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Behavioral Pharmacology > Ch 13: Nicotine and Caffeine > Flashcards

Ch 13: Nicotine and Caffeine Flashcards

1
Q

adenosine

A

Blockade of receptors for this substance is responsible for caffeine’s stimulant effects; serves a neurotransmitter-like function in the brain

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2
Q

caffeinism

A

Syndrome caused by taking excessive amounts of caffeine and characterized by restlessness, insomnia, anxiety, and physiological disturbances.

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3
Q

chronic obstructive pulmonary disease

A

Disorder of the respiratory system characterized by shortness of breath, wheezing, chronic coughing, and chest tightness. Two main conditions comprise COPD, namely emphysema and bronchitis.

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4
Q

cotinine

A

Principal product of nicotine metabolism by the liver; 70-80% is transformed into this

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5
Q

cytochrome P450 2A6

A

Specific type of cytochrome P450 that metabolizes nicotine into cotinine.

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6
Q

deprivation reversal model

A

Theory that smoking is maintained by mood enhancement (alleviation of irritability, stress) and increased concentration that occur when nicotine withdrawal symptoms are alleviated; proposes that smoking increases overall stress which must be countered by repeated smoking

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7
Q

mecamylamine

A

Drug that is an antagonist for nicotinic receptors; blocks action of residual nicotine

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8
Q

nicotine replacement

A

Method to stop smoking that involves giving the smoker a safer nicotine source, thereby maintaining a level of nicotine in the body and reducing nicotine withdrawal symptoms; chewing gum (nicotine polacrilex) is absorbed in the mouth

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9
Q

nicotine resource model

A

Theory that smoking is maintained due to positive effects of nicotine such as increased concentration and greater mood control.

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10
Q

nicotinic cholinergic receptors (nAChRs)

A

Family of ionotropic receptors that are activated by ACh and selectively stimulated by nicotine. They may also be called nicotinic receptors; ionotropic receptors comprising five separate protein units

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11
Q

osmotic minipump

A

Device placed just under the skin of an animal that allows a drug to be administered continuously over a set period of time.

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12
Q

tar

A

Mixture of hydrocarbons created by the vaporization of nicotine in tobacco. Tar is a major component of cigarette smoke.

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13
Q

nicotine

A

alkaloid found in tobacco leaves; large leaf (Nicotiana tabacum), small leaf (Nicotiana rustica); large leaf is what is used today; 5% of drug tobacco leaves

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14
Q

amount of nicotine in a typical cigarette

A

6 and 11 mg; no more than 1-3 mg actually reaches the blood stream; enters lungs via tar

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15
Q

entry of nicotine into the brain

A

reaches in about 7 seconds; smoking is the quickest and most efficient method of delivering nicotine to the brain; arterial nicotine rises more rapidly and reaches a greater peak than in venous blood

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16
Q

excretion of nicotine and related metabolites

A

urine

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17
Q

are there protective effects against cigarette smoking?

A

slow breakdown of nicotine (low CYP2A6 activity)

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18
Q

what does normal levels of CYP2A6 activity and variation in a gene cluster that codes for subunits of the nicotinic cholinergic receptor play a role in?

A

what contributes to smoking frequency, risk for lung cancer, and nicotine dependence

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19
Q

half life of nicotine

A

2 hours

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20
Q

which receptors are more sensitive to nicotine?

A

neuronal receptors containing two alpha4 or alpha3 subunits along with the beta subunits are much more sensitive to nicotine than those composed of five alpha7 subunits

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21
Q

where are nicotinic cholingeric receptors found?

A

cerebral cortex, thalamus, striatum, hippocampus, monoamine-containing nuclei (substantia nigra; ventral tegmental area; locus coeruleus; raphe nuclei)

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22
Q

cause of nicotine poisioning

A

high doses of nicotine lead to a persistent activation of nicotinic receptors and a continuous depolarization of the postsynaptic cell. this causes a depolarization block and the cell cant fire again until the nicotine is removed–biphasic effect

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23
Q

mood effects of nicotine

A

increase calmness and relaxation and reduction in negative affect in smokers (relief from nicotine withdrawal); tension, lightheadedness, dizziness, nausea (non smokers)

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24
Q

calming effect in smokers

A

little difference between nicotine-containing and denicotinized cigarettes in any of these conditions–> conditioned stimuli associated with smoking play a significant role in the calming effects of this behavior in regular smokers

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25
Q

nicotine and cognitive function

A

enhanced performance on many cognitive and motor tasks (attentional demands)–> alleviation of withdrawal effects; improvements in find motor performance, accuracy and response latency in certain types of attentional and memory tasks; animals (sustained attention/working memory)

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26
Q

use of 5-choice serial reaction time task and cognitive function in mice using nicotine

A

improved performance with either acute or chronic nicotine administration, but poorer performance during withdrawal from chronic nicotine

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27
Q

what nicotine receptors are important in enhanced cognitive function?

A

nicotinic receptors containing alpha7 subunits

28
Q

mesolimbic dopamina pathway and nicotine’s reinforcing effects

A

VTA to nucleus accumbens; high affinity nicotinic receptors located in the VTA stimulate the firing of DA neurons, which causes increased DA release in the nucleus accumbens; lesioning the dopaminergic innervation of this area with 6-hydroxydopamine (6 OHDA) significantly attenuated nicotine self-administration

29
Q

what nicotine receptors play a role in its rewarding effect?

A

VTA nicotinic receptors containing alpha6 and beta2 subunits; receptors in the nucleus accumbens contribue to reinforcement by modulating DA release

30
Q

what receptor reduces nicotine self-administration?

A

alpha5 receptors in the medial habenula (posterior dorsal thalamus)

31
Q

what does nicotine inhibit in the brain?

A

monoamine oxidase (MAO) A and B in the brain and the periphery; MAO breaks down DA–> may contribute to reinforcing effects

32
Q

physiological effects of nicotine

A

activates sympathetic and parasympathetic systems; stimulates release of epinephrine and norepinephrine; increased heart rate, elevated blood pressure, increased hydrochloric acid secretion in the stomach (ulcers); increased muscle contraction in the bowel (chronic diarrhea)

33
Q

Can nicotine be toxic?

A

Yes–60mg can be fatal.

34
Q

symptoms of nicotine poisioning

A

nausea, excessive salivation, abdominal pain, vomiting, diarrhea, cold sweat, headache, dizziness, disturbed hearing/ vision, mental confusion, marked weakness–> fainting, falling blood pressure, difficulty breathing, weakening of the pulse, rapid/irregular pulse, collapse–> convulsions, respiratory failure

35
Q

acute nicotine tolerance

A

short lived; smokers undergo a significant degree of nicotine tolerance during the course of the day; after an overnight period of abstinence, smokers awaken the next morning more sensitive to nicotine than at the end of the previous day

36
Q

receptors associated with acute nicotine tolerance

A

related to desensitization of central nicotinic receptors; receptors composed of BOTH alpha and beta subunits are desensitized at lower nicotine concentrations than alpha7-containing receptors; alpha5beta2 receptors recover more rapidly than alpha7 receptors

37
Q

chronic tolerance

A

long term nicotine tolerance; elicits a compensatory response manifested by an up-regulation of high-affinity nicotinic receptor expression in many parts of the brain

38
Q

nicotine abstinence syndrome

A

mediated by a combination of reduced DA activity in the nucleus accumbens and increased corticotropin-releasing factor (CRF) activity in the central nucleus of the amygdala

39
Q

Gender and nicotine

A

women smoke fewer cigarettes per day, prefer cigarettes with less nicotine, don’t inhale as deeply, more influenced by nonnicotine aspects of smoking, find it more difficult to quit

40
Q

does smoking as an adolescent lead to adult smoking?

A

early smoking increases the chances of smoking as an adult; 1/2 of all people who begin smoking during adolescence and continue with long-term smoking die prematurely from their habit

41
Q

Chippers

A

smokers who maintain a pattern of regular smoking of a new cigarettes a day without showing the typical signs of dependence

42
Q

what does the relaxing effect of smoking do to a smoker?

A

brings the smoker to the same state as a typical nonsmoker; first cigarette of the day may elevate mood, but later in the day the peaks in plasma nicotine level only maintain neutral mood

43
Q

what is being a smoker associated with?

A

increased stress, depressed mood

44
Q

what signifies onset of nicotine dependence (in adolescence)?

A

loss of autonomy over tobacco use–diminution of the individual’s ability to control their smoking behavior

45
Q

what characterizes abstinence syndrome?

A

tobacco craving, irritability, impatience, restlessness, anxiety, insomnia, difficulty concentrating, hunger, weight gain

46
Q

how long does abstinence syndrome last?

A

average levels of most symptoms (other than hunger and weight gain) were at or near baseline levels at 4 weeks

47
Q

what other factors, besides nicotine, play a role in smoking?

A

sensory stimuli associated with smoking (taste/smell) become conditioned to the reinforcing effects of nicotine; knowledge of upcoming opportunities to smoke

48
Q

behavioral interventions for nicotine

A

antismoking ads, warnings on cigarette packages, high taxes

49
Q

is over the counter nicotine replacement effective?

A

without additional supportive therapy–not really

50
Q

drugs to help quit smoking

A

bupropion (originally an antidepressant); varenicline (chantix)–partial agonist at high affinity alpha4beta2 receptors in the VTA

51
Q

major source of caffeine?

A

coffee beans from the plant coffea arabica; tea leaves have caffeine and theophylline

52
Q

pharmacology of caffeine

A

absorbed from the GI tract in 30-60 mins; begins in stomach but takes place mainly in the small intestine; half life of 4 hours; almost all its excreted through urine after being converted into metabolites in the liver

53
Q

biphasic behavioral effects of caffeine

A

low dose has a stimulating effects (increased locomotor activity); high dose animals show reduced activity and humans show tension and anxiety/ panic attacks

54
Q

positive subjective effects of caffeine

A

feelings of well-being, enhanced energy/ vigor, increased alertness and ability to concentrate, self-confidence, increased work motivation, enhanced sociability; these may be due to alleviation of withdrawal

55
Q

can you be dependent on caffeine?

A

yes– it can lead to dependence and abstinence related withdrawal symptoms

56
Q

caffeine and sports

A

benefits in endurance sports and high intensity activities perhaps by increased force of muscle contraction, enhanced arousal and alertness, and reduced pain perception

57
Q

chronic caffeine use

A

tolerance to some subjective effects; disruption of sleep; tolerance to the cardiovascular and respiratory effects; headache, fatigue

58
Q

caffeine withdrawal symptoms

A

headache, drowsiness, fatigue, impaired concentration, psychomotor performance, mild anxiety/ depression

59
Q

acute caffeine administration

A

leads to several effects on peripheral physiology, including increased blood pressure and respiration rate, enhanced water excretion, and stimulation of catecholamine release from the adrenal medulla

60
Q

chronic ingestion of excessive caffeine

A

1000mg or more per day; can lead to caffeinism

61
Q

medical uses of caffeine

A

mild analgesic effects; treatment of newborn infants suffering from apneic episodes (periodic cessation of breathing); treatment of asthma, type 2 diabetes, some neurodegenerative disorders (parkinson’s, alzheimer’s)

62
Q

mechanisms of action for caffeine

A

blockade of GABAa receptors, stimulation of Ca2+ release within cells, blockade of A1 and A2a receptors for adenosine

63
Q

what does blockage of receptors for adenosine do?

A

underlines caffeine-induced behavioral stimulation

64
Q

adenosine and caffeine’s effects

A

it can be released into the brain extracellular fluid, where it acts on several different types of specific adenosine receptors in nerve cell membranes. Four receptor subtypes (A1, A2a, A2b, A3). A1 and A2a are responsible for mediating most of adenosine’s effects in the brain–> major receptor for caffeine

65
Q

adenosine and sleep

A

is a key neurotransmitter/ neuromodulator in sleep production; caffeine promotes arousal–> antagonism of A1 receptor, studies on mice also implicate A2a

66
Q

adenosine and behavioral effects of caffeine

A

antagonism of A1 and A2a receptors in the striatum where adenosine interacts with DA to modulate locomotor activity

Behavioral Pharmacology (11 decks)

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