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LF260 Neuropharmacology > Lecture 8: Psychostimulants: use and abuse > Flashcards

Lecture 8: Psychostimulants: use and abuse Flashcards

1
Q

What are the two main nuclei in the brain that produce noadrenergic fibers?

A
  • Locus Coeruleus (LC)
  • Lateral Tegmental Area (LTA)
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2
Q
  • What is the primary function of the noradrenergic pathway in the brain?
A
  • To regulate behaviors associated with the “fight or flight” response
    • Arousal/wakefulness
    • Mood (in areas like the amygdala and hippocampus),
    • Pain contro (especially in the spinal cord)
    • Regulation of blood pressure/autonomic function
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3
Q

What brain region is affected in addiction and sends projections to the forebrain?

A

The Ventral Tegmental Area (VTA), especially to structures involved in executive function.

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4
Q

What role does the substantia nigra play in Parkinson’s disease?

A
  • The substantia nigra is a brain region with dopaminergic neurons that degenerate in Parkinson’s disease.
  • This degeneration leads to a deficit in dopaminergic transmission, resulting in the motor symptoms observed in Parkinson’s.
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5
Q

D1-like receptors (D1 receptor)

A
  • Coupled to the Gα5 protein subtype.
  • Increases cAMP and PKA activity.
  • Physiological responses include involvement in voluntary movement (e.g., Parkinson’s disease), reward pathways (e.g., drug abuse), and regulation of sleep.
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6
Q

D1-like receptors (D5 receptors)

A
  • Also coupled to the Gα5 protein subtype.
  • Increases cAMP and PKA activity.
  • Physiologically implicated in processes related to voluntary movement, reward, and sleep regulation.
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7
Q

D2-like receptors (D2 receptors)

A
  • Coupled to the Gαi protein subtype.
  • Reduces cAMP and PKA activity.
  • Decreases Gβgamma, influencing voltage-gated Ca channels and K+ channels.
  • Involved in mood regulation, cognition, attention (e.g., ADHD, schizophrenia), hormonal regulation (especially in the pituitary), sympathetic regulation, and nausea/vomiting.
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8
Q

D2-like receptors (D3 receptors)

A
  • Coupled to the Gαi protein subtype.
  • Reduces cAMP and PKA activity.
  • Influences mood, cognition, attention, hormonal regulation, sympathetic regulation, and nausea/vomiting.
  • Associated with various neurological and psychiatric conditions.
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9
Q

What is the primary nucleus associated with extensive projections throughout the brain?

A

Raphe nuclei

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10
Q

What functions is the raphe nuclei involved in?

A

Sleep, wakefulness, mood regulation, feeding behavior, and the control of sensory transmission, especially pain pathways

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11
Q

How many classes of G protein-coupled receptors (GPCRs) are there for serotonin (5HT)?

A

7

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12
Q

What type of receptor is the 5-HT3 receptor?

A

Ion channel receptor, composed of pentameric subunits, similar to nicotinic receptors.

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13
Q

What is the clinical significance of 5-HT3 antagonists?

A

Control of vomiting associated with chemotherapy.

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14
Q

What is the role of selective serotonin reuptake inhibitors (SSRIs) in treatment?

A

Treatment of depression

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15
Q

How are some subtypes of 5HT1 receptors utilized in medical treatment?

A

Agonists of subtypes of 5HT1 receptors are used in migraine treatment.

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16
Q

How do monoamines like dopamine, serotonin, and norepinephrine get taken up from the synaptic cleft?

A
  • Each monoamine neurotransmitter (dopamine, serotonin, norepinephrine) has its own specific plasma membrane uptake carrier (DAT for dopamine, SERT for serotonin, NET for norepinephrine).
  • These carriers facilitate the uptake of their respective monoamines from the synaptic cleft into the presynaptic neuron.
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17
Q

What facilitates the uptake of monoamines by the carriers?

A

ATPase enzyme that creates a hydrogen ion (H+) gradient, which in turn allows the uptake of monoamines into the presynaptic neuron.

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18
Q

How does dopamine respond in the synaptic cleft?

A
  • Dopamine is taken up by the dopamine transporter (DAT).
  • Cocaine effectively inhibits dopamine uptake, leading to an immediate rush when taken.
  • This mechanism explains its addictiveness.
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19
Q

What happens to serotonin in the synaptic cleft?

A
  • Serotonin is taken up by the serotonin transporter (SERT).
  • MDMA (ecstasy) is taken up by SERT, leading to accumulation of serotonin in the cell.
  • MDMA competes for uptake into vesicles, resulting in increased serotonin concentration in the synaptic cleft.
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20
Q

How is norepinephrine affected in the synaptic cleft?

A
  • Norepinephrine is taken up by the norepinephrine transporter (NET).
  • Amphetamine competes with norepinephrine, causing accumulation of norepinephrine in the synaptic cleft.
  • Amphetamine also competes with the vesicular monoamine transporter (VMAT), preventing norepinephrine from entering synaptic vesicles.
  • Additionally, amphetamine inhibits monoamine oxidase, leading to reduced breakdown of norepinephrine and other monoamines in the synaptic cleft.
  • These effects contribute to the rush and addictiveness of the drug.
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21
Q

What are the main effects of amphetamines?

A
  • Increased motor activity
  • Euphoria and excitement
  • Insomnia
  • Anorexia
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22
Q

What is the primary cause of the effects of amphetamines?

A

Increased levels of monoamines in the synaptic cleft

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23
Q

What is a notable outcome of amphetamine use in terms of psychological response?

A

Strong psychological dependence

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24
Q

What condition can occur with prolonged amphetamine use and what does it resemble?

A

Schizophrenia

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25
Q

In what medical conditions is amphetamine used therapeutically?

A
  • Attention Deficit Hyperactivity Disorder (ADHD) for focusing attention at low doses.
  • Narcolepsy (excessive sleepiness) at low doses.
  • Obesity, particularly in cases of severe obesity.
26
Q

What are the main effects of cocaine use?

A
  • Increased motor activity
  • Euphoria, excitement, and garrulousness
  • Increased peripheral sympathetic nervous system activity, leading to an increase in blood pressure and heart rate
27
Q

What is the primary reason behind the effects of cocaine?

A

The effects of cocaine occur due to increased levels of monoamines, especially dopamine, in the synaptic cleft.

28
Q

How do the duration of effects of cocaine compare to amphetamines

A

Cocaine has shorter-lasting effects compared to amphetamines.

29
Q

What trend has been observed regarding deaths related to cocaine use?

A

Deaths related to cocaine use are increasing, attributed in part to higher purity of the drug

30
Q

How does modafinil affect the dopamine transporter?

A

Binding strongly to stratum in the brain. When modafinil is provided, it displaces cocaine binding, suggesting that it targets the dopamine transporter.

31
Q

What is the perception of modafinil in terms of its effects

A

Modafinil is seen as an enhancing compound.

32
Q

For what condition is modafinil commonly used, and what are its primary effects in this context?

A

Modafinil is commonly used in narcolepsy to increase wakefulness. Its main effects include increased wakefulness and vigilance.

33
Q

How does modafinil interact with dopamine and norepinephrine transporters?

A

Modafinil binds with low affinity to both dopamine transporter (DAT) and norepinephrine transporter (NET).

34
Q

Apart from its actions on dopamine and norepinephrine systems, what other neurotransmitter systems does modafinil affect?

A

Modafinil has additional actions at a variety of neurotransmitter systems, including serotonin (5HT) and glutamate.

35
Q

What is the abuse potential of modafinil?

A

Modafinil has low abuse potential and does not typically produce a high or euphoria.

36
Q

What are cognitive enhancers and what is their primary function?

A
  • Cognitive enhancers: compounds that enhance cognition
  • Reduce mental fatigue (pilots)
  • Maintain attention n concentration
  • Increased motivation (esp for dull n repetitive tasks, eg exams)
  • Alter memory processing
  • Normalize behaviour (e.g. schizophrenia, autism disorders, addiction)
37
Q

What are some examples of cognitive enhancers?

A
  • Cognitive enhancers: compounds that enhance cognition
  • Reduce mental fatigue (pilots)
  • Maintain attention n concentration
  • Increased motivation (esp for dull n repetitive tasks, eg exams)
  • Alter memory processing
  • Normalize behaviour (e.g. schizophrenia, autism disorders, addiction)
  • Caffeine, modafinil, methylphenidate, ampakines
38
Q

How were rats tested for cognitive enhancement in an experiment involving ampakines?

A
  • Rats were placed in an operant chamber.
  • They had to perform tasks such as pressing a bar, traveling to the other side of the box and waiting for a light to go out, and then returning to press the opposite bar.
39
Q

What were the results of the experiment involving ampakines in rats?

A
  • Experimental rats administered with ampakines showed significantly enhanced performance compared to control rats.
  • Their performance levels were notably higher, indicating cognitive enhancement.
40
Q

What is the mechanism of action of ampakines?

A
  • Ampakines enhance the activation of glutamate AMPA receptors.
  • They also promote the release of brain-derived neurotrophic factor (BDNF).
41
Q

What evidence suggests the cognitive enhancement potential of ampakines?

A
  • Ampakines have shown evidence of enhancing cognition in a range of tests.
  • This indicates their potential for improving cognitive function.
42
Q

What is the monoamine theory for depression based on?

A

The theory suggests that drugs enhancing monoamine levels improve mood and alleviate symptoms of depression, while drugs lowering monoamine levels can worsen depression (e.g., reserpine).

43
Q

What are some other factors that may be involved in depression aside from monoamine levels?

A

Stress hormone levels and neurogenesis are among the factors that may contribute to depression.

44
Q

How do antidepressants work to alleviate depression according to the monoamine theory?

A

Antidepressants normalize the levels of monoamine neurotransmitters, which is believed to alleviate depression symptoms.

45
Q

What are examples of monoamine oxidase inhibitors used in depression treatment?

A

Phenelzine

46
Q

What is the function of monoamine oxidase (MAO) in the context of depression treatment?

A

MAO prevents the breakdown of monoamine neurotransmitters → increasing their availability in the brain → alleviate depression

47
Q

What are tricyclic antidepressants, and which neurotransmitter transporters do they target?

A

Tricyclic antidepressants like imipramine target the norepinephrine transporter (NET) and the serotonin transporter (SERT).

48
Q

What are examples of selective serotonin reuptake inhibitors (SSRIs), and which transporter do they selectively target?

A

Examples include citalopram and fluoxetine (Prozac), both of which selectively target the serotonin transporter (SERT).

49
Q

What is reboxetine, and which neurotransmitter transporter does it target selectively?

A

Reboxetine is a selective norepinephrine reuptake inhibitor (NRI), targeting the NET.

50
Q

What is duloxetine, and what is its mechanism of action as a dual-action antidepressant?

A

Duloxetine is a serotonin-norepinephrine reuptake inhibitor (SNRI), acting on both the serotonin transporter (SERT) and the norepinephrine transporter (NET).

51
Q

What are positive symptoms of schizophrenia, and what is their underlying mechanism involving dopamine receptors?

A

Positive symptoms involve over-activity in the mesolimbic dopaminergic pathway, leading to the activation of dopamine D2 receptors. These symptoms may include delusions, hallucinations, thought disorder, abnormal behavior, and catatonia.

52
Q

What are negative symptoms of schizophrenia, and how are they related to dopamine receptors?

A

Negative symptoms result from decreased activity in the mesocortical dopaminergic pathway, specifically affecting D1 receptors.

53
Q

Which neurotransmitter system is primarily implicated in schizophrenia?

A

Dopamine is primarily implicated in schizophrenia due to dysregulation in dopaminergic pathways.

54
Q

What are the main categories of antipsychotic drugs?

A

First-generation (typical, classical, conventional) antipsychotics and second-generation (atypical) antipsychotics.

55
Q

What are examples of first-generation antipsychotic drugs, and what receptors do they primarily target?

A

Examples include chlorpromazine and haloperidol, which primarily target dopamine D1 and D2 receptors.

56
Q

Which receptors do second-generation (atypical) antipsychotic drugs primarily target, and can you provide examples?

A

Second-generation antipsychotic drugs like clozapine and risperidone target dopamine D2 receptors, with some activity at D1 receptors as well.

57
Q

What are some common side effects of antipsychotic drugs, and how do they occur?

A
  • Motor effects such as extrapyramidal effects (resulting from D2 receptor antagonism in the nigrostriatal pathway), including symptoms resembling Parkinson’s disease like involuntary movements, tremors, spasms, and rigidity.
  • Other side effects include increased prolactin secretion leading to conditions like gynecomastia and galactorrhea, weight gain, and sedation or drowsiness.
58
Q

How is levodopa used in the treatment of Parkinson’s disease (PD)?

A

Levodopa, a precursor to dopamine, is administered to PD patients to replenish dopamine levels in the brain, compensating for the deficits caused by the loss of dopaminergic neurons.

59
Q

How is peripheral metabolism of levodopa prevented?

A
  • Peripheral metabolism of levodopa to one of its metabolites is prevented by using an inhibitor of the enzyme responsible for this metabolism.
  • These inhibitors do not cross the blood-brain barrier (BBB), ensuring that levodopa is available for conversion to dopamine within the brain.
60
Q

How are dopamine levels in the brain maintained?

A

Compounds that can cross the BBB are utilized to prevent the breakdown of dopamine, thereby keeping dopamine levels elevated in the brain.

61
Q

Apart from replenishing dopamine, what other therapeutic approaches are used in PD treatment?

A

Therapeutic approaches also target specific compounds and receptors involved directly in PD pathology, such as D1 and D2 receptors. Agonists of these receptors may lead to therapeutic effects.

62
Q

Describe a surgical treatment option for PD.

A

Surgical treatments, such as deep brain stimulation, involve the insertion of electrodes into specific brain regions, such as the subthalamic nucleus. By stimulating these regions, tremors associated with PD can be improved. Patients with the implant can activate it when performing tasks requiring motor control to avoid overstimulation of the tissue.

LF260 Neuropharmacology (14 decks)

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