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Final

PSYC 3030 Study Guide - Final Guide: Spatial Memory, Outline Of Object Recognition, Dentate Gyrus

9 pages64 viewsFall 2016

Department
Psychology
Course Code
PSYC 3030
Professor
Boyer Winters
Study Guide
Final

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Amino Acid Neurotransmitters I: Glutamate and Aspartate
Excitatory amino acids
Most amino acids serve a role in metabolism and protein synthesis, but some are used directly as
neurotransmitters
Glycine and GABA (inhibitory), glutamate and aspartate (excitatory)
Glutamate and Aspartate
Most abundant, free, non-essential amino acid in the mammalian brain
Synthesized by the body, not required in diet
Glutamate is important for metabolism and protein synthesis in all neurons and glia
Glutamatergic neurons have higher concentration of glutamate
Metabolic and neurotransmitter glutamate are kept separate from one another
Amino acids neurotransmitters are used by a large portion of neurons
Fast, excitatory neurotransmission via ionotropic receptors
Synthesis, Storage, Release, Uptake, Inactivation
Synthesis
Two possible mechanism
1. Alpha KG
Alpha-Ketoglutarate is synthesized from glucose
Transanimation by pydridoxal phosphate and alanine aminotransferase moves the amine group
from a donor amino acid to the alpha-KG, forming glutamate and a de-aminated amino acid
2. Glutamine Cycle
Most neurotransmitter glutamate is synthesized this way
Astrocytes and neurons interact to produce glutamate from glutamine
Glutamine is converted by glutaminase into glutamate and ammonia
Product Inhibition: glutamate and ammonia prevent further production of glutamate by
inhibiting glutaminase
Storage and Release
Glutamate is stored as glutamine (safer)
Glutamate is packaged into vesicles by VGLUT1-3: vesicular glutamate transporter
1 OR 2, and/or 3
VGLUTs are selective markers for glutamatergic neurons
Uptake
EEAT1-5: excitatory amino acid transporters
1 and 2 are on astrocytes
3 is the most widely used
Inhibition of 1 or 2 (astrocytes) leads to an increase of synaptic glutamate, but inhibiting 3 does
not
Inactivation
By glutamine synthetase
Both astrocytes and neurons
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Glutamatergic Pathways
Cerebral cortex, descending pathways from neocortical pyramidal cells: output neurons, have
numerous subcortical projections
Cerebellar cortex: parallel fibres, hippocampus
Intrahippocampal and hippocampal projection pathways (learning and memory, LTP)
Long range and intrinsic projections
Cell bodies are not clustered in one area
Receptors
Ionotropic
AMPA
Agonized by AMPA (alpha-amino-3-hydroxyl-5-methyl-4-isoxazole proprionic acid) and
quisqualic acid
Antagonized by CNQX and NBQX: sedation, ataxia, reduced brain excitability
Sodium and potassium channels
Kainate
Agonized by kainic acid and domoic acid
Antagonized by the same as AMPA receptors, but less so
Sodium and potassium channels
NMDA
Agonized by NMDA (N-methyl-D-aspartic acid) and ibotenic acid
Antagonized by CPP and AP-5 (competitivedamages efficacy), and MK-801, PCP, and
Ketamine (non-competitivedamages efficacy and potency)
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Sodium, potassium, and calcium channels (second messenger functions)
Metabotropic
mGLUR1-7
Use IP3, DAG, and cAMP as second messengers
Mostly autoreceptors, negative feedback
NMDA Receptor
Short-term memory does not require protein synthesis, not reliant on intracellular changes
(NMDA receptor is not needed)
Calcium eventually leads to protein synthesis
NMDA-Dependent-Receptor-Plasticity: increases efficacy of neuronal communication, LTP
Increase of Synaptic Weight: externally derived behaviours changes the circuitry of what
encoded it in the first place
1) Obligatory orthosteric binding sites for two glutamates
2) Obligatory Co-Agonists: glycine or D-serine, these are almost always present, making
glutamate the deciding factor
3) PCP (non-competitive antagonist) allosteric binding site, depressant effects if PCP is bound;
also recognizes other non-competitive antagonists (ketamine, MK801)
4) Mg2+ binding site, blocks the poreCa2+ cannot enter if magnesium is bound
Membrane Depolarizes
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