ELM 9 Synapses Flashcards

1
Q

What is the distinguishing characteristic of rectifying synapses?

A

Rectifying synapses allow for one-way transmission, with a high resistance barrier that makes ions more likely to diffuse out of the synapse.

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2
Q

What are the two types of synapses that solved the problem of high resistance barrier?

A

Electrical and chemical synapses.

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3
Q

What is the structure of an electrical synapse?

A

Electrical synapses are formed by gap junctions, with a distance of approximately 3.5 nanometers between neurons. These synapses allow for the direct transfer of ions.

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4
Q

what is 1/2 -way transmission also called?

A

1 = rectifying, 2 = non-rectifying.

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5
Q

What are the characteristics of electrical synapses?

A

Electrical synapses are non-rectifying, allow for fast transmission, and often exhibit signal attenuation, where the signal is smaller in the second neuron. They are highly reliable.

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6
Q

How do chemical synapses work?

A

hemical synapses involve the transmission of signals from one neuron to another through the release and reception of neurotransmitters. This process involves electrical-to-chemical-to-electrical signaling.

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7
Q

Who discovered the concept of chemical neurotransmission, and what was their experiment?

A

Otto Loewi discovered chemical neurotransmission in 1921 through his experiment involving the stimulation of the vagus nerve, which led to the release of a substance (later named “vagusstoff”) that affected the activity of a second heart.

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8
Q

What is synaptic delay?

A

Synaptic delay refers to the time taken for a signal to cross the synapse, which includes the time for neurotransmitter release, diffusion across the synaptic cleft, and binding to receptors on the postsynaptic membrane.

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9
Q

Can you give an example of an organism that utilizes electrical synapses for communication?

A

One example is the giant fiber system in Drosophila, which detects the shadow of a predator’s hand and triggers action potentials in neurons that form electrical synapses with leg and wing motor neurons.

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10
Q

What are the main steps involved in vesicular release at chemical synapses?

A
  1. SNARE proteins bind to each other and draw vesicle close to membrane. 2. Calcium ions (Ca²⁺) trigger vesicle fusion with the membrane. 3. Neurotransmitters are released into the synaptic cleft.
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11
Q

Define quantal release and describe its two forms.

A

Quantal release refers to the release of neurotransmitter vesicles in discrete packets or quanta. It has two forms: evoked release, triggered by an action potential and resulting in excitatory postsynaptic potentials (EPSPs), and spontaneous release, which occurs in the absence of an action potential and generates miniature EPSPs (MEPPs).

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12
Q

What is the role of SNARE proteins in vesicular release?

A

SNARE proteins facilitate vesicular release by binding to each other and drawing the vesicle close to the presynaptic membrane, initiating the fusion process.

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13
Q

: How is quantal content calculated, and what does it represent?

A

Quantal content is calculated by dividing the amplitude of the evoked postsynaptic potential (EPP) by the amplitude of a single quantal event. It represents the number of quanta released during evoked neurotransmitter release.

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14
Q

Describe the process of vesicular recycling.

A

After vesicular fusion with the presynaptic membrane, clathrin proteins surround the vesicle, forming a clathrin coat. This coat helps detach the vesicle from the membrane and internalize it into the presynaptic terminal for refilling with neurotransmitters. This process ensures constant vesicle size, number, and terminal size for efficient synaptic transmission.

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15
Q

What is the mechanism of action of Botulinum toxin?

A

Botulinum toxin is a proteolytic enzyme that cleaves SNARE proteins, preventing vesicles from docking with the membrane and thus inhibiting neurotransmitter release.

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16
Q

How does α-bungarotoxin from the banded krait affect synaptic transmission?

A

α-bungarotoxin blocks nicotinic acetylcholine receptors, leading to the inhibition of endplate potentials. It is a member of the alpha neurotoxin family.

17
Q

What is the role of physostigmine, found in the Calabar bean, in neuromuscular transmission?

A

Physostigmine, an acetylcholinesterase inhibitor, prevents the breakdown of acetylcholine, leading to increased concentrations of acetylcholine at the neuromuscular junction. This can counteract the effects of toxins that bind to acetylcholine receptors and is used to treat conditions like myasthenia gravis.

18
Q

How does ω-agatoxin IVA from the funnel web spider affect synaptic transmission?

A

ω-agatoxin IVA blocks P/Q-type voltage-gated calcium channels, inhibiting transmitter release. It is utilized by the spider to subdue its prey.

19
Q

What is the mechanism of action of ω-conotoxin MVIIA from the magician cone snail?

A

: ω-conotoxin MVIIA blocks N-type voltage-gated calcium channels, thereby preventing neurotransmitter release. Conotoxins are small peptides with disulfide bridges.

20
Q

what is MG?

A

. Myasthenia gravis (MG) is an autoimmune disease in which nicotinic receptors are attacked by antibodies. It causes muscle weakness and drooping eyelids are a common symptom (left)

21
Q

What is the causative agent of tetanus?

A

Tetanus is caused by the anaerobic bacterium Clostridium tetani.

22
Q

How does tetanus toxin affect synaptic transmission?

A

Tetanus toxin cleaves SNARE proteins, which are essential for neurotransmitter release. This leads to uncontrolled muscle spasms.

23
Q

How does tetanus toxin differ from botulinum toxin in terms of target neurons?

A

The difference lies in the types of neurons targeted by the toxins. Tetanus toxin primarily affects inhibitory neurons, while botulinum toxin primarily targets excitatory neurons.

24
Q

Describe the pathway of tetanus toxin from the site of infection to its action on neurons.

A

Tetanus toxin binds to and enters presynaptic terminals in the skeletal muscle neuromuscular junction (NMJ). It then travels retrogradely up the motor neuron axon into the central nervous system (CNS). Once inside inhibitory neurons, the toxin destroys their SNARE proteins, preventing them from releasing neurotransmitters.

25
Q

What are the consequences of tetanus toxin action on neurons?

A

The destruction of SNARE proteins in inhibitory neurons prevents them from regulating motor neurons that stimulate skeletal muscle contraction. This leads to uncontrollable muscle spasms, including those affecting respiratory muscles, which can result in breathing problems. Tetanus has a mortality rate of approximately 10%.