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Pharm Exam 1 > Kapatos - Introduction to Neuropharmacology > Flashcards

Kapatos - Introduction to Neuropharmacology Flashcards

1
Q

Glia: neuron ratio

A

Glia: outnumber neurons by ~10:1

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2
Q

Glia general:

How do they promote signaling between neurons?

Synthesize and release:

Other functions

A

General:

Promote signaling between neurons by accumulating or metabolizing NTs

Synthesize and release trophic factors that are important for neuronal survival (ie. GDGF)

Physically support the neurons, provide structure to the brain, and separate/insulate neuronal groups and synaptic connections

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3
Q

Microglia:

A

Scavengers that remove debris after cell death (like macrophages)

Activated microglia secret cytotoxic cytokines that induce cell death.

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4
Q

Macroglia

A

Oligodendrocytes
Schwann Cells
Astrocytes

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5
Q

Oligodendrocytes:

A

Produce myelin in CNS that insulates nerve cell axons (saltatory conduction)

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6
Q

Schwann Cells:

Produce:

Regulate:

A

Produce myelin in PNS that insulates nerve cell axons (saltatory conduction)

Regulate the properties of the presynaptic terminal at the nerve-muscle synapse

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7
Q

Astrocytes

A

Help form the blood brain barrier

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8
Q

Radial glia:
Guides:
Serves as:

A

Radial glia: a type of astrocyte

Guides migrating neurons

Serve as neuronal progenitors (constantly made) in some brain regions (ie. hippocampus- involved in memory)

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9
Q

Neurons:

Four defined regions:

A

Main signaling units of the nervous system

Four Defined Regions:

Cell body (soma)
Dendrites
Axon
Presynaptic Terminals

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10
Q

Cell body (soma):

A

Metabolic center containing the nucleus (stores genetic info) and endoplasmic reticulum (proteins synthesis)

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11
Q

Dendrites:

Voltage-gated Na channels?

Receptor types:

A

Dendrites: receive incoming signals

No voltage gated Na channels (do not convey classic APs)

Contain ionotropic NT receptors (glutamatergic) and voltage gated Ca channels (capable of propagating electrical signals to the soma)

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12
Q

Axon:

Contains

Where is AP initiated?

A

Axon: extends away from the cell body and is the output unit for neurons (conveys electrical signal)

Contains voltage gated Na channels (conduction of AP)

APs initiated in the axon hillock

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13
Q

Presynaptic Terminals:

Site of:

A

Presynaptic Terminals: form synapses to communicate with other neurons across the synaptic cleft

Site of classical NT biosynthesis (packages into vesicles and secreted by exocytosis)

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14
Q

State of dendritic spines:

Synaptic plasticity definition:

What happens when spines make contact with active nerve terminals?

A

Dendritic spines are in a constant state of flux.

Synaptic plasticity is defined as morphological alterations in dendritic architecture in response to changes in neuronal activity.

Spines that make contact with active nerve terminals are stabilized while spines that do not retract.

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15
Q

Types of Synapses:

A

Types of Synapses:

  • Axo-dendritic
  • Axo-somatic
  • Axo-axonic (synapse on a synapse)
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16
Q

Seven steps in synaptic transmission

A

Synaptic Transmission: each of the steps in transmission can be targeted by neuropharmacological intervention

  1. Neuron synthesizes NT and stores in vesicle
  2. Action potential travels down the neuron and depolarizes the presynaptic nerve terminal
  3. Activation of voltage-dependent Ca++ channels –> Ca++ enters nerve terminal
  4. Increase in Ca++ causes vesicle fusion with plasma membrane and release of NT into the synaptic cleft
  5. NT diffuse across cleft and binds to post-synaptic receptors
    Ionotropic and Metabotropic: binding activates intracellular signalling cascades
  6. Signal termination accomplished by removal of transmitter from synaptic cleft (degraded by enzymes or recycled by reuptake into presynaptic cell)
  7. Signal termination may also occur by enzyme degradation (ie. phosphodiesterase) of postsynaptic signaling molecules (ie. cAMP)
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17
Q

Ionotropic vs. Metabotropic

A

Ionotropic: binding causes channel opening and changes in permeability; may result in change in postsynaptic membrane potential

Metabotropic: binding activates intracellular signalling cascades

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18
Q

Amino acid NTs

A

primary excitatory and inhibitor NTs in the CNS
o Excitatory: glutamate and aspartate
o Inhibitory: glycine and GABA

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19
Q

Biogenic Amines:

3 types:

A

Biogenic Amines: primary modulatory NTs in the CNS
o Catecholamines: DA, NE, EPI
o Imidazole Group: histamine
o Indole Group: serotonin

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20
Q

Other small molecule NTs: (3)

A

ACh: found in diffuse modulatory systems in the CNS

Adenosine

Nitric Oxide (NO): atypical NT (made on demand and released by diffusion- not stored in/released by synaptic vesicles)

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21
Q

Peptide NTs:

Where?
co-localize with what?
synthesized on demand?
Examples:

A

Act as NTs in the brain

Typically co-localized with classical NTs (ie. monoamines)

Not synthesized upon demand in nerve terminals (made in cell body and transported intact down the axon)

Examples:
o Opioid peptides
o Tachykinins

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22
Q

Glutamate: type of NT.
Where?
Mechanism:
Channels activated:

A

Excitatory
Most neurons in the brain use it as a NT to mediate FAST EXCITATORY synaptic transmission

Mechanism: activates ligand gated ion channels (ionotropic receptors), resulting in depolarization of the membrane due to passage of Na+ and Ca++ down their electrochemical gradient

Channels Activated: AMPA, kainite and NMDA

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23
Q

GABA and Glycine

Mechanism

A

(Inhibitory):

Mechanism: activate another class of ionotropic receptors, resulting in the hyperpolarization of the membrane due to the movement of Cl- down its electrochemical gradient

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24
Q

Output of the neuron:

A

Output of the neuron is the sum of its inhibitory and excitatory inputs.

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25
Q

Metabotropic G Protein Coupled Receptors:
General:

Speed compared to ionotropic:

G proteins:

  • Actions mediated by:
  • Where do pharmacological interventions occur?
A

General: modulate the properties of the neurons themselves and thus how they integrate fast synaptic activity

Slower neurotransmission than ionotropic receptors

G proteins are heterotrimeric proteins that couple receptor activation with various effector mechanisms

  • Actions mediated by variety of second messenger systems
  • Very biologically complex and therefore a pharmacological intervention can occur at a number of different steps in the signaling pathway.
26
Q 
Beta Adrenergic (NE): types
o	Gs --> ? --> ?
A

Beta Adrenergic (NE): B1, B2, B3

o Gs –> Stimulates AC –> Increase in cAMP

27
Q

Alpha Adrenergic (NE):

Alpha1: Gq –> ? –> ?

Alpha2: Gi –> ? –> ?

A

Alpha1: Gq –> Stimulates PLC beta –> IP3 and DAG (from PIP2)

Alpha2: Gi –> Inhibits AC –> Decrease in cAMP

28
Q 
Dopamine Receptors (DA):
2 families:

Gs –> ? –> ?
Gi –> ? –> ?

A

D1 Family (D1, D5): Gs –> Stimulates AC –> Increase in cAMP

D2 Family (D2, D3, D4): Gi –> Inhibits AC –> Decrease in cAMP

29
Q

Muscarinic Receptors (ACh):

Classes

Gq –> ? –> ?
Gi –> ? –> ?

A

o M1,M3,M5: Gq –> Stimulates PLC –> IP3 and DAG (from PIP2)
o M2,M4: Gi –> Inhibits AC –> Decrease in cAMP

30
Q

NTs Acting as Fast and Slow NTs:

A

Glutamate:
Ionotropic R: AMPA, NMDA, kainite
Metabotropic R: mGluR1-5

ACh:
Ionotropic R: nicotinic (NMJ, GABAergic neurons of hippocampus and cortex)
Metabotropic R: muscarinic (CNS and PNS)

31
Q

Glutamate:
Ionotropic R:
Metabotropic R:

A

Ionotropic R: AMPA, NMDA, kainite

Metabotropic R: mGluR1-5

32
Q

ACh:
Ionotropic R:
Metabotropic R:

A

Ionotropic R: nicotinic (NMJ, GABAergic neurons of hippocampus and cortex)
Metabotropic R: muscarinic (CNS and PNS)

33
Q

MONOAMINES:

NTs in this Class: (5)

A

DA, EPI, NE, 5HT, histamine

34
Q

Druggable Targets for monoamines

A

Biosynthesis (DOPA decarboxylase)

Vesicular Storage: VMAT (vesicular monoamine transporter)

Reuptake and Metabolism: DA/NE/5HT transporters or MAO/COMT enzymes

35
Q

Monoamine neurotransmitters:

Derived from:

A

They are neurotransmitters and neuromodulators that contain one amino group that is connected to an aromatic ring by a two-carbon chain (-CH2-CH2-).

All monoamines are derived from aromatic amino acids like phenylalanine, tyrosine, tryptophan, and the thyroid hormones by the action of aromatic amino acid decarboxylase enzymes.

36
Q

AUTONOMIC NERVOUS SYSTEM INNERVATION:
Sympathetic:

Preganglionic Neurons: arise in:

Synapse: )

A

Sympathetic:
Preganglionic Neurons: arise in THORACIC and LUMBAR segments of the spinal cord (SHORT)

Synapse:
in ganglia that lie CLOSE TO THE SPINAL CORD (ie. paravertrbral and prevertebral ganglia

37
Q

Parasympathetic:

Preganglionic Neurons:

Synapse:
- Postganglionic Neurons:

A

Parasympathetic:

Preganglionic Neurons: arise in nuclei in the BRAINSTEM and the SACRAL segments of the spinal cord (LONG)

Synapse: in ganglia that lie close to the organs they innervate
- Postganglionic Neurons: short

38
Q

Neurochemical anatomy:

Primary NTs of 5 types of neurons

A

Primary NTs:

  • Dorsal Root Ganglia: glutamate, substance P, other peptides
  • Somatic Motor Neuron: ACh
  • Preganglionic Neuron: ACh
  • Postganglionic Neuron (SNS): NE
  • Postganglionic Neuron (PNS): ACh
39
Q

CNS Organizational Motifs (3):

A
  1. Long Tract Neurons
  2. Local Circuit Neurons
  3. Single Source Divergent Neurons
40
Q

Long Tract Neurons:
o Receive signals from:
o Synapse with:

A

Long Tract Neurons: act as relays between periphery and higher sites in CNS

o Receive signals from many different neurons (convergent signaling)
o Synapse with many downstream neurons (divergent signaling)

41
Q

Local Circuit Neurons:
Includes:
Used to:

A

Local Circuit Neurons: complicated and arranged in layers

Includes both excitatory and inhibitory neurons

Used to process information

42
Q

Single Source Divergent Neurons:

A

Originate in a nucleus in the brainstem and have axonal terminals that innervate thousands of neurons, usually in the cerebral cortex.

43
Q

Dopaminergic pathways:

Arise in:

Project to:

Involved in:

A

Arise in substantia nigra and ventral tegmental area

Project to striatum (SN) and cerebral cortex (VTA)

Involved in the initiation of movement the brain reward pathway

44
Q

Cholinergic pathways:

Arise in:

Project to:

Involved in:

A

Arise in the nucleus basalis, pedunculopontine nucleus, and medial septal nuclei

Project widely throughout the brain

Involved in maintaining sleep-wake cycles and regulating sensory transmission

45
Q

Cholinergic pathways:

Arise in:

Project to:

Involved in:

A

Arise in locus ceruleus

Project to the entire brain

Maintain alertness

46
Q

Serotonergic Pathways:

Arise in:

Project to:

Involved in:

A

Arise in raphe nuclei

Project to diecephalon, basal ganglia, and via the basal forebrain, to the cerebral hemispheres, cerebellum and spinal cord

Play a role in modulating affect and pain

47
Q

Retrograde Signaling by Cannabinoids and NO:

A

Cannabinoids endogenous (in post synaptic membrane)/NO or exogenous (ie. marijuana)

Bind cannabinoid receptor on presynaptic membrane to alter Ca++ influx and alter NT release

48
Q

Where is there a high density of Na channels?

A

Trigger zone of the dendrite

49
Q

How does glutamate activation of ionotropic receptors serve to depolarize the membrane?

A

Glutamate activation of ionotropic receptors serves to depolarize the membrane via the passage of Na+ and Ca2+ down their electrochemical gradients.

50
Q

How do GABA and glycine hyperpolarize the membrane?

A

GABA and glycine serve to hyperpolarize the membrane via the movement of Cl- down its electrochemical gradient.

51
Q

What inhibits axonal transport?

A

colchicine

52
Q

What converts excitatory glutamate into inhibitory GABA?

A

GAD (Glutamic acid decarboxylase)

53
Q

What is retrograde transport?

Where are small molecules recycled?

What inhibits programmed cell death?

A

Following exocytosis large dense core vesicles are returned to the cell body for reuse or degradation. This process is referred to as retrograde transport.

Small molecule synaptic vesicles are recycled in the nerve terminal.

Retrograde transport also transports trophic factors from the target cell to the cell body, where they inhibit programmed cell death.

54
Q

G Protein Coupled Receptor: targeted by many psychoactive drugs directly (4)

A 
o	Opiod analgesics
o	Antipsychotics (DA R)
o	Halluncinogens (5HT R)
o	Antihistamines (histamine R)
55
Q

What are the binding targets for cholera toxin and pertussis toxin?

A

G-proteins

56
Q

What released by the autonomic nerve produces both a fast excitatory postsynaptic potential (EPSP) and a slow EPSP?

A

ACh

57
Q

The fast EPSP is produced by:.

A

The fast EPSP is produced by activation of ionotropic nicotinic ACh receptors.

58
Q

The slow EPSP is produced by:

A

The slow EPSP is produced by
activation of metabotropic muscarinic
Ach receptors.

59
Q

Muscarinic activation stimulates PLC to:

A

Muscarinic activation stimulates PLC
to hydrolyze PIP2, yielding PIP3 and
DAG.

60
Q

What does the decrease in PIP2 cause?

A

The decrease in PIP2 causes the closure of the M-type delayed-rectifier K+ channel, which depolarizes the neuron.

Pharm Exam 1 (23 decks)

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