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Neuro > CNS Neurotransmission Information > Flashcards

CNS Neurotransmission Information Flashcards

1
Q

The brain is made of

A

neurons and glia

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2
Q

neurons

A

Neurons (~100 billion in the brain); each neuron can synapse with many other neurons

o Cell body, dendrites, axon

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3
Q

glia

A

Glia—largely not well understood; include astrocytes, oligodendrocytes, microglia

o May have roles in inflammation, brain injury, infection, myelination, neurotransmitter uptake, and more

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4
Q

Neurotransmission

A
  • How the neurons in the brain communicate with each other
  • Synapse: space between two neurons where neurotransmission occurs
  • Neurotransmission between neurons is usually chemical (using neurotransmitters, neuropeptides, etc)
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5
Q

Chemical neurotransmission

A
  • Synthesis of neurotransmitter
  • Packaging of neurotransmitter
  • Release of neurotransmitter
  • Receptors for neurotransmitter
  • Reuptake of neurotransmitter from synapse
  • Degradation of neurotransmitter
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6
Q

Synthesis of neurotransmitter

A

! Therapeutics can target production of neurotransmitter

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7
Q

Packaging of neurotransmitter

A

o Vesicles

o Active transport is needed to concentrate neurotransmitter into vesicle (requires ATP)

o Vesicular monoamine transporter (VMAT)  serotonin (5HT), norepinephrine (NE), dopamine (DA)

o Therapeutics can block packaging of neurotransmitter, causing their concentration in the axon terminal space to rise

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8
Q

Release of neurotransmitter

A
  • o Action potential! Turning electrical signal within the neuron into a chemical signal between neurons
  • o Action potential induced depolarization of the membrane at the axon terminal causes opening of calcium channels which are essential for vesicular release
  • o Classic neurotransmission: neurotransmitter released from axon terminal (presynaptic neuron) acts on either pre- or post-synaptic receptor
  • o Retrograde neurotransmission: neurotransmitter is released from post-synaptic neuron and acts on pre-synaptic neuron (like negative feedback), Ex: endocabbinoids
  • o Therapeutics can block calcium channels and block neurotransmitter release, or can affect ability of the neuron to carry the action potential (stabilizing the neuron membrane in a non-depolarized state)
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9
Q

Receptors for neurotransmitter

A
  • Post-synaptic vs. pre-synaptic
  • Excitatory vs. inhibitory effects
  • Ionotropic receptors
  • Metabotropic receptors

Therapeutics can be agonists, partial agonists/antagonists, or antagonists at receptors

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10
Q

Post-synaptic vs. pre-synaptic receptors

A

Pre-synaptic is usually acting as a negative feedback (inhibiting the release of more neurotransmitter from the pre-synaptic neuron)

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11
Q

Excitatory vs. inhibitory effects

A

Depends on receptor!!!

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12
Q

Ionotropic receptors

A

Ionotropic receptors (aka ligand-gated ion channels)

  • ▪ Fast (directly opens or closes channel)
  • ▪ Usually post-synaptic
  • ▪ Examples: nicotinic acetylcholine receptors, GABA A receptors, glutamate receptors, glycine receptors, 5-HT3 receptors
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13
Q

Metabotropic receptors

A
  • Metabotropic receptors (aka G-protein coupled receptors)
    • Slower than ionotropic receptors because they work by activation of ion channels or signal cascades/second messenger systems
    • Can be pre- and post-synaptically located
    • Subtype of G protein will determine whether it is excitatory (Gs) or inhibitory (Gi)
      • Gs receptor activation:
        • Increases adenylyl cyclase activity
        • Opens Ca2+ channels
        • Inhibits Na+ channels
      • Gi receptor activation:
        • Inhibits adenylyl cyclase activity
        • Closes Ca2+ channels
        • Opens K+ channels
      • Gq receptor activation:
        • Increases phospholipase C activity
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14
Q

Reuptake of neurotransmitter from synapse

A
  • o One method for removal of neurotransmitter from the synapse (ending its action), it “recycles” the neurotransmitter back into the pre-synaptic neuron
  • o Not believed to be active transport (transports with the concentration gradient from more concentrated in the synapse to less concentrated area in the axon terminal of the pre-synaptic neuron)
  • o Examples: serotonin reuptake transporter (SERT), norepinephrine reuptake transporter (NET), dopamine reuptake transporter (DAT), and more
  • o Therapeutics can block reuptake transporters, increasing the concentration of neurotransmitter in the synapse
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15
Q

Degradation of neurotransmitter

A
  • o Enzymatic degradation of neurotransmitter can occur in the synapse or in the pre- synaptic terminal
  • o In the synapse degradation of the neurotransmitter is one way of terminating the neurotransmitter’s action
  • o In the pre-synaptic axon terminal it can decrease the amount of neurotransmitter that is available for packaging into vesicles
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16
Q

Neuroanatomy: Cerebral Cortex

A

Cerebral cortex

  • a. Frontal lobe—planning
  • b. Motor lobe
  • c. Speech
  • d. Somato-sensory
  • e. Vision, smelling, hearing
17
Q

Neuroanatomy: Limbic System

A

Limbic areas

  • Regions include:
    • Hippocampus
    • Amygdala
    • Limbic cortex
  • Functions include:
    • Memory
    • Mood
    • Biological needs
18
Q

Neuroanatomy: Brain Stem

A
  • Brainstem
    • Regions include:
      • Reticular formation
      • Medulla
      • Pons
    • Functions include:
      • Sleep/wake, attention
      • Breathing
      • Blood pressure maintenance
19
Q

Neuroanatomy: Spinal Cord

A
  • Spinal Cord
    • Connects body to brain
    • Input of peripheral information
      • Pain
      • Position
    • Output of central message
      • Movement
      • Blood pressure maintenance
      • Body temperature maintenance
      • Respiration
20
Q

Neurotransmitters

A

Monoamine

Amino acids

Acetylcholine

21
Q

Monoamine Neurotransmitters

A

Dopamine

Norepinephrine

Serotonin

22
Q

Dopamine

A

Dopamine (DA; monoamine AND catecholamine)

  • ○ Synthesis→ tyrosine hydroxylase is the rate limiting step in production of dopamine (converts tyrosine to dopa)
  • ○ Vesicles→ vesicular monoamine transporter (VMAT) packages all monoamines into vesicles in the presynaptic terminal
  • ○ Degradation→ Monoamine oxidase (MAO, found in presynaptic terminal and synapse) and Catechol-O-Methyl tranferase (COMT, found in synapse only)
  • ○ Localization
    • ■ Cell bodies mostly limited to:
      • ● ventral tegmental area (reward, addiction)
      • ● substantia nigra (movement)
    • ■ Projectionstolimbicareas(emotion, memory), striatum, and cortex
  • ○ Reuptake→ Dopamine reuptake transporter (DAT)
    • ○ Receptors: Metabotropic
      • ■ D1family→coupled to Gs
      • ■ D2family→coupled to Gi, may be presynaptic (autoreceptors) or postsynaptic
    • ○ Central diseases/conditions associated with dopamine:
      • ■ Parkinson’sdisease
      • ■ Substanceabuse
      • ■ Schizophrenia
      • ■ ADHD
23
Q

Norepinephrine

A
  • ● Norepinephrine (NE; monoamine AND catecholamine)
    • ○ Synthesis→ synthesized from dopamine (dopamine betahydroxylase converts dopamine to norepinephrine)
    • ○ Vesicles→ vesicular monoamine transporter (VMAT) packages all monoamines into vesicles in the presynaptic terminal
    • ○ Degradation→ Monoamine oxidase (MAO, found in presynaptic terminal and synapse) and Catechol-O-Methyl tranferase (COMT, found in synapse only)
    • ○ Localization
      • ■ Cell bodies mostly limited to:
        • ● locus ceruleus (LC, near brainstem)
        • ● brainstem
      • ■ Projections to amygdala(partoflimbicsystem-emotion,memory),thalamus and cortex
    • ○ Reuptake→ Norepinephrine reuptake transporter (NET)
    • ○ Receptors: Metabotropic
      • ■ alpha1→coupledtoGq
      • ■ alpha2→coupledtoGi,maybe presynaptic (autoreceptors) or postsynaptic
      • ■ beta→coupledtoGs
    • ○ Central diseases/conditions associated with norepinephrine:
      • ■ Cognition
      • ■ Depression
      • ■ Posttraumaticstressdisorder(PTSD)
      • ■ ADHD
24
Q

Serotonin

A
  • Serotonin (5-HT; monoamine ONLY)
  • ○ Synthesis→ synthesized from tryptophan
  • ○ Vesicles→ vesicular monoamine transporter (VMAT) packages all monoamines into vesicles in the presynaptic terminal
  • ○ Degradation→ Monoamine oxidase (MAO, found in presynaptic terminal and synapse)
  • ○ Localization
    • ■ Cell bodies mostly limited to:
      • ● raphe nucleus
    • ■ Projectionstolimbic,midbrain,andcortex
  • ○ Reuptake→ Serotonin reuptake transporter (SERT)
  • ○ Receptors: 13 different receptor subtypes identified (12 metabotropic, 1 ionotropic)
    • ■ 5-HT3→ionotropic;antagonistsat5-HT3receptorsareusedforanti-nausea
    • ■ 5-HT1Dand1A→inhibitory,autoreceptors;agonistsareusedformigraine
    • treatment
    • ■ 5-HT2A→antagoniststothisreceptorareantipsychotics
  • ○ Central diseases/conditions associated with serotonin:
    • ■ Depression
    • ■ Antipsychotics
    • ■ Migraine
    • ■ Obesity/weightloss
25
Q

Acetylcholine

A
  • • Synthesis: Choline acetyltransferase combines choline and acetyl coenzyme A to make acetylcholine
  • • Vesicles: Vesicular acetylcholine transporter packages Ach into vesicles in axon terminal
  • • Degradation: Acetylcholinesterase is very efficient enzyme that breaks down ACh
  • • Localization:
    • o Cellbodiesinforebrainandbrainstem;interneuronsinstriatum
    • o Projectionstolimbicareas,cortex,striatum
  • • Reuptake: Choline transporter (transports only choline after it is degraded in synapse)
  • • Receptors:
    • o Muscarinic G-protei ncoupled receptors found pre- and post-synaptic
    • o Nicotinic Ionotropic receptors
  • • Central diseases/conditions associated with acetylcholine:
    • o Alzheimer’s/Dementia
    • o Parkinson’s
    • o Depression(?)
26
Q

Amino acid neurotransmitters

A

Glutamate-excitatory

GABA-inhibitory

Balance between excitation and inhibition is vitally important in the brain!

27
Q

Glutamate

A

Glutamate = Excitatory

○ Uptake by astrocytes with reuptake transporters specific to glutamate

○ Ionotropic receptors (FAST)

■ AMPA,NMDA,Kainate

○ Metabotropic receptors (mGluR, SLOWER)

■ Inhibitory, so coupled to Gi

28
Q

GABA

A
  • GABA = Inhibitory
  • GABA A receptors → Ionotropic receptors
    • GABA binding to these receptors causes Cl- to enter cell—hyperpolarizing it
    • Receptor where alcohol, barbiturates, benzodiazepines, inhalants all work!
  • GABA B receptors → Metabotropic/G-protein coupled receptors
    • Can be pre- or post-synaptically located
    • GABAB receptors on neurons that release glutamate, dopamine, norepinephrine or serotonin will decrease release of THOSE neurotransmitters
29
Q

Conditions related to some dysfunction or imbalance with glutamate and/or GABA

A
  • ○ Epilepsy
  • ○ Addiction
  • ○ Stroke
  • ○ Schizophrenia
  • ○ Anxiety
  • ○ Sleep disorders
  • ○ Anesthesia

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