Lecture 6: NTs; Small Molecule NTs, Neuropeptides, Endocannabinoids Flashcards
first criterion for identifying a NT
substance must be within the signaling (typically presynaptic) neuron
- looking at enzymes helps us know what they release: if they have glutaminase, they probably are a glutamatergic neuron
second criterion for identifying a NT
depolarization causes release of the substance in a Ca2+ dependent manner
third criterion for identifying a NT
receptors specific to the substance are found in the postsynaptic neuron or cellular target
- sometimes neurons synapse on themselves so we have to be careful with these definitions
types of small molecule NTs
acetylcholine, amino acids, biogenic amines
types of amino acid NTs
glutamate, GABA, glycine
types of biogenic amines
catecholamines, serotonin, histamine
types of catecholamines
dopamine, norepinephrine, epinephrine
types of neuropeptides
brain-gut, opioid, pituitary, hypothalamic-releasing
types of brain-gut neuropeptides
substance P, choleocystyokinin, vasoactive intestinal peptide
types of opioid neuropeptides
endorphines, ekephalins, dynorphins
types of pituitary neuropeptides
vasopressin, oxytosin, adrenocorticotropin hormone
types of hypothalamic-releasing neuropeptides
thyrotropin releasing hormone, leutinizing hormone-releasing
type of lipid-based NTs
endocannabinoids (anadamide (AEA), 2-arachidonoylglycerol (2-AG))
differences between NTs and neuromodulators
NTs carry info, have short range effects; neuromodulators affect how info carried by the primary NTs is processed, make a neuron more or less excitable, have long range effects
main role of dopamine as a neuromodulator
altering other conductances
what is the excitatory primary NT of the CNS
glutamate
- also technically a neuromodulator
what happens when glutamate acts on the metabotropic glutamate receptors
results in changes to voltage; really impacting the excitability of the cell
classes of metabotropic glutamate receptors
Gq coupled, G alpha io coupled
Gq coupled metabotropic glutamate receptor function
increase excitability
G alpha io coupled metabotropic glutamate receptor function
increase K+ or decrease Ca2+ conductance depending on which receptor & where
what are the primary inhibitory NTs of the CNS
GABA & glycine
what kind of channels do GABA & glycine work on
ligand-gated ion channels
where is GABA found
1/3 synapses in the brain (including the hippocampus)
where is glycine found
1/2 all inhibitory synapses in brainstem & spinal cord
- it is also found in the forebrain since it is a co-agonist for NMDA receptors, but there are no glycine receptors in the forebrain
why don’t GABAergic neurons release glutamate
because they don’t have VGLUT
