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202: Theme 1, Fundamental neuroscience and the brain > Chemicals in the brain > Flashcards

Chemicals in the brain Flashcards

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1
Q

Synaptic transmission sequence

A
  1. An AP arrives to the presynaptic button, causing depolarisation of the membrane.
  2. Depolarisation opens voltage gated calcium channels, there is an influx of calcium ions.
  3. Calcium ions cause the migration of vesicles with NT to dock at the plasma membrane.
  4. Vesicles fuse with plasma membrane and release NT into the synaptic cleft.
  5. NT diffuses across the cleft and binds to specific receptors on the post-synaptic plasma membrane, initiating a response by opening or closing channels- inhibitory or excitatory.
  6. NT is removed from the synaptic cleft by glial cells or enzymes.
  7. Vesicular membrane is recycled from the presynaptic membrane.
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2
Q

Glutamate

  • Where + What
  • Function
  • Synthesis
A

Amino acid NT, main excitatory NT found in the CNS

Function:
- Causes depolarisation of the post-synaptic membrane.

Synthesis:

  1. Made via the Kreb’s cycle from glucose.
  2. Converted from glutamine using glutaminase.
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3
Q

Re-uptake of glutamate

A

Into the presynaptic button using excitatory amino acid transporters (EAATs)

Relies on the electrochemical gradient formed by Na+/K+ ATPase
- 2Na+ co-transported with Glu.

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4
Q

Storage of glutamate

A

After synthesis in the cytoplasm, loaded into the vesicles via vesicular glutamate transporters (VGLUTs).

This relies on a proton gradient.

  • Exchanges H+ for glutamate.
  • H+ originally pumped into vesicles via H+- ATPase
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5
Q

GABA

  • Function
  • Speed of action
A

Gamma-aminobutyric acid
- An amino acid NT

Function:
Main inhibitory NT found in the brain.

Speed of action:
- Rapid, stored in small, clear core vesicles

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6
Q

Synthesis of GABA

A

Made from glutamate

- Using glutamic acid decarboxylase (GAD)

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7
Q

Storage of GABA

A

Pumped into vesicles using GABA transporter (GAT)

- Uses H+ gradient

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8
Q

Recycling of GABA

A

Re-uptake into the glial cells and neurones.
- Glial cells convert it t glutamine before transporting it back to neurone.

GABA is not recycled, it is made de novo whilst the vesicles are reformed.

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9
Q

The need for different types of neurotransmitters

A

Some neurotransmitters pass on information
- Glu, GABA

Others have modulating effect: active of inhibit entire circuits of neurone involved in specific brain functions.
- e.g Ach.

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10
Q

Glycine

  • Function
  • Storage
A

Inhibitory amino acid NT
- In the spinal cord and brain stem.

Storage:
- Transported into synaptic button using GABA transporter (GAT)

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11
Q

Vesicle docking

A

Influx of calcium ions from depolarisation
- Ca2+ binds to calmodulin kinase II

Calcium-bound calmodulin kinase II phosphorylates synapsin.

Phosphorylated synapsin is unable to bind to cytoskeleton, releases vesicles to active zone.

SNARE complex docks vesicle to plasma membrane.

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12
Q

Vesicle release

A

Mechanism= exocytosis.

  1. Synaptobrevin on vesicle membrane binds to plasma membrane proteins to form SNARE complex.
  2. SNARE complex pulls vesicular membrane to plasma membrane.
  3. Calcium influx binds Synaptotagmin.
  4. Calcium-bound synaptotagmin binds to SNARE complex and plasma membrane, causing them to fuse.
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13
Q

Botox

  • Species
  • Mechanism
  • Uses
A

Poison from Clostridium botulinum species.

Mechanism

  • Binds to SNARE protein, preventing release of Ach at neuromuscular junction.
  • Causes muscle relaxation.

Uses:
Treatment for muscle spasm.

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14
Q

Tetanus

  • Species
  • Mechanism
  • Uses
A

Clostridium tetani releases a toxin, acts as a poison.

Mechanism:

  • Binds to SNARE protein, preventing release of GABA and Gly.
  • Dis-inhibits cholinergic neurones
  • Permanent muscle contraction.
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15
Q

Excitotoxicity

A

The damage or death of cells cause by excess excitatory stimulation.
- Due to excess Glutamate or too little GABA/glycine.

Constant stimulation causes excess influx of Ca2+ which increases digestive enzymes, causing cell death.

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16
Q

Cerebral ischaemia

- Mechanism

A

Lack of blood flow to the brain.
- Leads to excitotoxic cell death.

Metabolic events are disrupted
- Reversed Na+/K+ channels, pumps out glutamate into the synaptic cleft via transporters

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17
Q

GHB- gamma hydroxybutyrate

A

Date rate drug

Metabolite of GABA, converted back to GABA which administered.

Causes excess inhibition of neurones leading to sedation/ unconsciousness.

18
Q

Congenital myasthenia syndromes

- What is the abnormality in neurones

A

Disruption of vesicle recycling.

19
Q

LEMS mechanism of pathology

A

Caused by autoimmune attack on Ca2+ channels.

Prevents release of NT.

20
Q

Latrotoxin

A

Poison that triggers vesicle fusion to the plasma membrane

- Excess release of NT

21
Q

Differential release of NT

A

Low frequency stimulation = Only small molecular NT in small, clear core vesicles are release.
- Due to localised increase in Ca2+.

High frequency stimulation= BOTH small molecular and large molecular NT released

22
Q

Serotonergic system

A

Modulatory system involved in:

  • Sleep
  • Pain
  • Emotion
  • Appetite

Small set of neurones arising from the brain stem (Raphe nuclei) are interconnected.

  • Basal ganglia
  • Thalamus + Hypothalamus
  • Temporal lobe
  • Cerebellum
23
Q

Serotonin

  • Function
  • Storage + re-uptake + removal
A

Indolamine NT, released in the CNS and enteric NS
- Affects mood, sleep, appetite and pain.

Storage:
Pumped into vesicles

Re-uptake:
- Into presynaptic terminal using Serotonin transporters (SERTs)

Degradation:
- Monoamine oxidase in the cytoplasm

24
Q

Synthesis of serotonin

A

Derived from amino acid tryptophan.

  1. Tryptophan —> 5-HTP
    - Uses tryptophan hydroxylase.
  2. 5-HTP —-> Serotonin
    - Using 5-HTP decarboxylase
25
Q

Dopamine

  • Function
  • Storage
  • Re-uptake
  • Degradation/ inactivation
A

Catecholamine NT made in presynaptic neurone cytoplasm.

Storage:
- Pumped into vesicles using vesicular monoamine transporters (VMATs)

Re-uptake:
- Into presynaptic terminal using (Dopamine transporters) DATs

Degradation:
- Monoamine oxidase (MAOs)

Inactivation:
- Catechol-o-methyl-transferase (COMTs)

26
Q

Dopamine synthesis

A

Derived from tyrosine , in the cytoplasm.

  1. Tyrosine —> Dopa
    - Using tyrosine hydroxylase (TH)
  2. Dopa—> Dopamine
    - Dopa decarboxylase.
27
Q

Adrenaline and noradrenaline synthesis

A

In the vesicles:

  1. Dopamine—-> Noradrenaline
    - Uses dopamine-beta-hydroxylase (DBH)
  2. In cytoplasm:
    NADR—-> adrenaline
    - Using PNMT
    - ADR stored into vesicles using vesicular monoamine transporter (VMAT)
28
Q

Fluoxetine/ Prozac

  • Drug type
  • Mechanism
  • Indications
A

Selective serotonin re-uptake inhibitor (SSRI)
- Blocks Serotonin transporter in presynaptic plasma membrane

Treatment:

  • Depression
  • OCD
29
Q

Fenfluramine

  • Drug type
  • Mechanism
  • Indications
A

Appetite suppressant

Mechanism:

  • Stimulates serotonin release
  • Inhibits serotonin re-uptake

Used to treat obesity.

30
Q

MDMA

  • Drug type
  • Mechanism
  • Indications
A

Psychoactive drug

Mechanism:

  • Reverses Noradrenaline and Serotonin transporters on the plasma membrane.
  • Increases release of these NT in the synaptic cleft

Currently being assessed to be used for PTSD.

31
Q

Amphetamine

  • Drug type
  • Mechanism
  • Indications
A

Stimulant drug

Mechanism:

  • Blocks dopamine and Noradrenaline re-uptake
  • Reverses the transporters on the plasma membrane for both NT.

Indications:

  • Narcolepsy
  • ADHD
32
Q

Cocaine + Methyphenidate

  • Drug type
  • Mechanism
  • Indications
A

Stimulants

Mechanism:

  • Blocks Dopamine transporters, thus re-uptake
  • Increases synaptic cleft dopamine.

Indications (Ritalin
):
- ADHD
- Narcolepsy.

33
Q

Selegiline

  • Drug type
  • Mechanism
  • Indications
A

Selective irreversible monoamine oxidase inhibitor

Mechanism:
- Blocks MAO, allowing more DA to be release on activation.

Indications:

  • Early stage Parkinson’s disease
  • Depression
  • Dementia
34
Q

Entacapone

  • Drug type
  • Mechanism
  • Indications
A

Selective, reversible inhibitor of COMT (catechol-o-methyl transferase)

Mechanism:

  • Inhibits COMT, preventing Dopamine inactivation.
  • Increases available DA

Indications:
Parkinson’s disease.

35
Q

Acetylcholine

  • Function
  • Synthesis
  • Storage
A

Small molecule neurotransmitter.

  • Main Modulatory NT in the brain
  • Parasympathetic system

Synthesis:
Choline + Acetyl CoA
- Using Choline transferase

Storage:
- Pumped into vesicles using vesicular acetylcholine transporter.

36
Q

Degradation and removal of Ach

A

Degradation:
Acetylcholinesterase enzyme in synaptic cleft.
- Choline is transported back into presynaptic terminal

37
Q

Neostigmine

  • Drug type
  • Mechanism
  • Indications
  • Removal
A

An acetylcholinesterase inhibitor.

Mechanism:
- Prevents breakdown of Ach, prolongs its effect.

Treatment for myasthenia gravis (MG)

Broken down by proteases extracellularly

38
Q

Neuropeptides NT

  • Speed of action
  • Function
  • Removal
A

Released slowly but its effects last for a longer period than small molecules.

They are created in the soma and packaged there- quickly transported to the axon terminal.

Many functions, including: sensory functions.

Broken down by proteases extracellularly

39
Q

NO as a NT

  • Synthesis
  • Action
  • Removal
A

Soluble gas

  • Made in the POSTsynaptic neurone
  • Nitric oxide synthase (requires Ca2+- calmodulin)

Retrograde signalling
- made in post-synaptic neurone and diffuses between the synaptic cleft

Action:
- Activates guanylyl cyclase—-> cGMP

Removal
- Converted into an inactive form.

40
Q

Endocannabinoids

- Function

A

Small lipids, act as a NT

Reduces GABA at certain terminals

Active compound in marijuana

202: Theme 1, Fundamental neuroscience and the brain (27 decks)

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