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IMS: Neuroanatomy > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

Mechanism of Neurotransmission

A
  1. Action potential causes rapid Ca2+ release at nerve terminal
  2. Rapid fusion of vesicles
  3. Diffusion of neurotransmitters across synaptic cleft
  4. Binding to postsynaptic receptor
  5. Change in membrane potential
    • Depoarlization: more positive membrane potential deviation sufficient to initate AP
    • Hyperpolarization: more negative membrane potential
    • Graded response: depolarization not sufficient to initiate AP
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2
Q

Defining

a

Neurotransmitter

A
  1. Present in neurons w/ enzymes involved in synthesis.
  2. Released from nerve terminal after depolarization in Ca2+ dependent process.
  3. Activates specific postsynaptic receptors causing depoarlization/hyperpolarization of postsynaptic membrane.
  4. Same effect with microiontophoresis as phsyiological.
  5. Blocked by specific antagonists.
  6. Action terminated by specific mechanism.
  7. Activates specific presynaptic autoreceptors which usually reduces release and regulates concentration in the synapse.
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3
Q

Neurotransmitter Classes

A
  1. Small Molecules
    • Acetylcholine (ACh)
    • Amino acids
    • Monoamines
  2. Peptides
    • Endorphins
    • Angiotensin
    • Substance P
  3. Di​ssolved Gases
    • Nitric oxide (NO)
    • Carbon monoxide (CO)
  4. Neurosteroids
    • Glucocorticoids
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4
Q

Amino Acid

Neurotransmitters

A
  • Glutamate (Glu) → major excitatory transmitter in cortex and spinal cord
  • Gama-aminobutyric acid (GABA) → major inhibitory transmitter in cortex
  • Glycine (Gly) → major inhibitory transmitter in spinal cord
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5
Q

Monoamine

Neurotransmitters

A
  • Catecholamines
    • Epinephrine (EPI)
    • Norepinephrine (NE)
    • Dopamine (DA)
  • Indolamines
    • Serotonin (5-HT)
  • Imidazoles
    • Histamine (HIS)
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6
Q

Ionotropic Receptors

(Fast)

A
  • 5 subunits form receptor binding site and ion channel
  • Maximized for speed
  • Neurotransmitter binding alters receptor conformation
    • permits fast exchange of ions across membrane
    • alters membrane permeability
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7
Q

Metabotropic Receptors

(Slow)

A
  • 7 membrane spanning subunits
  • Receptor binding activates second messenger systems through G proteins
    • Gs stimulates adenylate cyclase
    • Gi inhibits adenylate cyclase
  • +/- of adenylate cyclase will active/inhibit protein kinase
  • +/- of protein kinase will active/inhibit phosphoprotein phosphatase
  • +/- of phosphoprotein phosphatase will phosphorylate/dephosphorylate various ion channels, enzymes, and proteins
    • Protein phos/dephos can result in altered membrane permeability
    • Can have long-term consequences such as regulation of gene expression
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8
Q

Sensitization

A

Long Term Change

Decreased neurotransmitter levels result in increased receptor numbers leading to increased response.

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9
Q

Desensitization

A

Long Term Change

Increased neurotransmitter levels result in reduced receptor numbers leading to reduced response.

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10
Q

Plasticity

A

Long Term Change

Strengthening of synaptic connections that may allow for memory formation or recovery of function after injury.

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11
Q

Termination of Action

A
  1. Degradation/Recycling by specific enzymes
    • Acetylcholinesterase (AChE) for ACh
    • Monoamine Oxidase (MAO) for monoamines
    • Catechol-O-methyl transferase (COMT) for catecholamines
  2. Reuptake by high affinity membrane transporters
    • glutamate, GABA, glycine, serotonin, dopamine, norepinephrine
  3. Diffusion (removal by extracellular peptidases)
    • most neuropeptides
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12
Q

Effects of Drugs

Presynaptic

A
  1. Block reuptake (e.g. antidepressants)
  2. Change precursor availability (e.g. L-DOPA for Parkinson’s)
  3. Inhibit neurotransmitter synthesis (e.g. alpha methyltyrosine)
  4. Inhibit storage of neurotransmitter (e.g. reserpine)
  5. Alter release of neurotransmitter (e.g. amphetamine)
  6. Provide presynaptic regulation through autoreceptors
  7. Provide presyntaptic regulation through heteroreceptors
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13
Q

Effects of Drugs

Postsynaptic

A
  1. Agonists bind to receptor to produce a response.
  2. Antagonists bind to receptor and reduce or inhibit a response.
  3. Receptor adaptation ⇒ repeated doses of drugs lead to long-term changes in receptor number and affinity resulting in sensitization or desensitization
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14
Q

Effects of Drugs

Degradation Enzyme Inhibition

A

Inhibition of degrading enzymes increases amount of neurotransmitter in the synapse.

MAO inhibitors: selegilene

AChE Inhibitors: neostigmine or donepezil

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15
Q

Cholinergic System

A

Major nuclei for neurotransmitter synthesis:

  1. Septal nuclei project via fornix to hippocampus
  2. Nucleus Basalis of Meynert
    • projects to neocortex
    • degenerates in Alzheimer’s disease
  3. Striatum
    • contains cholinergic interneurons
    • degenerates in Hungtington’s disease
  4. Neocortex contains cholinergic interneurons
  5. Dorsal tegmental area of pontine reticular formation
    • projects to thalamus
    • involved in maintaining states of consciousness
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16
Q

Dopaminergic System

A

Major nuclei for neurotransmitter synthesis:

  1. Substantia nigra pars compacta
    • projects to striatum via nigrostriatal pathway
    • degenerates in Parkinson’s disease
  2. Ventral tegmental area of reticular formation
    • projects to many cortical and subcortical lumbic nuclei
    • Schizophrenia associated with increased DA production
  3. Arcuate nucleus of hypothalamus
    • projects to infundibular portal system
    • regulates prolactin release
17
Q

Noradrenergic System

A

Major nuclei for neurotransmitter synthesis:

  1. Locus coeruleus
    • projects diffusely to entire CNS
    • involved in attention and states of arousal
  2. Lateral tegmental area of reticular formation
    • involved in descending control of pain
18
Q

Serotonergic System

A

Major nuclei for neurotransmitter synthesis:

  1. Raphe nuclei
    • located all along the midline of the brainstem
    • projects diffusely to entire CNS
    • reduced 5-HT associated with depression and insomnia
    • increased 5-HT associated with mania
    • involved in descending control of pain
  2. Pineal gland
    • converts 5-HT to melatonin
    • regulates cicadian rhythms
19
Q

Alzheimer’s Disease

A
  • Caused by loss of cholineric neurons
  • Short term treatment:
    • Increase Ach at synapse
    • Donepezil
      • Inhibits acetylcholinesterase (AChE)
      • Also used with myasthenia gravis
20
Q

Parkinson’s Disease

A
  • Neurodegenerative disease
    • Progressive loss of dopaminergic neurons in the substantia nigra pars compacta
    • See low levels of dopamine
  • Short term treatment
    • Precuror loading with L-DOPA
      • Dopamine cannot cross BBB
      • L-DOPA can cross BBB
    • Carbidopa
      • false substrate for peripheral aromatic amino acid decarboxylase (AAAD)
      • AAAD acts on Carbidopa allowing L-DOPA to diffuse through BBB more efficiently
    • Central AAAD uses L-DOPA to make DA
21
Q

Anxiety

A
  • Involves inability to inhibit conflicting behaviors
  • Suspected that GABA-ergic neurons of limbic system imvolved with compensatory behavior
  • Stimulation of GABA-A receptors ⇒ Cl- mediated hyperpolarization of membrane potential
    • GABA-A receptor has benzodiazepine site
      • Binding incudes conformation in receptor
      • Potentiates GABA-induced inhibition
  • Treatment
    • Lorazepam (Ativan)
      • Binds benzo site of GABA-A receptor
      • Increases inhibitory action
    • Old drugs:
      • Diazepam (Valium)
      • Chlordiazepoxide (Libirum)
      • generally less tolerance when used for anxiety
      • more tolerance when used for anticonvulsive, sleep, and muscle relaxation
22
Q

Depression

Original Treatments

A
  • Theory that depression results mainly from serotonin imbalance
    • Then effects balance of other monoamines
  • Drugs that affect the monoaminergic system
    • Iproniazid
      • Monoamine oxidase inhibitor
      • Blocks MAO allowing monoamine levels to increase in synapse
        • NE, 5-HT, DA
    • Tricyclic antidepressants (TCAs)
      • Block reuptake of monoamines
      • Increases levels of monoamines at synape
      • Many act on NE and 5-HT reuptake
      • Different affinities and effects
      • Not always effective
      • Many side effects
23
Q

Depression

Second Generation Treatment

A
  • Selective serotonin reuptake inhibitors (SSRI)
    • specifically targets serotonin reuptake system
    • Ex. Fluoxetine (Prozac)
    • fewer side effects
    • Also have a lesser affinity for NE and DA transports
    • May take 2-3 weeks before clinical effects
      • Most likely cause long term sensitization or desensitization changes in post-synaptic receptors
      • Involves mechanisms that restore synapses to normal function
24
Q

Schizophrenia

A
  • Attributed to an imbalance in dopaminergic system
    • LIkely involves overstimulation of the dopamine receptor
    • Positive symptoms ⇒ hallucinations
    • Negative signs ⇒ withdrawal, lack of affect
    • Often starts in teenage years
    • Proportion of positive/negative symptoms change with disease progression
  • Treatments:
    • haloperidol (Haldol)
      • Receptor antagonist of dopamine receptor
      • Prevents overstimulation
      • Modulate postive signs better than negative ones
    • Clinical improvements associated with mesocorticolimbic system
    • Side effects associated with:
      • nigrostriatal system ⇒ tardive dyskinesia
      • tuberoinfundibular system ⇒ hyperprolactinemia
25
Q

Pleasure Pathway

A
  • Pathway always activated during pleasurable events
  • Part of limbic pathway called Medial Forebrain Bundle
  • Dopaminergic neurons involved in drug abuse and addition
    • Located in Ventral tegmental area (VTA)
    • VTA neurons project to limbic area called nucleus accumbens
      • Modulates prefrontal cortex activity
  • Cocaine overactivates pathway in unregulated fashion
  • Sets up a behavioral state
    • User expects same degree of overactivation each time
    • Chronic cocaine users experience same autonomic effects of taking the drug if put in an environment of previous exposure
    • Adds to addictive cycle
26
Q

Drugs of Abuse

Direct Effectors

A
  • Cocaine > Amphetamine and methamphetamine
  • Directly affects the dopamine system ⇒ most potential for abuse
  • Blocks the dopamine reuptake transporter
  • Cocain most addictive
    • High affinity and fast onset drug
    • Single dose of cocaine can permanently alter function of the dopamine receptor system
    • Long term changes include:
      • Sensitization
      • Plasticity
      • Neurotoxic effects
  • Fast onset and amount of drug that reaches the brain that determines pleasurable effects vs addictive/dangerous effects
27
Q

Drugs of Abuse

Indirect Effectors

A
  • Heroin, nicotine, and ethanol indirectly effects pleasure pathway
    • Blocks interneurons that normally inhibit VTA cycle
    • “Less addictive”
  • Heroin ⇒ opiod receptors (usually bind endorphins)
    • Treat with Methadone
      • Drug substitute for heroin
      • Prevents heroin or morphine from interacting with opiod receptors
      • Can cause mild euphoria and drowsiness
      • Continued use can restor sexual, immune, and adrenal function
      • Cessation can result in methadone withdrawal
  • Nicotine ⇒ acetylcholine receptors
    • Treatment:
      • Nicotine patches
        • Concentration progressively reduced
      • Buproprion (Wellbutrin)
        • produce dopamine release in mucleus accumbens & modulate limbic circuitry
  • Ehtanol ⇒ GABA receptors
    • Treat with disulfiram (Antabuse)
      • Blocks acetaldehyde dehydrogenase
      • Causes build up of acetaldehyde
      • Produces immediate and severe negative reaction to alcohol intake

IMS: Neuroanatomy (23 decks)

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