Besides for the amount of time it takes for their signals, what is another important component of slow IPSPs/EPSPs?

Their intensity is stronger (about 2mV vs 6mV for fast vs slow EPSPs respectively)

What two major classes of receptors mediate postsynaptic responses to neurotransmitters?

Ligand-gated ion channels (ionotrophic receptors) and G-protein coupled receptors (metabotrophic receptors)

What is the neurotransmitter that is present at all vertabrate neuromuscular junctions?

Acetylcholine

What is the general structure of nicotinic ACh receptors?

There are 5 subunits which each have 4 transmembrane domains so there are 20 different membrane crossing segments; neuronal receptors have 3 alpha and 2 beta subunits

What subunits of the nicotinic ACh receptor binds ACh?

The alpha subunit

What happens in the synaptic cleft once acetylcholine has been utilitized to open sodium channels?

ACh is quickly broken down by acetylcholinesterase

Where are nicotinic acetylcholine receptors found?

In skeletal muscle

What is the general flow of cause-and-effect through nicotinic acetylcholine receptors?

2 ACh bind, sodium channels open, depolarization occurs and there is an EPSP

How do muscarinic ACh receptors in the CNS function and what is extremely important about them?

They are metabotrophic (GPCR) and generate an inhibitory response

Which is more important in determine the final signal: the neurotransmitter involved or the type of receptor?

Type of receptor

In the presence of a neurological toxin such as curare, what happens when motor axons, which lead to N-ACh receptors, are stimulated?

Subthreshold EPSPs are generated so the signal is not generated; this leads to paralysis

What effect does an antagonist have on receptor sites?

Antagonists bind to receptor sites but do not have the complete conformational similarity to generate the same response; typically, there is no response

Describe the general postsynaptic response to ACh

There is a fast inward current and conductance but there is a slower PSP which is caused by the slow discharging of potassium ions through leak channels

How are endplate currents related to certain inputs of membrane voltage through voltage clamp experiments?

They are directly linear with a small rush of current which eventually decreases

At positive membrane potentials, ACh causes (blank) current; at negative membrane potentials, ACh causes (blank) current

Outward, inward

Does ACh conductance increase or decrease with successive hits?

Increase

How would E-reversal vary based on which ions a membrane receptor passed?

If the membrane were only permeable to either potassium or sodium, E-rev would equal either E-Na or E-K

(This) = g_ACh (V_M - E_ACh)

EPC (endplate currents)

Lowering the external sodium concentration causes EPCs to reverse at more (blank) potentials because ENa is more (blank)

Negative, negative

Raising the external potassium concentration makes the reversal potential more (blank) because EK is more (blank)

Positive, positive

GABA and glycine receptors are both what kinds of channels?

Ionotrophic chloride channels

Benzodiazepines and barbituates are modulators of the GABA receptor which (blank) the GABA current (chloride ion flow)

Enhance

The cell's normal resting potential is approximately equal to what?

E-Cl

GABA conductance increases postsynaptic G_Cl to typically cause an (blank) PSP

Inhibitory

If E-rev is more hyperpolarized than the membrane potential, GABA will have an (blank) effect on the neuron

Inhibitory

When E-rev is more depolarized than the membrane potential, GABA will have an (blank) effect on the neuron

Excitatory

What role do GABA receptors play in developing vs. mature brain cells?

GABA receptors allow for depolarizing responses in the developing brain (there is a high concentration of chloride in the cell) while they allow for hyperpolarizing responses in the more mature brain (there is a low concentration of chloride in the cell)

How are PSPs that arrive on different dendrites added together?

They are added together in spatial configuration, signals stacked one on top of another

How to PSPs arriving at slightly different times add together?

They slightly separate on a time scale and slightly overlap on the vertical polarization axis

What impact does the distance of excitatory synapses have on membrane voltage?

The impact decays with distance

Where are inhibitory synapses typically located?

They are axosomatic or occur down the signaling pathway along the axon and away from the soma