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Structure and Function 2- Exam 1 > Neurotransmitters and Neuromodulator > Flashcards

Neurotransmitters and Neuromodulator Flashcards

1
Q

Ionotropic

A

These receptors are ion channels. Muti-unit channels that form a poor

  1. Neurotransmitter binds
  2. Channel opens
  3. Ion flows acrosse membrane

RAPID ACTING MECHANISM (either depolarization/repolarize)

Example: Ligand gates ion channels

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2
Q

Metabotropic

A

Require secon messenger pathway

“SLOW ACTING”

(phosphorylate/dephosphorylate channel)

  1. Neurotransmitter binds
  2. G-proteins is activated
  3. G-proteins subunits or intracellular messengers modulae ion channels
  4. Ion channels flow
  5. Ions flow across membrane
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3
Q

Where are neurotransmitters found?

A

Synthesized in the neuron and present in the presynaptic terminal, and its release exerts a defined action on the post synaptic cell

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4
Q

When a neurotransmitter is administered exogenously, it mimics what?

A

Mimics the action of the endogenous chemical

(same effect in the lab as in the body)

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5
Q

What are the different processes that can occur to remove neurotransmitters from the synaptic cleft?

A

Reuptake

degradation

diffusion

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6
Q

What are the diffeent type of neurotransmitters?

A

Small molecule transmitters

Neuropeptides

Steroid Hormones as Neuromodulators

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7
Q

What are the different type of Small molecule neurotransmitters?

A

•Amino acid neurotransmitters:

glutamate

GABA

glycine

•Brain stem neurotransmitters:

acetylcholine

biogenic amines (brain stem monoamines)

catecholamines: dopamine, norepinephrine

Indoleamines: seratonin

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8
Q

What are the different types of Neuropeptides?

A

Opiods

tachykinins

gastrins

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9
Q

What is Glutamate?

A

it is a amino acid transmitter

Predominant excitatory NT in the the CNS (ALWAYS)

Has a widespread distribution of neurons and receptors (Pyramidal cells of the cerebral cortex)

Released at about 90% of CNS synapses

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10
Q

How is Glutamate removed from the synaptic cleft?

A

Via diffusion (since it is a very small molecule)

and

glial uptake

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11
Q

Glutamate is involved in what pathway of the body?

A

Involved in synaptic plasticity

Long term potentiation, long term depression

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12
Q

What two medical conditions involve Glutamate?

A

Seizures (neurons firing out of control) and epilepsy.

Excitotoxity

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13
Q

Glutamate - Ionotropic Receptors

A

•NMDA RECEPTORS (big player in cytotoxity)

Binding site for glutamate, NMDA, and glycine

Permeabel to Cations (Na+, Ca2+, K+) , rapid depolarization

Blocked by Mg2+ at resting membrane potential (so initial depolarization stimulus is required to get ion out. Glutamate has to first act at one of the other two receptors to start depolarization)

  • AMPA RECEPTORS
  • KAINATE RECEPTORS
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14
Q

Glutamate - Metabotropic Receptor

A

• Metabotropic glutamate receptors may be on the presynaptic neuron (autoregulation, self binding after release of glutamate), on the post-synaptic neuron, or on glia cells.

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15
Q

What is GABA?

A

It is a amino acid transmitter

Glutamate -> “Gamma-aminobutyric acid” (loss of carboxygroup)

(enzyme = Glutamic acid decarboxylase)

•Predominant inhibitory neurotransmitter in the CNS

Caused chlorine influx

•Widespread distribution of neurons and receptors

Lots of interneurons are GABA

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16
Q

How is GABA removed from the synaptic clet?

A

Via Diffusion

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17
Q

What are the Pharmocological drugs that utilize GABA?

A

Benzodiazepines - antianxiety (Valium and Xanax)

anti-anxiety

Barbiturates

anesthesia

(makes it harder for neurons to fire because they are hyperpolarized)

“Highly Adictive”

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18
Q

GABA Ionotropic Receptor

A

GABAA Receptors

  • Binding sites for GABA, benzodiazepines, barbiturates.
  • Permeable to chloride ions, hyperpolarization

Cause hyperlorization and make it more diffictul to have a AP

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19
Q

GABA Metabotropic Receptor

A

GABAB Receptor

(have to subunits that work together - allosteric modulation. B1 binds GABA and then activate B2, which is the G protein couple part that will hyperpolarize the neuron)

  • Dimerization, “allosteric modulation”.
  • Actions through G-protein mechanisms
  • Increased K+ conduction, hyperpolarization
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20
Q

What is acetycholine?

A

It is a brainstem neurotransmitter

(Produced in the Pedunculopontine nucleus and Nucleus basalis)

• Implicated as playing a role in cognition and learning.

Acts through nicotinic (ionotropic, excitatory/neuromuscular junction)

or

muscarinic (metabotropic; excitatory or inhibitory/Second messenger pathways) cholinergicreceptors.

• Synthesized by choline and a actetly group with the help of choline acetyltransferase. Choline is not biosynthesized and must be obtained through the diet.

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21
Q

How is excess acetycholine degraded?

A

degraded in the synapse by the enzyme acetylcholinesterase

22
Q

Acetycholinesterase inhibitors is clinically used to help manage which disease?

A

Myasthenia Gravis

23
Q

What is Dopamine (DA)?

A

It is a catecholamine that falls under brainstem monoamines

•Dopamine exerts its actions through metabotropic receptors (primarily D1 and D2).

D1 receptor activation stimulates adenylyl cyclase (excitatory).

D2 receptor activation inhibits adenylyl cyclase (inhibitory).

24
Q

What is the Nigrostriatal pathway

A

Dopamine pathway from Substantia Nigra to basal nuclei (basal ganglia)

“Dopamine nuerons that dies in Parkinson’s”

25
Q

Describe the cinical symptoms and pathology hallmarks of Parkinson’s Disease?

A

Clinical symptoms

  • Hypokinetic movement
  • Cogwheel rigidity

Pathology hallmarks

  • Nigrostriatal degeneration
  • DA neuronal degeneration in substantia nigra

The Nigrostriatal Pathway is affeced

26
Q

What is the Mesolimbic pathway?

A

Dopomanine receptors from the ventral tegmental area to the nucleus accumbens to the prefrontal cortex

involved with motivation and reward. It is heavyly implicated in addiction.

27
Q

Norepinephrine goes through what synthesis before is becomes norepinephrine?

A

It goes through dopamine synthesis

(enzyme is Dopamine Beta-hydroxylase)

28
Q

What is Norepinephrine?

A

It is a Catecholamine that is classified as the brain stem monoamine.

•primarily involved in stress and arousal, but is also implicated in higher cognitive functions.

Widespread distribution

•Its actions are exerted through alpha and beta adrenergic receptors.

Metabotropic receptors, excitatory or inhibitory depending on the receptor subtype and on the target cells.

29
Q

How is norepi removed from the synaptic cleft?

A

Presynaptic reuptake mechanism

(uptake proteins on the pre-synaptic terminal)

Monoamines synthesiszed in the nerve terminal

30
Q

What is the basis of Indolamines?

A

Tryptophan based

31
Q

What is Seratonin (5-Hydroxytryptamine)?

A

It is an Indolamine (Brain stem monoamine)

Alson known as 5HT

  • Involved in mood, and heavily implicated in anxiety disorder and depression.
  • Actions are exerted through multiple subtypes of metabotropic receptors, which may cause excitatory or inhibitory responses.
32
Q

How is Seratonin (5HT) removed from the synaptic cleft?

A

Presynaptic reuptake mechanism

33
Q

Reuptake inhibitors (SSRIs) cause there to be more 5HT in the synaptic cleft, how does that affect the body?

A

Change Mood

SSRI are effective in treating mood disorders

34
Q

Small molecule transmitters

Site of Synthesis

Type of Vesicle

Mechanism of Release

Release and Replenishment

A

Site of Synthesis: Synthesized locally in nerve terminalis

Type of Vesicle: smaller “lucent” vesicles

Mechanism of release: Localized release at active zone, “docking” recycling of vesicles

Release and Replenishment: Release can be rrapid and sustained

35
Q

Neuropeptides

Site of Synthesis

Type of Vesicle

Mechanism of Release

Release and Replenishment

A

Site of Synthesis: Synthesized in cell body (ribosomes) (require protein sythesis and need gene)

Type of Vesicle: Large ‘dense core’ vesicles (have Leucent and dark vesicles)

Mechanism of Release: “Secretory Pathway” not localized to active zone, no recycling of vesicles

Release and Replenishment: slower secretory release (Metabotropic), slower replenshment

36
Q

Peptides co-transmit with what?

A

Peptides and small molecule transmitters typically coexist in the same neuron and are released together (co-transmission)

37
Q

Types of Neuropeptides

A

Edorphines - pain killers (inhibitory)

Tachykinins - pain transmitters (excitatory)

Somatostatin - hypothelamic peptide (inhibitory)

Cholecystokinin - brain gut peptide (excitatory) - inhibit appetite

38
Q

Nuerotransmitters

Source

Receptors

Mechanism of action

Speed and duation of actions

A

Source: Released from presynaptic nerve terminals

Receptors: Bind to membrane receptors (ionotropic and metabotropic)

Mechanism of Action: Ion flow or second messenger signaling alters membrane potential

Speed and duration of actions: Rapid, acute, localized actions

39
Q

Steroid Hormone

Source

Receptors

Mechanism of action

Speed and duation of actions

A

Source: Circulate in the blood stream (can cross the BB)

Receptors: diffuse into cell to bind intrecellular receptors (receptor in the cell)

Mechanism of action: “Genomic signalin” alters transcription of hormone-responsive genes (transcription factor turning genes on and off)

Speed and duation of actions: Slow, extended, “global” actions

ONLY LIMITING FACTOR - DO YOU OR DONT YOU HAVE THE RECEPTOR TO EXPRESS

40
Q

Organizational Effect of Steroid Hormones

A

“There are Sex diffences in the brain”

  • Early development exposure to gonadal steroids. Permanetly shape hormone-sensitive brain circuits
  • Shape the neurocircuitry that controls reproductive functions (male shuts down ovulation center)
  • Widspread effect developin limbic and cortical Systems
  • sex difference in cognitive task:
    • males have hot spot of intense activity and female have widspread activity with math
    • better performance by males with 3-D puzzles
    • females are more intune to suttle difference like color change
41
Q

What is the default brain?

A

The default brain is female. So the organizational effects that occur in development typically happen in males.

“burst of testosterone exposure”

42
Q

Activational Effects of Steroid Hormones

A
  • After Puberty
  • Females hormones flunctuate/Cyclic, male hormones are more steady
  • Receptor dependent
  • Adrenal Steroids
    • Hippocampus is affected by Cortisol (high levels are neurotoxic)
  • Gonadal Steroids
    • Limbic System is affected by Estrogen, Testosterone, and Progesterone (impact mood)
43
Q

What are the activation effect of adrenal Steroids in the brain?

A
  • A number of studies in the last several years have confirmed a strong connection between stress, high cortisol levels, damage to the hippocampus and memory.
  • This connection shows up across a wide range of human medical conditions including post-traumatic stress disorder, Cushing’s disease, and depression.
44
Q

Which disorders are more likely in men than women?

A
  • Autism
  • Early onset schizophrenia
  • Alcoholism
  • Antisocial personality disorder
  • ADHD
45
Q

Which disorders are more common in women than men?

A
  • Depression
  • Anxiety disorder
  • Somatic complaints
  • PTSD
  • Alzheimer’s disease
46
Q

Most neurotransmitters are what type?

A

Small molecule neurotransmitters

47
Q

In the CNS how does Glycine behave?

A

It is excitatory

48
Q

This type of NT begins with Tyrosine?

A

All catecholamines

(enzyme Tyrosine hydroxylase convertes Tyrosine to L-DOPA, which is the precursor for dopamine)

49
Q

Dopamine does not cross the BBB so how can you treat a patient with Parkinson’s?

A

You give the L-DOPA which can cross the BBB and then it is converted to Dopamine

50
Q

Norepinephrine is converted to epinephrine? Where is this completed?

A

Made in the adrenal gland

51
Q

Where is norepinephrine made?

A

In Bilateral nuclei called Locus Coeruleus (pigmented neurons that are blue) that are located in the PONS.

52
Q

Seratonin is found in the brianstem just like dopamine. It is produced by which type of nuclei?

A

Raphe Nuclei

(Nuclei along the midline around the midline, ventrally and dorsally)

Structure and Function 2- Exam 1 (13 decks)

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