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Neuro > CNS neuropharmacology - french > Flashcards

CNS neuropharmacology - french Flashcards

1
Q

For a neuron to receive information what are the possible axonic connections?

A
  • Axodendritic
    • Axosomatic
    • axoaxonic
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2
Q

What are hierarchical systems in the brain?

A
  • Clearly delineated pathways that are directly involved in motor control and sensory perception
    • Large myelinated neurons with rapid conduction velocity
    • Sensory information is processed sequentially and is integrated successively at relay nuclei on the way to the cortex
    • Any leasion at any link disrupts the whole pathway
    • Relay neurons and local circuit neurons are present in each nuclei
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3
Q

What are local circuit neurons?

A
  • Smaller and branch in immediate vicinity of cell body, synapsing primarily on cell bodies of relay neurons
    • Can act as feed-forward and recurrent feedback pathway mechanisms
    • Spinal cord - special class forms axoaxonic synapses on terminals of sensory relay neurons
    • Most are inhibitory releasing GABA (some glycine)
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4
Q

What are relay neurons?

A
  • Form interconnecting pathways that transmit signals over long distances
    • Cell bodies are large and axons project over long distances
    • Smaller collaterals that synapse on local interneurons are present as well
    • Neurons are excitatory, releasing glutamate and activating ionotropic receptors
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5
Q

What is the main function of the diffuse systems?

A
  • Modulate the functions of the hierarchical systems
    • NT in diffuse neuronal systems including ach, dopamine (da), norepinephrine (ne), serotonin (5ht) are produced in neurons whose cell bodies lie in small discrete nuclei, most often in the brainstem
    • Despite limited cell number, these nuclei project widely and diffusely throughout brain and spinal cord
    • The axons here are divergent enough to innervate functionally distinct parts of the CNS
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6
Q

What is important about the monamine diffuse systems?

A
  • Cannot convey topographically specific information
    • CAN affect vast CNS areas simultaneously subserving global functions
    • Attention, sleep-wake cycle, appetite, emotions
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7
Q

What are the six key neurotransmitter systems that are targeted by psychopharmacologic agents?

A
  • GABA
    • Glu
    • Ach
    • Da
    • Ne
    • 5-HT (serotonin)
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8
Q

What should go through your mind as you use symptoms and circuits as a guide to pick a neuro pharm agent?

A
  • Match disease symptoms to hypothetically malfunctioning circuit
    • Consider neurotransmitter systems that theoretically regulate each circuit
    • Select treatment to target the relevant neurotransmitter system
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9
Q

What are the two broad categories of the rational approach to selecting a neuro-psychopharmacologic agent?

A
  • Using symptoms and circuits

* Specific behaviors hypothetically linked to brain regions

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10
Q

What behaviors are linked to the PFC?

A
  • PFC = pre frontal cortex
    • Executive function
    • Attention
    • Concentration
    • Emotions
    • Impulses
    • Obsessions
    • Compulsions
    • Motor
    • Fatigue
    • Ruminations
    • Worry
    • Pain
    • Negative symptoms
    • Guilt
    • Suicidality
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11
Q

What behaviors are linked to the NA?

A
  • NA = nucleus accumbens
    • Delusions
    • Hallucinations
    • Pleasure
    • Interests
    • Libido
    • Fatigue
    • Euphoria
    • Reward
    • Motivation
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12
Q

What behaviors are linked to the S?

A
  • S = striatum
    • Motor
    • Critical relay site from PFC
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13
Q

What behaviors are linked to the thalamus?

A
  • T = Thalamus
    • Pain
    • Sensory relay TO cortex
    • Sensory relay FROM cortex
    • alertness
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14
Q

What behaviors are linked to the BF?

A
  • BF = basal forebrain
    • Memory
    • Alertness
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15
Q

What region of the CNS is pain associated with?

A

• Spinal cord and brain stem

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16
Q

What part of the brain are memory and reexperiencing linked to?

A

• H = hippocampus

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17
Q

What behaviors are linked to the C?

A
  • C = cerebellum

* Motor coordination

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18
Q

What behaviors are linked to the Hy?

A
  • Hy = hypothalamus
    • Sleep
    • Appetite
    • Endocrine
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19
Q

What does GABA stand for?

A

• Gamma-aminobutyric acid

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20
Q

How is GABA synthesized?

A
  • Synthesis is intertwined with the synthesis of glutamate (which is major excitatory transmitter)
    • Via the GABA shunt
    • GAD = glutamic acid decarboxylase, the enzyme that makes GABA from glutamate
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21
Q

What do the receptors for GABA do?

A

• GABA-a
○ Opens ligand-gated Cl channel, decreases neuronal excitability
• GABA-b
○ GPCR, inhibits adenylyl cyclase, decrease Ca conductance, open K channel (hyperpolarizes)

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22
Q

What does vigabatrin have to do with GABA?

A
  • Inhibits degradation by GABA-T
    • T = transaminase
    • Works in the glial cells mostly
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23
Q

How does Tiagabine interact with GABA?

A

• Inhibits reuptake of GABA by transporter

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24
Q

What do benzodiazepines do in relation to GABA?

A

• bind to GABA-a receptor to facilitate GABA inhibitory action

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25
How is GABA terminated?
* Action of GABA at synapse terminated by reuptake into the presynaptic nerve terminal and surrounding glial cells * GABA transporter similar to monoamine reuptake transporters
26
Where is GABA found in the CNS?
* Found in high concentrations in the brain and spinal cord * Absent pretty much from the peripheral tissues * Functions as major inhibitor NT in CNS * 30-40% of all CNS synapses both postsynaptically and presynaptically
27
Is GABA-a receptor presynaptic or postsynaptic?
* GABA-a is postsynaptic | * GABA-b is both pre and postsynaptic
28
In which diseases does GABA play a pathophysiological role?
* Generalized anxiety disorders * Seizure disorders * Sleep disorders * Alcohol abuse and withdrawal * Huntington disease
29
How is glutamate synthesized?
* Dependent on interaction between nerve terminals and glial cells * Glutamate is formed from glutamine by the action of glutaminase in the nerve ending. * Newly synthesized glutamate is stored in synaptic vesicles for subsequent release
30
What are the various receptors for glutamate?
``` • Ionotropic receptors ○ NMDA - increases calcium influx ○ AMPA - increase Na and Ca influx ○ Kainate - increase Na influx • Metabotropic receptors ○ R1-R5 - Gq - GPCR - increases PLC activity ○ R2-3 - Gi - decreases AC activity and inhibits VSCC, activates K channels ○ R4,6,7,8 - Gi - inhibit VSCC ```
31
How is released glutamate terminated?
* Reenters the neuron via a neuronal glutamate transporter (Gt-n) * or is taken up by the glial cell transporter (Gt-g) * Converted to glutamine by glutamine synthetase * Glutaminase will convert glutamine to glutamate for re-use as a NT
32
What two enzymes are responsible for synthesizing glutamate from alpha-ketoglutarate?
* OAT and AAT | * Both convert alpha-ketoglutarate to glutamate if there is either omithine or aspartate present
33
Where is glutamate present as a NT in the CNS?
* Virtually all neurons in CNS * Highest in hippocampus, cortex, lateral septum, striatum, cerebellum * Functions as the major excitatory NT through AMPA receptors * Trigger neuroplasticity * When overactivated can trigger excitotoxicity
34
In what diseases does glutamate play a pathophysiological role?
* Epilepsy * Ischemic brain damage * Addiction * schizophrenia
35
How is Ach synthesized?
* CAT = choline acetyl transferase | * Choline uptake is the rate limiting step so this enzyme is pretty amazingly fast
36
How is ach packaged into the vesicles for release?
• VAT - vesicle associated transporter
37
What is meant by VSSC in french's notes?
* VSSC = voltage senstitive (sodium) channel | * You could have VSCC for calcium channel too
38
In what diseases does ach play a pathophysiological role?
* Alzheimer's * Parkinson's * schizophrenia
39
What is meant by MSN, DB, Ch5-Ch8 in terms of ach?
* These are the regions of the brain where cell bodies make ach as their NT and project into hippocampus and cerebral cortex * MSN = medial septal nuclei * DB = diagonal band of Broca * Ch5-Ch8 = cholinergic brainstem nuclei (numbered)
40
Where is ach found in the CNS?
* Remember it's used in all NMJs * In the CNS, specifically produced in cell bodies in the brain stem and basal forebrain of neurons that widely project to cerebral cortex and hippocampus * MSN, DB, Ch5-Ch8
41
What are the different receptors for ach?
• Muscarinic receptors ○ M1, M3 - Gq - increases PLC activity ○ M2, M4 - inhibits adenylyl cyclase activity • Nicotinic receptors ○ N-n - opens receptor gated cation channel (ionotropic)
42
How is the ach "signal" terminated?
* Ach is terminated in the synapse by enzymatic degradation (ache = acetylcholinesterase) * Both in the synapse anchored to cells and free in blood (periphery)
43
What causes ach release?
• Action potential, VSSC opening, VSCC opening, Calcium influx, synaptotagmin binding of calcium and fusion of stored ach vesicles
44
What NT should come to mind when you hear "monoamines"?
* Catecholamines and indoleamines * Catecholamines - dopamine and norepinephrine * Indoleamines - serotonin (5-HT)
45
How might drug action mess with the storage of the monoamines
* Ultimately by shifting balance between NT being stored in vesicles and being broken down by MAO * Inhibitors of VMAT - reserpine - block vesicular uptake, increase degradation by MAO, decrease monoamine release and action overall * Inhibitors of MAO - phenelzine-selegiline) decrease degradation by MAO, allowing greater vesicular storage by VMAT, increases monoamine release and action overall * All of these affect all 3 monoamine transmission dynamics
46
How are the monoamines stored?
* Transmitter is taken up into storage vesicle via the vesicular monoamine transporter (VMAT) * Packaged for release AND protected from degradation by intraneuronal monoamine oxidase (MAO)
47
How are the monoamines synthesized?
• Catecholamines ○ NE and DA ○ Rate limiting enzyme in pathway is tyrosine hydroxylase (TH) ○ Tyrosine is the start, dopamine an intermediate of norepinephrine ○ MAO is quite involved in the later stages of the pathway • Indoleamine ○ 5-HT (serotonin) ○ Rate limiting enzyme in pathway is tryptophan hydroxylase (TpH) ○ Tryptophan is the start ○ MAO is involved in the later part of the pathway
48
How is monoamine release different from ach?
* It's not different at all | * Action potential, VSSC, VSCC, vesicle fusion and release
49
What are the different receptors for norepinephrine?
``` • NE is a catecholamine, which is a monoamine • Alpha-1 adrenergic ○ Gq - stimulates PLC activity • Alpha-2 adrenergic ○ Gi - inhibits adenylyl cyclase, opens K channels • Beta-1 adrenergic ○ Gs - stimulates AC activity • Beta-2 adrenergic ○ Gs - stimulates AC activity ```
50
What would be the overall effect of blocking specific monoamine transporters?
• Increase duration of synaptic activity and enhance MA neurotransmission
51
How is the monoamine signal terminated?
* Primarily by presynaptic membrane transporters that suck back up transmitter (reuptake) * In cytosol, ever-present MAO can destroy it OR it can be re-packaged by VMAT * Each vesicle will have a specific monoamine transporter to package that vesicle * Each of these transporters can be inhibited pharmacologically
52
What are the receptors for dopamine?
* D1 - Gs - stimulates AC | * D2 - Gi - inhibits adenylyl cyclase
53
What are the receptors for 5-HT?
* 5-HT = serotonin * 5HT 1a, 1b, 1d - Gi- inhibition of AC, opens K channel * 5HT 2a, 2b, 2c - Gq - stimulates PLC, closes Ca channel * 5HT3 - ligand-gated cation channel - excitatory (ionotropic) * 5HT4 - Gs - stimulates AC
54
Where can you find Dopamine in the CNS?
* [These are all successive links in a chain] * Substantia nigra * Neostriatum pathway (nigrostriatal), ventral tegmental area * Limbic cortex (mesolimbic), ventral tegmental area * Frontal cortex pathway (mesocortical), hypothalamus * Pituitary (tuberoinfindibular pathway)
55
Where can you find norepinephrine in the CNS?
* Cell bodies in pons and brain stem (lucus ceruleus) * Projecting to all levels of brain * A1,2,5,7 = adrenergic brainstem nuclei * Locus coeruleus projects into cerebellum as well
56
Where can you find serotonin in the CNS?
* Cell bodies in raphe regions of the pons/upper brain stem * Project to all levels of brain * Think Raphe nuclei in brainstem
57
What is the function of dopamine in the CNS?
* Initiation of voluntary movement * Necessary for reward-related behaviors * Cognitive control of behavior including working memory and control of attention
58
What is the function of norepinephrine in the CNS?
* Regulation of arousal, attention, vigilance, sleep-wake cycle * Fear response/anxiety * Mood/emotion * Descending pathways modulate afferent pain signals
59
What is the function of serotonin in the CNS?
* Influences sleep, arousal, attention, processing of sensory information in cerebral cortex * Important aspect of emotion and mood regulation, pain pathways, eating and drinking behaviors
60
In what diseases does Dopamine play a pathophysiological role?
* Schizophrenia * Parkinson's * Restless leg syndrome * Obsessive-compulsive anxiety disorder * Attention deficit/hyperactivity disorder * Drug abuse
61
In what diseases does Norepinephrine play a pathophysiological role?
* Mania * Depression * Anxiety disorders (panic, PTSD) * ADHD
62
In what diseases does Serotonin play a pathophysiological role?
* Depression * Anxiety disorders * Schizophrenia * Eating disorders

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