intro to neuro EXAM #2

Explain the basic structural differences between post-synaptic ionotropic receptors (ligand-gated ion channels) & metabotropic receptors (g-protein coupled receptors). Key functional differences. How do the structural differences explain the functional differences?

Explain how the permeability of an ion through a post-synaptic NT ion channel changes with changing membrane potential when the membrane is at resting potential.

Explain how the permeability of an ion through a post-synaptic NT ion channel changes with changing membrane potential when the membrane is at the ion’s equilibrium potential.

Explain how the permeability of an ion through a post-synaptic NT ion channel changes with changing membrane potential when the membrane’s potential is more positive than that ion’s reversal potential.

Explain how the permeability of an ion through a post-synaptic NT ion channel changes with changing membrane potential when the membrane’s potential is more negative than that ion’s reversal potential.

Explain the basic general principle of excitatory versus inhibitory postsynaptic potentials (PSPs) based on the reversal potential of the ion moving through the channel and the neuron’s threshold for generating an action potential

What is the receptor type & basic properties of nicotinic receptors?

Nicotinic receptors are ligand-gated ion channels (ionotropic receptors).

They are large protein complexes consisting of 5 subunits. Allowing positively charged ions like Na and Ca to rush into the cell.

What is the receptor type & basic properties of muscarinic receptors?

What is the receptor type & basic properties of acetylcholine receptors?

What is the receptor type & basic properties of ionotropic receptors?

What is the receptor type & basic properties of glutamate receptors?

What is the receptor type & basic properties of GABA receptors?

Explain the differences between how a molecule like acetylcholinesterase and how reuptake molecules in the presynaptic membrane or in glial cells remove their NT from the synaptic cleft after transmitter release from the presynaptic neuron

Explain the special properties of the glutamatergic NMDA (n-methyl-D-aspartate) receptor. Why is it called a “coincidence activity detector)

What are the biogenic amines & their subclass?

• Dopamine

• Epinephrine

• Norepinephrine

• Histamine

• Serotonin

What is the psychological & psychiatric importance of catecholamines?

Dopamine: d2 produced in the ventral tegmental is believed to be involved in motivation, reward, & reinforcement.

Epinephrine: project to the hypothalamus and thalamus.

Norepinephrine: regulates arousal, attention, alertness, fight or flight. Synthesized within locus coeruleus.

Explain how an SSRI (selective serotonin reuptake inhibitor) achieves its pharmacological effect.

Why is tetrahydrocannabinol, the psychologically active agent in marijuana, so efficient at activating specific neurons?

What features make nitric oxide (NO) such an unusual NT?

Describe the main components of cyclic adenosine monophosphate (cAMP)

This is a major second messenger linked to metabotropic NT receptors… FINISH!

Explain one further effect (beyond the diagram) of increasing protein phosphorylation that the second messenger system- cAMP- produces.

What are the basic steps in the activation & deactivation of a G-protein coupled receptor?

Define Cell signaling molecule + example from the neurobiology of synaptic plasticity

Define Receptor + example from the neurobiology of synaptic plasticity

Define second messenger + example from the neurobiology of synaptic plasticity

Define Heterotrimeric G-protein + example from the neurobiology of synaptic plasticity

Define Transcription factor + example from the neurobiology of synaptic plasticity

Protein kinases & phosphates are major targets of second messenger systems in neurons. Explain how each helps to regulate protein phosphorylation and what effects each has on key proteins in intraneuronal signaling pathways.

Explain facilitation (the short-term changes in synaptic strength & the basic mechanism by which each is produced). How can these short term changes contribute to the study of learning and memory?

Explain synaptic depression (the short-term changes in synaptic strength & the basic mechanism by which each is produced). How can these short term changes contribute to the study of learning and memory?

Explain augmentation (the short-term changes in synaptic strength & the basic mechanism by which each is produced). How can these short term changes contribute to the study of learning and memory?

Explain (post-tetanic) potentiation (the short-term changes in synaptic strength & the basic mechanism by which each is produced). How can these short term changes contribute to the study of learning and memory?

What are some behavioral differences between short-term and long-term sensitization? What is the synaptic basis for short-term sensitization in Aplysia? What additional changes underlie long-term sensitization in Aplysia?

What is long-term potentiation(LTP)? Explain how LTP can be generated experimentally in neurons in the CA 1 region of the mammalian hippocampus.

What is long-term depression (LTD)? How is it generated experimentally? Compare & contrast the intracellular signaling pathways involved in LTP versus LTD.

Explain the mechanisms for the initial acquisition of LTP in mammalian neurons (so-called “early” or “E-LTP”)? What additional mechanisms are needed for long-lasting (“late” or L-LTP)?