Synaptic Physiology Lab [3]

Question 1

Describe the mechanisms by which curare and elevated Mg/low Ca solutions produced their effects.

Answer 1

Curare blocks the nicotinic receptors, post-synaptically

Low Ca causes low transmitter release, pre-synaptically

Question 2

Recognize and understand the events that underlie the visually‐observed transition from individual muscle twitches to a tetanus as the frequency of stimulation to the motor nerve is increased.

Answer 2

x

Question 3

Describe the main experimental observations that underlie the Quantum Hypothesis of transmitter secretion

Answer 3

The pretty step-wise graft!

Question 4

Describe the effects on synaptic transmission of bathing a preparation in a solution containing curare, and a solution containing elevated Mg/low Ca ion concentrations

Answer 4

Curare: blocks the nicotinic receptors which mimics myasthenia gravis (destroying of the Ach receptors)

Elevated Mg/low Ca: Low transmitter release, mimics myasthenic syndrome

Question 5

Recognize the effects of neostigmine on synaptic transmission, and describe the drug’s mechanism of action

Answer 5

Neostigmine is a treatment for Myasthenia Gravis. It inhibits Acetylcholinesterase, allowing more ACh to be present in the cleft, allowing more possible ACh molecules to interact with the limited receptors.

Question 6

Describe synaptic facilitation and synaptic depression and how they interact during repetitive stimulation in curare and in elevated Mg/low Ca solutions.

Answer 6

x

Question 7

Describe the causes of myasthenia gravis and the myasthenic syndrome, and the effects of these diseases on synaptic transmission at the neuromuscular junction.

Answer 7

Myasthenia Gravis: circulating antibodies that block/damage acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors at neuromuscular junctions.

Myasthenic Syndrome: presynaptic disorder of neuromuscular transmission in which quantal release of acetylcholine (ACh) is impaired due to autoantibody-mediated removal of a subset of the Ca2+ channels involved with neurotransmitter release

Question 8

Differentiate between spontaneous miniature end plate potentials (MEPPs) and nerve‐evoked end plate potentials (EPPs).

Answer 8

MEPP is result of one vesicle (one quantum) release. Even when motor neuron is not stimulated, neurotransmitter can be released spontaneously

EPPs are in the addition of 0, 1, 2, 3, 4, and so on ( can see the quantal nature of nerutrnasmitter release). Some EPP has amplitude of 0 because nothing was released

You see MEPP that does not correlate with stimulation (this is how you can tell between the EPP and MEPP)