CNS Neurotransmitters Flashcards
What are the monoamine neurotransmitters?
- Norepinepherine (NE)
- Serotonin (5-HT)
- Acetylcholine (ACh)
What are the amino acid neurotransmitters?
- Glutamate (Excitatory)
- GABA (Inhibitory)
- Glycine (Inhibitory)
What are the neuropeptide neurotransmitters?
- Endorphin
- Angiotensin
- Substance P
- Many others
What type of staining showed the nervous system was a collection of individual neurons?
Golgi staining
Describe the two types of transmission speeds and the charactestics of each.
- Fast
- Rapid, point-to-point, transient (doesn’t last long)
- Involve transmitter-gated ion channels (ionotropic)
- Typicall triggered by a single depolarizatoin
- Slow
- Slow, diffuse, lasting
- Involve G-protein coupled receptors (metabotropic)
- Typically triggered by prolonged or repetative depolarization
What functional groups do monoamine neurotransmitters consist of? What is the exception to this?
-
Amine group connected to an aromatic ring by a two carbon chain
- ACh is not a monoamine but is clumped together with this group
What enzyme converts glutamate (excitatory) to GABA (inhibitory)?
Glutamic acid decarboxylase (GAD)
- Wherever there is glutamate, there is also GAD
What determines if a neuron is inhibitory or excitatory? What is the exception?
- It’s receptor
- Gluatamate - Always excitatory
- GABA - Always inhibitory
What neurotransmitters work together to tightly regulate different neural functions?
Glutamate & GABA
- Glutamate released into cleft
- Binds post-synpatic neurons
- Neurons can take up Glutamate and convert to GABA
What receptor is believed to be the source of learning?
Glutamate-NMDA receptor
Describe the Glutamate-NMDA recptor firing.
NMDA is a slective agonist to glutamata
- NMDA, Glutamate, and depolarization from -80mV to -40mV are required to fire
- Depolarization frees a Mg<strong>2</strong>+ that blocked channel
- Ca2+ influx results (Voltage gated)
What is synaptic plasticity?
Regulation of strength of connection between two synapses
- Seen in Glutamate-NMDA receptor
What is glutamate toxicity?
Too much glutamate from:
- Excessive gluatamate release
- Poor glutamate reuptake
Excessive Ca2+ intake triggers neuronal injury/death
What can cause glutamate toxicity?
Stroke: Anoxia can release toxic amounts of glutamate
What is the mechanism of the GABAA receptor and what drugs act on it?
Hyperpolarization via Cl- influx into neuron
Drugs:
- Benzodiazepines
- Barbituates
What is the mechanism of the GABAB receptor and what drugs act on it?
Hyperpolarization via K+ outflux from neuron
Drugs:
- GHB
- Baclofen
What is the disease model for Huntington’s?
Destruction of GABAergic neurons in basal ganglia
What is the disease model for Tetanus and Strychnine?
Inhibition of presynaptic GABA release (results in shortage of GABA in synaptic cleft)
What is the disease model in Stiff-Person Syndrome?
Antibodies destroy GAD and prevent GABA production, causing autoimmune or paraneoplastic syndrome
What drugs can treat excessive glutamate? (Increased glutamate can cause seizures)
- Benzodiazepines (increase GABA efficiency)
- Valproate (Inhibit enzymes that deactivate GABA)
- Topiramate (Inhibit GABA re-uptake)
What are the side effects of treating excessive glutamate with GABA?
- Sedation
- Cognitive slowing
What are the non-therapeutic uses of drugs that increase GABA?
- Anxiolysis, hypnosis, amnesia (occasionally)
- High addictive potential
- “Date-rape” drugs
- GHB (Gamma-hydroxybutrate)
- Benzodiazepines
What nuclei produce Dopamine?
- Pars compacta (substantia nigra) - largest
- Ventral tegmental area
- Hypothalamus
Describe the Nigrostriatal tract.
- Substania nigra → Striatum (D2 receptors)
- Regulates fluid and smooth muscle action