Synaptic Transmission Flashcards by Emily Wagner

What is the intermembrane structure that connects cells for gap junctions called?

connexons

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in what direction does conduction flow through a gap junction?

both directions (gap junctions are bidirectional)

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at what speed does conduction travel through the gap junction?

fast, there is no synaptic delay like that seen in chemical synapses that must undergo secretory process)

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what is an important characteristic of gap junctions for electrical conduction?

allow large number of cells to contract simultaneously

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in what ways does a gap junction differ from other membrane channels?

the normal state of the channel is to be open.
the gap junction channel spans two cell membranes.
both ends of the gap junction channel are intracellular.
both cations and anions can pass through the same channel.

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can gap junctions close?

Gap junction channels can close so that cells are no longer electrically coupled. This may protect normal cells from neighboring cells that are damaged

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what might make a gap junction close?

high Ca
high H (or low pH)
depolarization of one cell

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what are the first two parts of synaptic transmission?

Release of a chemical transmitter from the presynaptic nerve terminal.
Diffusion of the transmitter to the postsynaptic membrane

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what are chemical synapses?

Distinct cytoplasmic discontinuity that separate the presynaptic
and postsynaptic membranes, synaptic cleft.

Contains a high concentration of mitochondria and synaptic
vesicles

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what is the third and fourth steps of synaptic transmission?

Binding of the transmitter to the postsynaptic receptor and response.
Inactivation or removal of the transmitter

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what direction co chemical synapses flow?

only one direction

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at what speed do chemical synapses work?

slightly slower than electrical due to the synaptic delay of 0.5 msec

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what criteria’s needed in order for something to be considered a neurotransmitter?

Synthesis of the neurotransmitter occurs in the neuron itself
It can be found in the presynaptic membrane
Its release into the synaptic cleft causes a change in the postsynaptic membrane
Its effect on a neuron is the same whether released exogenously (i.e., from outside the organism as a drug) or endogenously (from the presynaptic terminal)
Once released, the molecule is specifically removed from the synaptic cleft either by reuse or degradation

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what are examples o neuroactive peptides?

a. Opioid peptides (enkephalins, endorphins, dynorphins)
b. Nonopioid peptides (Substance P, vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK)

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what are examples of other neuromodulators?

a. Purine nucleotides (ATP)
b. Purines (adenosine)

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Neuromuscular junctions as well as other chemically mediated synapses act as _____

amplifiers

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what does amplification do for NMJ?

Amplification allows the relatively tiny currents in a 5 μm α-motoneuron axon to
elicit an action potential in a 100 μm muscle fiber

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in humans the neuromuscular
synapse is ________

always excitatory, never inhibitory.

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The presynaptic terminal of NMJ has large concentrations of _____

mitochondria

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what is the active zone of the NMJ?

where synaptic vesicles containing transmitter accumulate around presynaptic dense bars.

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what is the synaptic cleft?

The synaptic cleft is filled with an
amorphous network of connective tissue called the basal lamina

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what is the steps of transmission at the NMJ?

-AP conducted
-VG Ca channels open
-Ca flows in causing release of Ach
-Ach diffuse across cleft
-activates Ach receptor, opens ligand gated Na/K channels
-Na depolarizes triggers AP
-muscle contracts

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what is evoked transmitter release?

-nerve terminal depolarized by AP, VG Ca channel open and Ca enters
-Ca intracellular messenger allowing synaptic vesicles to exocytosis contents
-Ca removed
-amount NT released is proportional to amount of Ca

how does increase intracellular Mg change NT release?

increasing Mg decreases NT because Mg competes with Ca for entry to Ca channel

less Ca=less NT

how is Ach synthetized?

ac CoA and choline in cytoplasm

how is choline made/enter cell?

Choline is made from serine and is pumped into the nerve terminal by a sodium dependent, secondary active transport system

how is Ach get loaded into vesicles?

-exchanging place with proton (does not require ATP) - however to get the H to get into the vesicle it needs a pump that needs ATP

How does docking happen for NT release?

specific proteins (SNAREs) that undergo transformation when Ca binds can then bind the vesicle so it can release the NT into the cleft

what is synaptic delay?

time it takes the vesicle to fuse and exocytosis the NT

Does the time it takes for NT to cross the synaptic cleft play a role in Synaptic delay?

how is Ach released?

ACh is released in packets with each packet corresponding to the release of one synaptic vesicle

Under resting conditions, synaptic vesicles release their contents (about 2,000 molecules of ACh) at a rate of approximately _____

1 per second

The spontaneous release of ACh produces ______________

miniature end plate potentials (MEPPs)

what is a MEPP the result of?

Each mepp is the result of the release of an integral number (mostly 1 but occasionally 2) of quanta

Do MEPPS excite muscle or cause contrition?

neither

why are Ach receptors called nicotinic?

because they are activated by nicotine and competitively inhibited by curare

what does the nicotine endplate receptor consist of?

binding site for neurotransmitter and chemically gated ionic channel

the nicotinic receptors contain what subunit?

5 subunits of α2βγδ (two A subunits have binding sites for ach)

what happens when Ach binds to both a subunits?

it makes the ionic channel permeable to both Na+ and K+. Both ions have the same conductance in this channel & depolarize the cell

is the nicotinic Ach receptor voltage dependent?

what are ionotropic receptors?

neurotransmitter receptor is part of one of the ion channel protein subunits itself so NT has direct effect on the ion channel conductance (ex Ach receptor at end of NMJ)

what are metabotropic receptors?

usually G-protein coupled receptors that when NT binds undergo a change in the post synaptic cell but not by binding to a receptor that is part of an ion channel (ex. Ach binding to muscarinic receptor in heart can open K channel)

what are excitatory end plate potentials?

electric changes in muscle fibers that occur when neurotransmitters bind to receptors in the neuromuscular junction. These changes depolarize the muscle fibers, which can lead to muscle contractions

what is the safety factor and what is it caused by?

The EPP reaches -30 mV but the membrane potential only needs to reach about -50 mV to trigger an action potential; there is a 20 mV “safety factor”

Excitatory ion channels are permeable to ______

Na+ and K+

Because of the electrical and concentration gradient does more K or Na move into cell

during excitatory post synaptic potential what happens to the charge inside the cell?

becomes more positive because of a the Na (if it depolarizes enough it will fire AP)

inhibitory ion channels are permeable to which ions?

Cl and K

during inhibitory potential which ion moved into the cell the most? and what does this do to the charge?

Cl makes more negative, hyperpolarizing the cell preventing AP

what is summation?

The local excitatory depolarizations or inhibitory hyperpolarizations are graded (passive) potentials and therefore can summate or cause additive changes to the post-synaptic membrane potential

what is spatial summation?

multiple synapses in nearby locations are stimulated simultaneously

what is temporal summation?

same channel is repeatedly opened (for example, because the presynaptic cell receives many impulses in a row), thereby altering the membrane potential further before it has the time to return to normal

how is NT inactivated?

degradation reuptake auto receptors (detect how much NT is around and inc/dec release as needed)

what what types of drugs are used to treat myasthenia gravis? MG is autoimmune disease that attacks Ach receptors causing muscle weakness

drugs that bock the action of acetylcholine esterase to prevent the degradation of Ach

review the NMJ/Chemical synapse chart