lobe

366
Q

Identify the precental sulcus

367
Q

Identify the precental gyrus. What does it control?

A

Primary MOTOR cortex

368
Q

Identify the superior frontal sulcus

369
Q

Identify the inferior frontal sulcus

370
Q

Identify the 1st (superior) frontal gyrus

371
Q

Identify the 2nd (middle) frontal gyrus.

372
Q

Identify the 3rd (inferior) frontal gyrus.

373
Q

Identify Broca’s Area. What is it’s function?

A

Speech production

Of note - it is asymmetric; stronger on left (in most people)

374
Q

Identify the frontal pole

375
Q

Identify the postcentral gyrus. What is its function?

A

Primary SOMATOSENSORY cortex

376
Q

Identify the postcentral sulcus

377
Q

Identify the intraparietal sulcus

378
Q

Identify the superior parietal lobule

379
Q

Identify the inferior parietal lobule. What is its function?

A

Primary vestibular cortex (synthesis of information, conscious perception of balance)

380
Q

Identify the occipital pole. What function is associated with it?

381
Q

Where is the interhemispheric fissure?

A

Between the two hemispheres of the brian.

382
Q

Identify the superior temporal sulcus

383
Q

Identify the superior temporal gyrus

384
Q

Identify Heschl’s Gyri. What is its function?

A

Primary auditory cortex

385
Q

Identify Wernicke’s Area. What is it’s function?

A

Speech recognition/comprehension

386
Q

Identify the temporal pole

387
Q

Identify the middle temporal sulcus/gyrus

388
Q

Identify the inferior temporal sulcus/gyrus

389
Q

Where is the insular lobe? What is it’s function?

A

Primary GUSTATORY cortex

390
Q

Identify the frontal pole (and occipital pole).

391
Q

Identify the central sulcus

392
Q

Identify the olfactory bulb

393
Q

Identify the olfactory tract

394
Q

Identify the olfactory stria

395
Q

Identify the anterior perforated space (substance).

396
Q

Identify the olfactory fissure.

397
Q

Identify the gyrus rectus.

398
Q

Identify the orbital gyrus.

399
Q

Identify the primary olfactory cortex.

400
Q

Identify the optic nerve, chiasm, tract.

401
Q

Identify the pituitary (infundibulum) and its stalk.

402
Q

Identify the median eminence

403
Q

Identify the tuber cinereum.

404
Q

Identify the mammillary bodies

405
Q

Identify the uncus

406
Q

Identify the parahippocampal gyrus

407
Q

Identify the collateral sulcus

408
Q

Identify the rhinal fissure

409
Q

Identify the corpus callosum.

410
Q

Identify the rostrum of the corpus callosum.

411
Q

Identify the genu of the corpus callosum

412
Q

Identify the body of the corpus callosum

413
Q

Identify the splenium of the corpus callosum

414
Q

Identify the callosal sulcus

415
Q

Identify the cingulate gyrus.

416
Q

Identify the cingulate sulcus

417
Q

Identify the paracentral lobule.

418
Q

Identify the parieto-occipital sulcus.

419
Q

Identify the calcarine fissure.

420
Q

Identify where the primary visual cortex is.

421
Q

Identify the limbic lobe.

422
Q

Identify the isthmus (retrosplenial cortex)

423
Q

Identify the subcallosal gyri of the limbic lobe

424
Q

Identify the thalamus.

425
Q

Identify the epithalamus

426
Q

Identify the subthalamus.

427
Q

Identify the hypothalamus.

428
Q

Identify the midbrain

429
Q

Identify the Pons/cerebellum.

430
Q

Identify the medulla.

431
Q

Identify the cerebral peduncle.

432
Q

Identify the pyramid

433
Q

Identify the olfactory nerve.

A

Cranial Nerve I

434
Q

Identify the optic nerve.

A

Cranial Nerve II

435
Q

Identify the oculomotor nerve.

A

Cranial Nerve III

436
Q

Identify the trochlear nerve.

A

Cranial Nerve IV

437
Q

Identify the Trigeminal Nerve

A

Cranial Nerve V

438
Q

Identify the Abducens Nerve

439
Q

Identify the Facial Nerve.

A

Cranial Nerve VII

440
Q

Identify the vestibulo-cochlear nerve.

A

Cranial Nerve VIII

441
Q

Identify the glossopharyngeal nerve

A

Cranial Nerve IX

442
Q

Identify the Vagus Nerve.

A

Cranial Nerve X

443
Q

Identify the Spinal Accessory Nerve.

A

Cranial Nerve XI

444
Q

Identify the Hypoglossal nerve.

A

Cranial Nerve XII

445
Q

Identify the superior cerebellar peduncle

446
Q

Identify the middle cerebellar peduncle

447
Q

Identify the inferior cerebellar peduncle

448
Q

Identify the pyramidal decussation. Why is it important?

A

It marks the transition from the brainstem to the spinal cord

449
Q

Identify the posteromedian fissure

A

1 in the diagram

450
Q

Identify the posterolateral fissure.

A

2 in the diagram

451
Q

Identify the sensory fibers.

A

3 in the diagram

452
Q

Identify the DRGs.

A

8 in the diagram

453
Q

Identify the sensory tracts.

A

5 in the diagram

454
Q

Identify the anterolateral fissure.

A

1 in the diagram

455
Q

Identify the motor fibers.

A

2 in the figure

456
Q

Identify the DRGs

A

3 in the figure

457
Q

Identify the sensory fibers

A

4 in the figure

458
Q

What is a ventricle?

A

A continuous fluid-filled sac (of CSF)

459
Q

Identify the lateral ventricle

460
Q

Identify the anterior horn of the left ventricle

461
Q

Identify the body of the lateral ventricle

462
Q

Identify the inferior (temporal) horn of the lateral ventricle

463
Q

Identify the posterior (occiptal) horn of the lateral ventricles

464
Q

Identify the atrium of the lateral ventricle

465
Q

Identifyt he interventricular foramen of Monro

466
Q

Identify the third ventricle

467
Q

Identify the optic recess

468
Q

Identify the infundibular recess

469
Q

Identify the habenular recess

470
Q

Identify the pineal recess

471
Q

Identify the interthalamic adhesion

472
Q

Identify the cerebral aqueduct of Sylvius (the aqueduct)

473
Q

Identify the fourth ventricle

474
Q

Identify the foramen of Magendie

A

13 (Midline Magendie)

475
Q

Identify the foramina of Luschka

A

15 (Lateral Luschka)

476
Q

Identify the central canal

477
Q

Identify the obex

478
Q

Identify the lateral ventricle

479
Q

Identify the interventricular foramina of Monro

480
Q

Identify the third ventricle

481
Q

Identify the optic recess

482
Q

Identify the infundibular recess

483
Q

Identify the habendular recess

484
Q

Identify the pineal recess

485
Q

Identify the cerebral aqueduct of Sylvius

486
Q

Identify the fourth ventricle

487
Q

Identify the central canal

488
Q

Identify the lateral ventricle

489
Q

Identify the Third Ventricle

490
Q

Identify the foramen of Monro

491
Q

Identify the aqueduct

492
Q

Identify the fouth ventricle

Brain and Behavior (9 decks)

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