Module 7 - Neuropharm - CG Flashcards

1
Q

What is the primary excitatory neurotransmitter in the CNS?

A

Glutamate

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2
Q

Which two sources can produce glutamate?

A

Glucose metabolism in the Kreb’s Cycle and GABA metabolism in glial cells.

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3
Q

What are the two most important glutamate receptors?

A

AMPA and NMDA receptors.

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4
Q

What enzyme converts glutamine into glutamate?

A

Glutaminase.

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5
Q

How is glutamate inactivated at the synapse?

A

It is rapidly taken up by neighboring glial cells and converted back into glutamine by
glutamine synthetase.

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6
Q

What is excitotoxicity, and which neurotransmitter is primarily involved?

A

Excitotoxicity is excessive stimulation by glutamate leading to neuronal damage or death
due to high intracellular calcium levels.

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7
Q

Which ion channel is regulated by NMDA receptors?

A

A non-specific ion channel that allows Na+ and Ca2+ to enter while allowing K+ to leave.

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8
Q

Why is NMDA receptor activity important for long-term potentiation (LTP)?

A

It is necessary for memory formation and synaptic plasticity.

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9
Q

What neurotransmitter is the primary inhibitor in the CNS?

A

GABA (Gamma-Aminobutyric Acid).

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10
Q

What enzyme synthesizes GABA from glutamate?

A

Glutamic Acid Decarboxylase (GAD).

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11
Q

How is GABA inactivated after release?

A

Reuptake into glial cells or presynaptic neurons, followed by metabolism via GABA
transaminase (GABA-T).

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12
Q

Which ion does the GABA-a receptor primarily regulate?

A

Chloride (Cl-).

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13
Q

What class of drugs modulates GABA-a receptors to enhance inhibition?

A

Benzodiazepines (BDZs).

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14
Q

Which neurotransmitter imbalance is implicated in epilepsy?

A

Excess glutamate or insufficient GABA.

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15
Q

What is the mechanism of action of valproic acid in seizure treatment?

A

It inhibits GABA transaminase (GABA-T), increasing GABA activity.

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16
Q

What role do enkephalins play in pain modulation?

A

They act on opioid receptors to inhibit pain signals.

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17
Q

What is the primary receptor for enkephalins?

A

The mu-opioid receptor.

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18
Q

Which drug is a competitive antagonist for opioid receptors?

A

Naloxone.

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19
Q

What is the function of the AMPA receptor?

A

It mediates fast excitatory synaptic transmission by allowing Na+ and K+ flux.

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20
Q

What is the role of serotonin (5-HT) in pain modulation?

A

It is involved in descending pain inhibition by promoting enkephalin release.

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21
Q

What is cortical spreading depression (CSD), and what condition is it associated with?

A

CSD is a wave of neuronal depolarization linked to migraines.

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22
Q

Which two neurotransmitters are co-released with glutamate in pain pathways?

A

Substance P (SP) and Calcitonin Gene-Related Peptide (CGRP).

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23
Q

What is the gate theory of pain modulation?

A

The concept that non-painful stimuli (A-beta fiber activation) can inhibit pain signals via
inhibitory interneurons.

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24
Q

How do benzodiazepines enhance GABA activity?

A

They increase chloride ion conductance at the GABA-a receptor, enhancing inhibitory
effects.

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25
Q

What is the relationship between chronic pain and central sensitization?

A

Prolonged excitatory signaling leads to a lowered threshold for pain perception, causing pain without actual tissue damage.

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26
Q

What are the key roles of glutamate in the nervous system?

A

Learning, memory, epilepsy, and Huntington’s Disease.

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27
Q

How does glutamate contribute to memory formation?

A

It activates NMDA receptors, which play a key role in long-term potentiation (LTP), essential
for memory storage.

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28
Q

What is the role of AMPA receptors in synaptic transmission?

A

They mediate fast excitatory synaptic transmission by allowing Na+ and K+ flux.

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29
Q

Why is calcium (Ca2+) influx through NMDA receptors tightly regulated?

A

Excess calcium can cause excitotoxicity, leading to neuronal damage and cell death.

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30
Q

What is the difference between AMPA and NMDA receptors in glutamate signaling?

A

AMPA receptors mediate fast synaptic transmission, while NMDA receptors require
depolarization to remove the Mg2+ block and allow Ca2+ influx.

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31
Q

How does excessive glutamate lead to neurodegeneration?

A

Overactivation of NMDA receptors leads to excessive Ca2+ influx, triggering cell damage
and apoptosis.

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32
Q

What is the function of excitatory amino acid transporters (EAATs)?

A

They regulate glutamate levels by removing it from the synaptic cleft to prevent
excitotoxicity.

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33
Q

How do astrocytes contribute to glutamate recycling?

A

They take up glutamate and convert it to glutamine via glutamine synthetase, which neurons then use to regenerate glutamate.

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34
Q

What is the primary inhibitory neurotransmitter in the brain, and what is its main function?

A

GABA; it reduces neuronal excitability and helps regulate anxiety and sleep.

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35
Q

How do GABA-T inhibitors help treat seizures?

A

By inhibiting GABA transaminase (GABA-T), they increase GABA levels, enhancing inhibition
and preventing excessive neuronal firing.

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36
Q

What is the main difference between GABA-a and GABA-b receptors?

A

GABA-a receptors are ionotropic (control Cl- influx), while GABA-b receptors are metabotropic (linked to second messenger systems).

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37
Q

What is the role of benzodiazepines in anxiety treatment?

A

They enhance GABA-a receptor activity, increasing chloride ion influx and leading to greater neuronal inhibition.

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38
Q

Why do benzodiazepines require both GABA and a benzodiazepine to bind for full receptor activation?

A

BDZs are allosteric modulators, meaning they enhance GABA’s effects but cannot activate
the receptor alone.

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39
Q

What are common side effects of benzodiazepines?

A

Sedation, dizziness, dependency, and memory impairment.

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40
Q

What is the relationship between GABA and glutamate in the brain?

A

They have opposing roles; glutamate is excitatory, while GABA is inhibitory, and they are
metabolically linked.

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41
Q

What is the function of enkephalins in the nervous system?

A

They modulate pain perception by acting on opioid receptors, reducing pain signals.

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42
Q

What are the three main types of opioid receptors?

A

Mu (μ), Delta (δ), and Kappa (κ).

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43
Q

What are the effects of activating the mu-opioid receptor?

A

Analgesia, respiratory depression, euphoria, and sedation.

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44
Q

How does naloxone work to reverse opioid overdoses?

A

It is a competitive antagonist at opioid receptors, displacing opioids and blocking their
effects.

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45
Q

How do opioids cause respiratory depression?

A

They inhibit respiratory centers in the brainstem by increasing K+ conductance and reducing neuronal excitability.

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46
Q

What neurotransmitters are involved in the transmission of pain signals?

A

Glutamate, Substance P (SP), and Calcitonin Gene-Related Peptide (CGRP).

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47
Q

What is Substance P’s role in pain transmission?

A

It binds NK-1 receptors and enhances pain signaling and neurogenic inflammation.

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48
Q

How does the gate control theory of pain work?

A

Non-painful stimuli (A-beta fibers) activate inhibitory interneurons, reducing pain signal
transmission in the dorsal horn.

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49
Q

How does enkephalin contribute to the gate control theory of pain?

A

It inhibits pain signals by reducing neurotransmitter release from nociceptive neurons.

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50
Q

What are the two types of pain fibers, and how do they differ?

A

• A-delta fibers: Myelinated, fast conduction, sharp localized pain.
• C-fibers: Unmyelinated, slow conduction, dull aching pain.

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51
Q

What is neurogenic inflammation?

A

Inflammation triggered by neurotransmitter release from primary afferent nociceptors,
including Substance P and CGRP.

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52
Q

How does serotonin (5-HT) modulate pain perception?

A

It enhances descending inhibition by promoting enkephalin release, reducing pain
transmission.

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53
Q

How do SSRIs affect pain perception?

A

They increase serotonin levels, which can enhance descending pain inhibition.

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54
Q

What is cortical spreading depression (CSD), and why is it significant?

A

A wave of neuronal depolarization linked to migraines, triggered by excessive glutamate
release.

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55
Q

What role do calcium pumps play in preventing excitotoxicity?

A

They actively remove excess intracellular Ca2+ to maintain neuronal homeostasis.

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56
Q

How does excessive glutamate release contribute to chronic pain?

A

It leads to central sensitization, making neurons hyperexcitable and increasing pain
perception.

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57
Q

What is the primary mechanism of chronic pain?

A

Central sensitization, where prolonged excitatory signaling lowers the pain threshold, leading to persistent pain perception.

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58
Q

How does chronic inflammation contribute to central sensitization?

A

It maintains a heightened state of excitability in dorsal horn neurons, making pain perception more intense.

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59
Q

What is the role of the periaqueductal gray (PAG) in pain modulation?

A

It activates descending pain inhibition pathways that release serotonin and norepinephrine.

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60
Q

How do opiates reduce pain at the spinal cord level?

A

They inhibit Ca2+ influx presynaptically (reducing neurotransmitter release) and increase K+
efflux postsynaptically (hyperpolarization).

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61
Q

Why can prolonged opioid use lead to hyperalgesia?

A

It causes increased sensitivity to pain due to receptor desensitization and changes in
neurotransmitter balance.

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62
Q

What is the function of norepinephrine in pain modulation?

A

It contributes to descending pain inhibition by activating opioid-releasing interneurons.

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63
Q

What neurotransmitters are involved in the descending pain modulation system?

A

Serotonin (5-HT), norepinephrine (NE), and enkephalins.

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64
Q

What is central biasing in pain perception?

A

The brain’s ability to modulate pain perception based on past experiences and emotional
factors.

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65
Q

How does glutamate contribute to epilepsy?

A

Excessive glutamate activity leads to overexcitation of neurons, increasing the likelihood of
seizures.

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66
Q

What role does glutamate play in Huntington’s Disease?

A

Excess glutamate release causes excitotoxicity, leading to the degeneration of GABAergic
neurons in the caudate nucleus.

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67
Q

How does GABA contribute to anxiety disorders?

A

Reduced GABA activity leads to increased neuronal excitability, contributing to heightened
anxiety.

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68
Q

What are the two main types of GABA receptors, and how do they differ?

A

• GABA-a: Ionotropic, controls Cl- influx, leads to fast inhibition.
• GABA-b: Metabotropic, uses second messenger systems for slower inhibition.

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69
Q

What is the function of GABA transporters (GATs)?

A

They remove GABA from the synaptic cleft to terminate its action.

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70
Q

What is the mechanism of action of barbiturates?

A

They enhance GABA-a receptor activity, prolonging Cl- channel opening for stronger
neuronal inhibition.

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71
Q

Why are benzodiazepines considered safer than barbiturates?

A

They only enhance GABA’s effect rather than directly opening Cl- channels, reducing
overdose risk.

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72
Q

How does alcohol affect GABA neurotransmission?

A

It enhances GABA-a receptor activity, leading to sedative and depressant effects.

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73
Q

What is the role of AMPA receptors in synaptic plasticity?

A

They mediate fast excitatory transmission and play a role in synaptic strengthening and LTP.

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74
Q

How do NMDA receptors contribute to synaptic plasticity?

A

They allow Ca2+ influx, which activates intracellular signaling pathways crucial for memory
formation.

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75
Q

How does magnesium (Mg2+) regulate NMDA receptor activity?

A

It blocks the NMDA receptor channel at resting membrane potential, requiring depolarization to be removed.

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76
Q

What are the consequences of excessive NMDA receptor activation?

A

Increased Ca2+ influx leads to excitotoxicity, neuronal damage, and possible neurodegeneration.

77
Q

How does memantine work as a treatment for Alzheimer’s disease?

A

It blocks NMDA receptors to prevent excessive Ca2+ influx and reduce excitotoxicity.

78
Q

What is the function of EAAT transporters in glutamate regulation?

A

They remove excess glutamate from the synaptic cleft to prevent excitotoxicity.

79
Q

How does glycine interact with NMDA receptors?

A

It acts as a co-agonist, necessary for NMDA receptor activation alongside glutamate.

80
Q

What happens when GABA levels are too low?

A

Increased neuronal excitability, leading to anxiety, insomnia, and potentially seizures.

81
Q

What is the function of GABA-T inhibitors in seizure treatment?

A

They prevent GABA breakdown, prolonging its inhibitory effect.

82
Q

What role does Substance P play in inflammation?

A

It promotes vasodilation, increased vascular permeability, and activation of immune cells.

83
Q

How does CGRP contribute to migraines?

A

It is a potent vasodilator involved in the pathophysiology of migraine headaches.

84
Q

What is the primary function of the periaqueductal gray (PAG)?

A

It is a key structure in descending pain modulation, activating inhibitory pathways.

85
Q

How do opioids affect neurotransmitter release at the spinal cord level?

A

They inhibit presynaptic Ca2+ influx, reducing the release of excitatory neurotransmitters like glutamate and Substance P.

86
Q

Why does opioid tolerance develop over time?

A

Repeated opioid use leads to receptor desensitization and downregulation, reducing drug effectiveness.

87
Q

What is opioid-induced hyperalgesia?

A

A condition where prolonged opioid use paradoxically increases pain sensitivity.

88
Q

How do NSAIDs reduce pain and inflammation?

A

They inhibit cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis.

89
Q

How does serotonin contribute to descending pain modulation?

A

It enhances inhibitory interneuron activity, reducing pain signal transmission.

90
Q

What is the relationship between norepinephrine and pain control?

A

It enhances descending inhibition by activating opioid-releasing interneurons.

92
Q

How do antidepressants like SSRIs and SNRIs help in chronic pain?

A

They enhance serotonin and norepinephrine activity, boosting descending pain inhibition.

93
Q

What is the significance of central sensitization in chronic pain?

A

It leads to heightened pain perception due to persistent excitatory neurotransmitter activity.

94
Q

How does the spinal cord regulate pain before reaching the brain?

A

Through inhibitory interneurons that modulate nociceptive transmission in the dorsal horn.

95
Q

What is the primary pathway for pain perception in the brain?

A

The spinothalamic tract, which transmits pain signals to the thalamus and cortex.

96
Q

What is the main function of the dorsal horn in pain processing?

A

It serves as the first synaptic relay for nociceptive information, where pain signals can be
modulated.

97
Q

How does ketamine work as an analgesic?

A

It blocks NMDA receptors, preventing excessive excitatory signaling and reducing pain
perception.

98
Q

What neurotransmitters are involved in descending pain control?

A

Serotonin (5-HT), norepinephrine (NE), and enkephalins.

99
Q

How does touch-based therapy like massage modulate pain?

A

It activates A-beta fibers, engaging the gate control mechanism to inhibit pain signals.

100
Q

How does stress influence pain perception?

A

Chronic stress increases cortisol levels, which can enhance excitatory neurotransmission
and lower pain tolerance.

101
Q

How does acupuncture modulate pain perception?

A

It stimulates endogenous opioid release, reducing pain transmission.

102
Q

What is the role of TRPV1 receptors in pain sensation?

A

They detect heat and capsaicin, contributing to pain signaling and neurogenic inflammation.

103
Q

What are endozepines, and what is their function?

A

E ndogenous benzodiazepine-like compounds that modulate GABA-a receptor activity.

104
Q

How do cannabinoids influence pain perception?

A

They act on CB1 receptors to inhibit neurotransmitter release, reducing pain signaling.

105
Q

Why are GABAergic drugs used in muscle relaxation?

A

They enhance inhibition in the spinal cord, reducing muscle tone and spasms.

106
Q

How does glutamate contribute to addiction?

A

It plays a role in synaptic plasticity, reinforcing drug-seeking behavior through NMDA
receptor activation.

107
Q

Why is NMDA receptor activation important in opioid withdrawal?

A

It contributes to hyperexcitability and withdrawal symptoms when opioid inhibition is
removed.

108
Q

What are the two primary excitatory neurotransmitters in the brain?

A

Glutamate and aspartate.

109
Q

What is the role of glutamate in reflexes?

A

It mediates excitatory signaling in the afferent limb of reflex arcs.

110
Q

Why is glutamate considered the most important neurotransmitter for cognition?

A

It is essential for synaptic plasticity, learning, and memory.

111
Q

How does glutamate interact with astrocytes?

A

Astrocytes take up excess glutamate and convert it into glutamine for recycling.

112
Q

What happens when glutamate transporters (EAATs) are dysfunctional?

A

Excess glutamate accumulates, increasing the risk of excitotoxicity and neurodegeneration.

113
Q

What is the relationship between glutamate and schizophrenia?

A

Hypofunction of NMDA receptors is associated with cognitive deficits in schizophrenia.

114
Q

What are the primary inhibitory neurotransmitters in the CNS?

A

GABA and glycine.

115
Q

How do benzodiazepines affect sleep?

A

They enhance GABAergic inhibition, promoting sedation and sleep.

116
Q

How does alcohol withdrawal cause seizures?

A

Chronic alcohol use enhances GABA activity, and withdrawal causes a rebound excitability
due to reduced inhibition.

117
Q

Why does GABA deficiency contribute to movement disorders?

A

Lack of GABAergic inhibition leads to excessive motor activity, as seen in Huntington’s
Disease.

118
Q

What is the function of the GABA-b receptor?

A

It inhibits neurotransmitter release via G-protein-coupled mechanisms, leading to prolonged inhibition

119
Q

What is the role of glutamate in stroke-induced brain damage?

A

Ischemia leads to excessive glutamate release, causing excitotoxicity and neuronal death.

120
Q

How does memantine differ from other NMDA receptor antagonists?

A

It is a low-affinity antagonist that blocks excessive NMDA activity without disrupting normal
function.

121
Q

What is the effect of chronic stress on glutamate signaling?

A

It increases glutamate release, leading to synaptic remodeling and potential neurotoxicity

122
Q

What role does dopamine play in regulating glutamate and GABA balance?

A

Dopamine modulates excitatory and inhibitory transmission in the basal ganglia to control
movement.

123
Q

What is the primary function of opioid peptides like enkephalins?

A

They inhibit pain transmission in the spinal cord and brain.

124
Q

How does morphine produce analgesia?

A

It binds to mu-opioid receptors, inhibiting neurotransmitter release and reducing pain
signaling.

125
Q

How do chronic pain conditions alter neurotransmitter function?

A

They lead to increased glutamate and Substance P activity, along with reduced inhibitory
control.