Chapter 5 Flashcards

(29 cards)

1
Q

Q: What is a synapse?

A

A: A specialized junction where a neuron communicates with another cell (neuron, muscle, or gland) through either chemical or electrical means.

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2
Q

Q: What are the two main types of synapses?

A

A: Chemical synapses (neurotransmitter-mediated) and electrical synapses (gap-junction-mediated).

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3
Q

Q: What are the advantages and limitations of electrical synapses?

A

A: Advantages – fast, synchronous activity; Limitations – lack of signal modulation or amplification.

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4
Q

Q: How do chemical synapses transmit signals?

A

A: Neurotransmitters are released from the presynaptic terminal into the synaptic cleft, binding to receptors on the postsynaptic membrane.

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5
Q

Q: What are the basic steps of chemical neurotransmission?

A

A: (1) Synthesis/storage, (2) AP-induced Ca²⁺ influx, (3) Vesicle fusion/release, (4) Receptor binding, (5) Termination (reuptake/degradation).

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6
Q

Q: What structural features define a chemical synapse?

A

A: Presynaptic vesicles, active zones, a synaptic cleft, and postsynaptic receptor densities (e.g., PSD).

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7
Q

Q: What triggers neurotransmitter release at the presynaptic terminal?

A

A: Opening of voltage-gated Ca²⁺ channels and Ca²⁺ influx in response to an arriving action potential.

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8
Q

Q: Which protein complex mediates synaptic vesicle fusion?

A

A: The SNARE complex (syntaxin, synaptobrevin/VAMP, SNAP-25) assisted by synaptotagmin (Ca²⁺ sensor).

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9
Q

Q: What are the main mechanisms for terminating neurotransmitter action?

A

A: Enzymatic degradation, reuptake by transporters, or diffusion away from the cleft.

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10
Q

Q: What are small-molecule neurotransmitters and where are they synthesized?

A

A: Classical transmitters like ACh, dopamine, glutamate, etc.; synthesized in the presynaptic terminal.

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11
Q

Q: What are peptide neurotransmitters and how are they synthesized?

A

A: Neuropeptides made in the soma, packaged in dense-core vesicles, and transported to terminals.

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12
Q

Q: What are the four major activating (modulatory) systems of the brain?

A

A: Cholinergic, Dopaminergic, Noradrenergic, and Serotonergic systems.

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13
Q

Q: What roles does acetylcholine play in the CNS and PNS?

A

A: CNS – arousal, attention, memory; PNS – neuromuscular junction activation of skeletal muscle.

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14
Q
  1. Q: Where are dopaminergic cell bodies located and what are their pathways?
A

A: Substantia nigra (motor control) and ventral tegmental area (reward/motivation).

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15
Q

Q: Which disorder results from degeneration of nigrostriatal dopamine neurons?

A

A: Parkinson’s disease.

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16
Q

Q: What is the primary function of the noradrenergic system?

A

A: Modulates alertness, attention, and stress responses via projections from the locus coeruleus.

17
Q

Q: What is the serotonergic system’s major role and origin?

A

A: Mood, sleep, appetite regulation; neurons originate in the raphe nuclei of the brainstem.

18
Q
  1. Q: Which neurotransmitter is the main excitatory transmitter in the CNS?
A

A: Glutamate.

19
Q

Q: Which neurotransmitter is the principal inhibitory transmitter in the brain?

A

A: GABA (γ-aminobutyric acid).

20
Q

Q: How do ionotropic receptors differ from metabotropic receptors?

A

A: Ionotropic = ligand-gated ion channels causing fast EPSPs/IPSPs; Metabotropic = G-protein-coupled receptors producing slower, modulatory effects.

21
Q
  1. Q: How can a neurotransmitter produce different effects in different tissues?
A

A: By acting on distinct receptor subtypes that open or close different ion channels or activate different signaling cascades.

22
Q

Q: What determines whether a synapse is excitatory or inhibitory?

A

A: The type of receptor and the ion conductances it controls, not the neurotransmitter itself.

23
Q

Q: What is a neuromuscular junction (NMJ)?

A

A: A specialized chemical synapse between a motor neuron and skeletal muscle fiber where ACh triggers muscle contraction.

24
Q

Q: What is synaptic plasticity?

A

A: The ability of synapses to strengthen or weaken in response to activity, forming the basis of learning and memory.

25
Q: What is long-term potentiation (LTP)?
A: A long-lasting increase in synaptic strength following high-frequency stimulation, often mediated by NMDA-type glutamate receptors.
26
Q: What is long-term depression (LTD)?
A: A sustained decrease in synaptic strength following low-frequency stimulation or asynchronous activity.
27
Q: How do astrocytes participate in synaptic signaling?
A: They take up neurotransmitters, buffer K⁺, release gliotransmitters, and modulate synaptic efficacy (forming the tripartite synapse).
28
Q: What are some pharmacological agents that act at synapses?
A: SSRIs (block 5-HT reuptake), benzodiazepines (enhance GABA_A), nicotine (stimulates nicotinic AChRs), botulinum toxin (blocks ACh release).
29
Q: Why are synapses central to neurophysiology and behavior?
A: They are the sites where neural information is transmitted, integrated, and modified—forming the cellular basis of all brain function and cognition.