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Biological Basis (Test 1) > Chapter 4 (from the slides) > Flashcards

Chapter 4 (from the slides) Flashcards

1
Q

What is an agonist?

A
  • drug that facilitates the effect of NT on the postsynaptic membrane
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2
Q

What is an antagonist?

A
  • drug that opposes, or interferes with the effect of a neurotransmitter on the postsynaptic membrane
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3
Q

what is a partial agonist?

A
  • drug whose action depends on neurotransmitter concentrations
  • depends on the NT
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4
Q

What is affinity?

A
  • the speed.readiness with which a drug binds to its target
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5
Q

what is tolerance?

A
  • decrease in drug effectiveness with repeated administration likely due to compensatory mechanisms
  • due to the fact that our body develops compensatory mechanisms that work against the drug
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6
Q

What is withdrawal?

A
  • unopposed compensatory mechanisms after drug discontinuation
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7
Q

What is the function of the autoreceptors?

A
  • receive neurotransmitters released by the terminal button they are on; they regulate (usually inhibit) synthesis and release of neurotransmitter
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8
Q

Axonic synapse?

A
  • it can be effected by drugs
  • the effect of the stimulation depends on what they do
  • the heteroreceptor will open the channels and release the neurotransmiters
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9
Q

What is the function of the dendritic autoreceptors?

A
  • have a regulatory effect of preventing the neurons from becoming too active.
  • the drugs binding to these autoreceptors are antagonist whereas drugs blocking them are agonists
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10
Q

What is an antagonist action?

A
  • drugs that activate presynaptic autoreceptors and reduce the amount of neuroransmitters released
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11
Q

What is an antagonist action?

A
  • drugs inactivate presynaptic autoreceptors and increase the amount of neurotransmitters released
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12
Q

heteroreceptors at axonic synaptes?

A

HRs at ASs are sensitve to neurotransmitters elease by another neuron, can be inhibitory or facilitory

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13
Q

What would a drug be though of as if a drug activates a heteroreceptor that produces presynaptic inhibition (closes the calcium channel)?

A
  • an antagonist
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14
Q

Direct antagonist and angonist binding site?

A
  • binds directly to the neurotransmitter binding cite

- when a drug bind there, then there is competition for the binding sites

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15
Q

Inirect antagonist and angonist binding site?

A
  • drug does not bind to the same site as the neurotransmitters
  • no competition for the binding sites
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16
Q

What two neurotransmitters are used for all information processing networks?

A
  • glutamate (produces EPSP’s)

GABA (produces (IPSP’s)

17
Q

What is the function of a other neurotransmitters?

A
  • they are neuromodulators that alter the action of entire networks of neurons that transmit information using either glutamate or GABA
18
Q

Function of Acetylcholine (ACh)?

A
  • primary neurotransmitter secreted by efferent CNS cells
  • In periphery: found in the autonomic ganglia (e.g, the heart) and neuromuscular junction (motor movement)
  • in the brain: found in dorsalateral pons, medial septum, basal forebrain, ACh release in brain results in facilitatory effects
19
Q

Why is ACh involved in REM sleep?

A
  • dorsolateral pontine keeps the muscles under control

the basal forebrain is in control of cortical learning and the medial septum is in control of modulating the hippocampus

20
Q
  • what occurs with a black widow spider bite?
A
  • too much ACh is released

- it is i an agonist so it causes severe muscle weakness and tremors.

21
Q

What occurs with botulism?

A
  • this is an antagonist

- produces muscle weakness, and issues with breathing

22
Q

What occurs with curare?

A
  • this is also antagonist
  • can be use as an anesthetic and is a muscle relaxant
  • loss of muscle function
  • trouble with breathing and swallowing
23
Q

What are the ACh receptors?

A
  • nicotinic receptors

- muscarinic receptors

24
Q

What is the function of the nicotinic receptors?

A
  • these receptors are found in skeletal muscle
  • rapid ionotropic effect
  • Agonist: nicotine
  • Antagonists: d-tubocurarine…puts you to sleep!
25
Q

What is the function of the muscarinic receptors?

A
  • receptors are found in heart, smooth muscle and CNS
  • slower metabotropic effect
  • Agonist: muscarine
  • Antagonists: atropine and scopolamine
26
Q

what are monomines?

A
  • class of amines that includes indolamine (serotonin) and catecholamines (dopamine, norepinephrine, and epinephrine)
27
Q

what is the cholinergic system?

A
  • networks activate cortical areas for learning functions but what is learned is transmitted by glutamate and GABA
28
Q

What is the pathway process channel?

A
  • Tryosine –> L-DOPA—> Dopamine—> Norepinephrine
29
Q

What is dopamine and what is its function?

A
  • one of the catecholmines
  • this can be EPSP or IPSP depending on the postsynaptic receptor
  • DA has been implicated in control of movement, attention, learning, and reinforcement/reward circuits
  • DA deficiency is the hallmark pathology of Parkinson’s disease
  • all receptors are metabotropic
  • Sustantia Nigra is important with this NT
  • Amphetamine is a very powerful agonist
    DA agonists have been given where DA deficiency is suspected to be a major etiologocal factor
30
Q

More about DA agonists

A
  • L-dopa & Sinemet (Levodopa & carbidopa) for PD: makes more precursor available for DA synthesis
    - Methylphenidate for ADHD: inhibits reuptake of DA
    - Monoamine oxidase (MAO) inhibitors (e.g., selegiline/deprenyl) for PD and depression: destroys MAO-B, which inactivates DA; therefore is a DA agonist
    DA antagonists have been traditionally given where overactivity of DA was suspected:
    - chlorpromazine: old antipsychotic that blocks postsynaptic D2 receptors
31
Q

What is the function of tryosine?

A
  • it is a dietary precursor for dopamine
32
Q

What is the Norepinephrine pathway and how does it work?

A
  • noradrenergic
  • NE is the final product in the biosynthesis of DA.
    - This final step occurs in the vesicles where DA is converted to NE.
  • NE is generally associated with vigilance, wakefulness, and attentiveness, and is believed to have a role in depression. The most important noradrenergic system projects from the locus coeruleus in the dorsal pons.
    • NE is released from axonal varicosities rather than from terminal buttons.
  • Noradrenergic receptors have both excitatory and inhibitory functions (α1 produces postsynaptic depolarization, α2 slow hyperpolarization)
33
Q

What is serotonin and what is its pathway?

A
  • are mostly located in the gut (98%) with only 2% of serotonin cells in the brain
  • 5-HT cell bodies are located in brainstem raphe nuclei and project to cortex. Behavioral effects are complex: 5-HT neurons have been associated with the regulation of mood, eating, sleep, arousal, possibly with dreaming, and pain.
    Biosynthesis starts with the essential amino acid tryptophan. NT is released from axonal vesicles.
  • SSRIs, e.g. fluoxetine for depression
  • Sumatriptan, 5-HT1 receptor agonist, for migraine
  • Drugs of abuse including LSD and MDMA (ecstasy)
34
Q

What is the function of GABA in the CNS?

A
  • the most important inhibitory neurotransmitter in the brain
  • Produces IPSP’s
  • absolutely essential to neuronal communication (consider likely GABA dysfunction in seizure disorders).
  • Receptor has binding sites for benzodiazepines, barbiturates, possibly alcohol, and steroid hormones like progesterone.
35
Q

What is glutamate?

A
  • principal excitatory neuotransmitter in the CNS. Possibly it is one of the first neurochemically active substance that has evolved
  • by broduct of the cell’s metabolism, therefor ubiquitous
36
Q

What is the function of glutamate?

A
  • Glutamate interacts with four receptor types
    - NMDA receptor: controls a CA++ channel
    - Important for learning and new memory formation
    - Normally blocked by Mg2+
    AMPA receptor: most common, controls Na+ channel
    PCP (Angel dust) binds at glutamate sites

- Channel opens if glutamate and glycine bind to their sites, and the magnesium ion is expelled from its binding site (only under conditions of partial polarization)

- Note: alcohol acts as antagonist at NMDA receptor
Excitotoxic mechanisms at glutamatergic synapses: There are many conditions (e.g., hypoxia, seizures, stroke) that cause excessive to catastrophic depolarization of neurons. This causes excessive release of glutamate and detrimental accumulation of calcium in the postsynaptic neuron that results in necrosis and ultimately apoptosis.

Biological Basis (Test 1) (4 decks)

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