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Neurologic & Psych > CNS Pharmacology Dr. Pond > Flashcards

CNS Pharmacology Dr. Pond Flashcards

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1
Q

Where is the nucleus located?
Neuron cell

A

Cell body

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2
Q

What are the Processes (extensions) of a neural cell?

A

Dendrites: receive signals

Axon: send signals to other cells (communicate)

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3
Q

What is the part of the neuron where the action potential originates?

A

-sending signals through the axon starts with the action potential

-the action potential is elicited in the “Initial segment” or axon hillock

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4
Q

What are breaches of the axon called?

A

-Axon collateral

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5
Q

At which part of the neuron do chemicals get released to communicate with other neurons?

A

Axon terminals

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6
Q

Different forms of Neurons in reference to axon and dendrites?

A

-Multipolar: 3 or more processes coming off the cell bodies
-> Motor neuron (muscle), but many others

-Bipolar: 2 processes: 1 axon, 1 dendrites
-> retina, olfactory cortex

-Pseudounipolar: 1 process coming off the cell body, but it branches in two different directions: 1 axon, 1 dendrite
-> dorsal root ganglion, sensory (afferent) neurons (pain neurons)

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7
Q

What are the different Glia cells?

A

-Astrocytes: regulate neuronal microenvironment, since neurons are very excitable (through ions), the concentration of ions and chemicals must be regulated, part of the BBB

-Microglial cells: resident immune cells in the CNS, since the BBB exclude leucocytes, these cells act as immune cells in the brain

-Myelinating cells: Oligodendrocytes (myelinate axons in the CNS (brain and spinal cord) and Schwann cells (myelinate cells in the periphery)

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8
Q

What is the purpose of myelinating cells?

A

-lipid region that doesn’t conduct electrical signal
-the signal skips myelinated part -> fast conduction

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9
Q

Which cells form and circulate cerebrospinal fluid?

A

Ependymal cells

they have beads that circulate the fluid in the ventricular space

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10
Q

Function of the ATP pump

A

takes 3 Na(+) from inside to the extracellular space
-> thereby using ATP (hydrolyze to ADP)

takes potassium from outside to inside

inside: net negative
outside: net positive

-the pump is constitutive (always on) - creating a gradient: a lot Na outside and lots of potassium inside
-Primary active transporter

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11
Q

Which channels transport ions through facilitated diffusion?

A

Ion channels (ions can’t cross the membrane since the membrane is lipophilic and nonpolar)

-transport down the gradient
-no energy required

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12
Q

What are the different typed gated channels?

A

-mechanical

-chemical/ligand: opens when a ligand binds to the channel

-voltage-gated: net positive outside and net negative inside -> when the charge of the membrane changes -> opening of the gate

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13
Q

How do ion channels transport specific ions?

A

Because they are charge-specific (consisting of amino acids), depending on the charge they will transport specific chemicals

-either cation channel (+) or anion channel (-)

or size-specific:
-they may conduct sodium but not potassium

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14
Q

What does it mean when the membrane is polarized?

A

-net charge inside is more negative than outside

-Depolarization: movement of membrane potential back to 0

-Overshoot: membrane potential moves beyond 0 to the positive

-Repolarization: bringing the membrane potential back to resting (negative membrane potential = -70mV)

-Hyperpolarization: taking membrane potential more negative than resting -70 mV

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15
Q

Why do we see over-repolarization?

A

K channels are slow to close

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16
Q

Which ion channels cause depolarization?

A

Na (+) channels (Na moves inside)

also overshoot

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17
Q

Which channels cause Repolarization?

A

-Potassium channel (moves out)
-Chloride channel (moves in?)

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18
Q

Which channels are involved in the action potential?

A

-voltage-gated Na-channel
open - inactivate rapidly - shut closed

-voltage-gated K-channel
open - close slowly

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19
Q

What is the purpose of the deactivated state of the Na channel?

A

-as the membrane depolarizes the Na channel opens and the inside of the membrane becomes positive

-after inactivation, the Na channel stays shut for a while: to make sure the membrane potential stays positive and the action potential doesn’t spread but move from axon hillock to axon terminal in one direction;
-and to ensure the refractory period

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20
Q

What is the Equilibrium potential?

A

The potential that is desired by specific ions

E(Na): +72 mV - when Na channel open, it tries to get the membrane potential to +72 mV by Na moving in - during depolarization

E(K): -89.7 by K moving out - during repolarization
E(Cl-): -89.2 by Cl moving in - during repolarization

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21
Q

What is the absolute (ARP) and relative refraction period (RRP) phase?

A

absolute: no action potential can fire no matter how strong the stimulus is, bc there are no enough open Na channels

relative: some Na channels open again, it is still hard to elicit the action potential -> the action potential is weak

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22
Q

Which channels are located in the terminal axon?

A

high-treshhold Ca2+ channels (strong depolarization (+) needed)

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23
Q

How does signal transduction in the synapsis work?

A

action potential moves from axon hillok to axon terminal -> open Ca2+ channel -> Ca2+ binds to proteins on the vesicles that contains neurotransmitter

it facilitates the fusion of vesicles and the axon membrane -> release of NT at synaptic cleft

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24
Q

What are the receptors on the postsynaptic neuron that receive Neurotransmitter?

A

-ionotropic receptors (ligand-gating ion channels)
-> the Neurotransmitter is the ligand -> causes opening of the ion channel and ions to move through the channel

-Metabotropic receptors (G-protein-coupled)
NT binds -> alpha subunit of the G-protein (alpha, beta, gamma) cleaves and binds to:

effector protein -> opening/close ion channel
OR
ion channels for -> opening/close ion channel

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25
Q

How does ion channel opening occur with an effector protein?

A

-effector protein: enzyme
f.e. adenylate cyclase -> converts ATP to cAMP

cAMP (second messenger) opens/closes the ion channel

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26
Q

How fast do channels on the postsynaptic neurons open upon activation?

A

ion channels: ACTION is fat but brief

metabotropic: Action is slow and long-lasting due to activation through second messenger

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27
Q

What are ways the postsynaptic neurons respond to neurotransmitters?

A

NT causes ion channels to open which causes

Excitatory Postsynaptic Potential (EPSP) - elicited by depolarization events
or
Inhibitory Postsynaptic Potential (IPSP) - elicited by repolarization events

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28
Q

Which ions cause EPSP?

A

Na -> depolarization towards treshhold -> EPSP

K and Cl cause IPSP

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29
Q

What type of postsynaptic potential is caused by closing K channels?

A

K usually moves out causing repolarization
-> when K channel closes it causes depolarization
-> EPSP

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30
Q

A single EPSP is enough to trigger an action potential. T/F

A

False, multiple are required

-Temporal summation: 2 EPSP fire with a short gap
-Spatial summation: 2 EPSP in same area combined (same space)

-Spatial summation of EPSP and IPSP -> cancel out

31
Q

Presynaptic inhibition/facilitation

A

-axoaxonic synapsis (dominantly in
spinal cord)

-presynaptic axon communicate with postsynaptic dendrite + another postsynaptic axon connected to the first postsynaptic axon

the presynaptic neuron is influenced by the other axon -> axon releases GABA and block Ca channel on the the other presynaptic neuron

-> blocking Ca channel causes lower NT release and reduced signal transduction to the next postsynaptic neuron

32
Q

Which NT has an inhibitory/facilitation effect on the presynaptic neuron (axoaxonic)

A

inhibitory: GABA

facilitation: Serotonin

33
Q

What is the purpose of axoaxonic inhibition/facilitation?

A

it is homoeostatic

since NT gets released and diffuses uncontrolled and may over-induce neurons

34
Q

Which of the Neurotransmitters are called Monoamines?

A

-Dopamine, Norepinephrine, Noradrenaline, Serotonin

-Catecholamine = Noradrenaline, Norepinephrine, Dopamine are

-all have a single amine group

35
Q

Catecholamines are derived from which amino acids?

A

Tyrosine

Serotonin is derived from Tryptophane

36
Q

GABA is derived from which amino acid?

A

Glutamate

37
Q

What is the main excitatory NT?

A

Glutamate

-seen all over the CNS

-synthesized from Glutamine via Glutaminase in the presynaptic neuron -> Glutamate is then stored in the vesicle (vesicle glutamate transporter vGLUT)

-

38
Q

How is Glutamate turned off?

A

Reuptake from synaptic cleft by Glutamate transporter into Astrocytes

-converted back into Glutamine

-released back to the presynaptic neuron

39
Q

What are the Glutamate receptors?

A

3 ionotropic receptors
-AMPA (Na transport): uniformly distributed in the brain - often next to NMDA receptors
-NMDA (Na and Ca transport): uniformly distributed in the brain - often next to AMP receptors

-Kainate (Na transport): HIP, cerebellum, spinal cord

40
Q

Why are NMDA receptors considered ligand and voltage-gated?

A

Glutamate binds as a ligand
-Mg blocks the channel until the membrane charge changes

-the membrane changes when Na moves in through the AMPA receptor -> as depolarization occurs, Mg will move away from the NMDA-r -> the NMDA-r will allow Ca2+ and Na to move in

41
Q

How does Ca2+ influx influence Glutamate receptors on the membrane?

A

-Ca2+ (2nd messenger) activates specific pathways that will add more AMPA receptors

-more AMPA receptors will cause more Na to enter and a greater chance for depolarization
-> this will again makes it more likely for Mg2+ to be lifted from NMDA receptors and allow for more Ca2+ and Na+ influx

POSITIVE FEEDBACK

42
Q

What important role are NMDA and AMPA receptors believed to play?

A

Learning and Memory

43
Q

What is the major role of Glycin receptors?

A

Glycin receptor

-major inhibitory!
-Chloride channel -> Cl causes hyperpolarization
-IPSP
-brain stem, spinal cord

44
Q

What is the major inhibitory Neurotransmitter?

A

GABA

-40% of brain neurons

45
Q

How is GABA recycled/removed?

A

-it derived from Glutamate

GABA is taken up by Gliacell (astrocyte) -> converted to Glutamate -> Glutamine
Glutamine is transferred back to the presynaptic neuron and converted to Glutamate -> GABA

-also there is a transporter that transports GABA or Glutamate or Glutamine back to the presynaptic neuron (favors Glutamine)

46
Q

Which ions pass through the GABA receptors?

A

Chloride
-inhibitory -> IPSP
-hyperpolraization

47
Q

Drugs targeting GABA(a) receptor

A

-Benzodiazepines
-Barbiturates
-Alcohol

48
Q

How is Acetylcholine synthesized?

A

-in the presynaptic neuron

Acetyl (from Acetyl-CoA) combined with choline

49
Q

Role of GABA (b)

A

-metabotropic -> act via second messenger
-inhibitory
-decrease adenylate cyclase activity

-controls K(+) channels = IPSP (postsynaptic neuron)
-controls Ca2+ channels: closing -> decrease NT release on presynaptic neuron

-can be found on pre or postsynaptic neuron

GABA (c): control Cl(-) channels = IPSP

50
Q

How is Acetylcholine recycled from the synaptic cleft?

A

Acetylcholine esterase cleaves Acetylcholine to Acetyl group and choline

-> Choline moves back to the presynaptic neuron and is reused to form new Acetylcholine

51
Q

What are the major cholinergic pathways?

A

-Nuclei of the basal forebrain
projects throughout the cortex (learning)
projects throughout the limbic areas (memory)

-Nuclei of the brain stem
projects throughout
thought to control the REM sleep

52
Q

What are the subtypes of Acetylcholine receptors?

A

-Nicotinic receptors (ion channels)
influx of Na(+) and efflux of K(+)
-> still EPSP bc more Na(+) coming in than K(+) going out

-Muscarinic receptors (metabotropic)
M1: tend to close K(+) channels -> EPSP (depolarization)
M2: tend to open K(+) channels -> IPSP (hyperpolarization)

53
Q

Synthesis of Catecholamines

A

from Tyrosine -> Dopa -> Dopamine -> Norepinephrine -> Epinephrine

54
Q

How are Catecholamines and Monoamines removed/recycled?

A

Dopamine transporter: reuptake of dopamine from the synaptic cleft back to the presynaptic neuron

COMT: extracellular degradation of catecholamines (dopamine, norepinephrine)

Monoamine oxidase (MAO): intracellular degradation of dopamine, norepinephrine, serotonin

80% of dopamine is taken up by dopamine transporter back to the presynaptic neuron

20% is degraded by COMT

55
Q

Where does the Nigrostriatal pathway lead to?

A

Neurons from the substantia nigra to caudate-putanem (striatum)

motor control, death of these neurons results in Parkinson’s disease

56
Q

Where does the Tuberoinfundibular pathway lead to?

A

from the Hypothalamus to the pituitary gland

Hormonal regulation
Maternal behavior (nurturing) - dopamine inhibits prolactin release (for milk production)

57
Q

Where do the Mesolimbic and mesocortical pathways lead to?

A

from the ventral tegmental area (VTA, midbrain) to the limbic areas or prefrontal cortex

Memory
Motivation and emotional response
Reward and desire
Addiction
possibly misregulated in schizophrenia

58
Q

How do Dopamine receptors affect cAMP?

A

D1 and D5: increase adenylate cyclase activity -> increase cAMP

D2, D3, D4: decrease adenylate cyclase activity -> decrease cAMP

59
Q

Are dopamine receptors metabotropic or ionotropic?

A

metabotropic

60
Q

How is Norepinephrine synthesized?

A

Tyrosine -> Dopa -> Dopamine -> Norepinephrine

80% reuptake by NET
20% degraded by COMT

61
Q

Where do Norepinephrine neurons lead to?
Noradrenergic pathways

A

major nucleus is called: locus coeruleus
-runs through the brainstem and midbrain

controlling and arousing
-regulates many behavioral & physiological processes
sleeping, waking, attention, appetite, emotions

62
Q

Are the Noradrenergic receptors depolarizing or hyperpolarizing?

A

-Beta-1 (b1)
-Beta-2 (b2)
-Alpha-1 (a1)
-> depolarizing by closing K(+) channels

-Alpha-2 (a2)
-> hyperpolarizing by increasing K(+) conducance

63
Q

How is the amount of Norepinephrine regulated?

A

Feedback inhibition with alpha-2 receptors

Feedback Excitation with ß-2 receptors

64
Q

How is Serotonin recycled?

A

-Reuptake by SERT

-some degraded by MAO

65
Q

Where do Serotonin neurons lead to?

A

stems from the Raphe nuclei, concentrated in the upper brainstem

-> projects throughout the brain, spinal cord, cerebellum

mood, appetite, sleep, temperature, arousal

66
Q

Are Serotonin receptors metabotropic or ionotropic?

A

-All are metabotropic except for 5-HT3
5-HT3 is a Na/K channel

67
Q

Role of Serotonin receptors

A

-5-HT1A: presynaptic/postsynaptic - inhibitory
-5-HT1D: mostly presynaptic - inhibitory

-5-HT2A: mostly postsynaptic - excitatory

68
Q

Histaminergic pathways

A

The tuberomammillary nucleus of the hypothalamus
-> project throughout the brain: cerebral cortex, corpus callosum, cerebellum, pons, medulla, spinal cord

69
Q

How is histamine synthesized/recycled?

A

-Synthesized from histidine by histidine decarboxylase

-loaded into vesicles by VMAT

-degraded by histamine methyltransferase, diamine oxidase (gut)

70
Q

Which peptides affect the activity of individual
neurons?

A

-opioid peptides, orexins (hypocretins), POMC, neuropeptide Y, substance P, neurotensin, and somatostatin

-often released with low MW transmitters (Monoamines: dopamine, norepinephrine, epinephrine, serotonin)

71
Q

Opioid peptides and their receptors

A

-mu (μ) receptors –β endorphin (preferentially)

-delta (δ) receptors – enkephalins
-kappa (κ) receptors – dynorphin

72
Q

What are the two Endocannabinoids?

A

-anandamide

-2-arachidonylglycerol

73
Q

How do Endocannabinoids affect NT in the brain?

A

-suppress release of neurotransmitter GABA

-Synthesized in response to Ca2+

-Activate cannabinoid receptors (CB1- brain and
CB2- periphery)

Neurologic & Psych (37 decks)

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