8 Mar 2015
School
Department
Course
Professor
•Inside the cell: A-(impermeable, so stay inside at the resting state), K+
•Outside the cell: Na+(at the resting state, ion channels are closed; impermeability; after depolarization,
sodium ion channel opens, freeing to rush inside), Cl-
•-60: threshold of excitation
•+40: Na+ ion channel refractory; membrane potential starts hyperpolarization; sodium is actively pumped
out, potassium actively pumped in to go back to the normal resting state
•Influx of calcium ion leads to biochemical and structural changes in the postsynaptic cells
•Nigrostrial, Mesocortical and Mesolimbic systems are examples of dopaminergic pathways
•What causes and action potential membrane: permeability to Ca+
•What causes hyperpolarization: K+ leaving the cell through elect
•Microtobules are involved in axoplasmic transport
•Muscimol, a GABA agonist, is used to commonly in experimental studies to increase the amount of GABA,
creating a temporary lesion by stopping the activity in the affected area
•
•NMDA and AMPA
o NMDA controls both sodium and calcium ion channels where AMPA only controls calcium ion
channel
oAMPA is only a voltage-dependent receptor while NMDA is a voltage and neurotransmitter-
dependent receptor, requiring Magnesium ion channels
•Inotropic receptor: neurotransmitter binds to the receptor at the binding site open ion channel
•Metabotropic receptor: neurotransmitter binds to the receptor at the binding channel, G-proteins
Second messengers Open ion channel; takes longer to begin but lasts longer
•Autoreceptors
oType of metabotropic receptor
oRespond to neurotransmitters released by that neuron itself
oRegulate internal processes
oMost cases inhibitory
•Tolerance
oDiminishing effect of drug after repeated administration
oThe body attempts to compensate for the effects of the drug
Decrease in effectiveness of binding (decrease in # or receptor and/or their affinity to the
drug)
Less effective coupling of receptors to ion channels and/or production of second messengers
•Withdrawal
•Agonists: increase the release of neurotransmitters
oDrugs is a precursor of a neurotransmitter
oDrugs stimulates postsynaptic receptor
oDrugs blocks autoreceptors
oDrugs stop reuptake
•Antagonists
oDrugs inhibits synthesis of neurotransmitter
oDrugs inhibits release of neurotransmitter
oDrugs prevents storage of neurotransmitter in vesicles
oDrug blocks postsynaptic receptors
oDrugs activate autoreceptors