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PYB260 > W 6 - Nicotine > Flashcards

W 6 - Nicotine Flashcards

1
Q

What are the forms of nicotine?

A

o Smoking tobacco
• Cigars, pipes ect
o Smokeless tobacco
• Snuff, chewing tobacco ect

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2
Q

How is nicotiine absorbed through smoking?

A

o 90% absorbed through the mucuous membrane in the lungs
o Directly to the heart and reaches brain in 7 sec
o Amount absorbed is determined by:
• How a cigarette is smoked
• vol of smoke
o Some nicotine absorbed through the mouth
o NOTE: alkaline so absorbed fast through mucous membranes
o Snuff
o Most nicotine absorbed through nasal cavity membranes
o Nasal Spray
o Most similar to smoking route of administration and absorption

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3
Q

What is the absorption when nicotine taken orally?

A

• Not as good as smoking because not readily absorbed through mucous membrane
• Chewing = tobacco absorbed through mouth membranes
• Ingestion = tobacco rarely swallowed
o Poorly absorbed
o Most metabolized in liver
o Usually induces vomiting
• Nicotine Gum
o Nicotine levels rise and fall with chewing
o Peak © approx. 1/3 that of smoking

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4
Q

What is the absorption when Nicotine taken transdermally?

A

• Patches
o Slow build up of nicotine
o Constant level of nicotine maintained for hours

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5
Q

What is the time of distribution of nicotine, and where is it concentrated?

A
  • Depends on route of admin and time of admin

* Nicotine leaves the brain approx. 30 min and concentrates in liver, kidneys, salivary glands and stomach

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6
Q

Where is nicotine found?

A

• Nicotine crosses most barriers and is found in sweat, saliva, breast milk and placenta

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7
Q

How is nicotine extreted in the kidney’s?

A

o Depends on pH – i.e. 30-40% excreted in pH<7

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8
Q

How is nicotine metabolized/excreted in liver?

A

o Metabolized to:
• Cotinine (~80%)
• Nicotine - `/-N-oxide

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9
Q

What is the half life of nicotine

A
  • Half life ~90-150 mins in adults

* Minimal day-to-day accumulation

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10
Q

What does metabolism depend on?

A

• Metabolism depends on:
o Gender
o Smoker vs non-smoker
o Genetics (e.g. CYP2A6 gene expression)
• If there is mutation then have people who are slower at metabolizing – protective (doesn’t need to smoke as much)

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11
Q

What are the physiological effects of nicotine?

A

• ↑ Heart Rate
• ↑ Blood Pressure – narrower vessels
• Vasoconstriction in skin
o Decreased skin temperature
o Cold Touch
o Because doesn’t have good blood supply to skin – aging and wrinkles
o Decreased blushing
• Inhibits stomach secretion – over long period of time can stimulate
• Stimulates bowel activity – laxative effect

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12
Q

What types of receptor sites does nicotine target?

A

Cholinergic

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13
Q

What are the types of receptor sites, and what are they named after?

A
  • Named after agonists (activates receptor)
  • Muscarinic
  • Nicotinic (cHChR)
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14
Q

What is an agonist

A

Naturally occurring in the body

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15
Q

What is muscarinic receptors stimulated and blocked by?

A

o Stimulated by muscarine; blocked by atropine

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16
Q

What are nicotinic receptors?

A
  • Mainly ionotropic - entry and exit of ions (Na+, K+, Ca2+ ions) - allows entry into cell when it binds
    o Stimulated by nicotine
    o Blocked by curare (neuromuscular), mecamylamine (neuronal)
    o Body regulates homeostasis but by taking nicotine disturb balance
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17
Q

What are the three states of nChRs

A
  1. Basal state: closed ion channel at rest; high affinity for antagonists
  2. Active state: open channel; low affinity for agonists and antagonists
  3. Desensitized state: closed channel; insensitive to agonists/antagonists
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18
Q

What is the effect of nicotine on receptors?

A

o At low doses nicotine stimulates nicotinic cholinergic receptors
o At high doses it blocks these receptors

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19
Q

Where are nicotinic receptors located?

A

PNS and CNS

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20
Q

Whare neurotransmitters do nicotinic receptors release when stimulated

A

Dopamine (DA ) and norepinephrine (NE)

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21
Q

What does nicotine also stimulate the release of?

A

o Serotonin
o Beta-endorphin
o Hormones

22
Q

What is the Nucleus Accumbens

A

reward centre

→ General the area of the brain that is effected in addiction

23
Q

What is the Mesolimbic reward pathway

A

• Dopamine brought to NAc from VTA (ventral tegmental area)– this connection bringing in dopaminergic neurons is mesolimbic reward pathway

24
Q

What happens to dopamine in withdrawal? - In mesolimbic reward pathways?

A
  • Dopamine goes below normal in withdrawal – cravings

* Need to take drugs to feel ‘normal’

25
Q

What happens in NcA?

A
  • Ventral Striatum processes withdrawal and motivation

* Dorsal Striatum = habit forming behaviours

26
Q

What type of control is done on NcA?

A
  • Ventral Striatum processes withdrawal and motivation

* Dorsal Striatum = habit forming behaviours

27
Q

What happens in people who take drugs? What is this called?

A

top down control from cortex to NA is weakened
• Can understand that behavior is not good for them but continues to do it
—> Increased impulsivity

28
Q

What happens to cause compulsivity in drug takers?

A
  • Habit – pleasurable and rewarding behaviours become a habit and start being controlled by dorsal striatum
  • Control of DS by cortex is weakened – start compulsivity
  • Something that starts recreational can start to become compulsive
29
Q

What type of ion channels are nicotinic receptors (nAChRs)?

A

• nAChRs are pentarmeric legand-gated ion channels consisting of different combinations of a2 – a10 and B2 – B4 subunits

30
Q

What are nicotine and acetylcholine

A

ligands to nAChR

31
Q

Where are nAChRs distributed

A

widely distributed in the brain including the NAc, VTA, prefrontal cortex and amygdala

32
Q

What are the effects on the PNS?

A
  • Nicotinic receptor sites located at neuromuscular junctions of striated muscles
  • Nicotine stimulation = muscle tremors
  • Nicotine causes release many neurotransmitters that affect the PNS, e.g. adrenaline/epinephrine (E)
33
Q

What are the effects on the CNS?

A

• Direct effect on synapses
• Release of adrenaline from various sites (synapses and adrenal glands)
• Stimulation of reticular activating system
o All result in increased arousal

34
Q

What are the neurological effects?

A

• Stimulation of medulla – increased respiration
• Inhibition of reflexes due to stimulation of inhibitory cells in spinal cord
• Vomiting centre also stimulated
• Release of NE and DA - & stimulation of systems that use these NTs (e.g. reward system)
o Increase in DA activity in Nacc; correlates with rated pleasure
o nAChRs with alpha2, alpha4 & beta2 subunits appear to mediate nicotine reinforcement
• Serotonin systems also affected – antidepressant action

35
Q

What are the subjective effects of nicotine?

A

o Acute effects
• Pleasurable (by smokers)
o Chronic effects
• Stress, decreased well being ratings

36
Q

What are the effects on sleep?

A

o I.V. nicotine – REM sleep in cats but not humans

o Withdrawal may affect sleep (increased REM)

37
Q

What do the effects on performance depend on?

A
  • Smokers vs non-smoker

- Withdrawal

38
Q

What are the general effects of nicotine on performance?

A

• Increased speed & accuracy of vigilance, attention & information processing
o Increased short-term episodic memory, but not LTM
o Increased alerting attention accuracy (vigilance)
o Increased speed of alerting and orienting attention and working memory (N-back task RT only) – motor system
• Faster motor reaction time – e.g. finger tapping speed; faster RT on N-back task

39
Q

What are the effects on cognitive functioning?

A

• Effects of smoking similar to arousal – thus effect on learning
• Immediate recall impaired, but later recall improved
• Alzheimer’s disease
• Contentious area of research: many other studies show null or negative effects of nicotine on cog function
Animal Studies

40
Q

What were the findings of SMA in rats?

A

• SMA in rats usually depressed initially, but increased after 7 days
o Initial decrease SMA due to increased Ach – then tolerance
o Increased adrenalin produces SMA similar to amphetamines

41
Q

What are the conditioned responses to nicotine?

A

• Nicotine and amphetamine effects on conditioned behavior are similar:
o Nicotine seems to slow high rates of behavior and increase low rates of behavior
o Does not increase punished responses
o Withdrawal can disrupt shock-avoidance behavior

42
Q

What may the conditioned responses be due to?

A

catecholamine release associated with nicotine, though nAChRs important (effects blocked by mecamylamine)

43
Q

What is the self-administration in animals

A

• Most animals do not self-administer nicotine
• Monkey research
• Reinforcement depends on:
o Forces consumption
o Paired stimuli
o Reinforcement schedules which impose abstinence between administration
• Nicotine can also serve as a punisher

44
Q

What is the self-administration in humans?

A
  • Reinforcing in humans

* Self-administration is less frequent with higher doses and more frequent with lower doses

45
Q

What are the theories of self-administration in humans?

A
  1. Maintain constant nicotine level – not true as doesn’t remain constant
  2. Trying to achieve high doses (bolus)
  3. Situation & expectations
  4. Dual reinforcement model
    a. MOST LIKELY EXPLANATION
    b. States that you have neurological and social cues which causes individual to engage in behavior
46
Q

What are the discriminitive properties of nicotine?

A

• 0.2 mg/kg can be successfully discriminated – does not generalize to adrenalin, pentobarbital, caffeine

47
Q

Do the effects generalise?

A

• May partially generalize to amphetamines & cocaine
o Suggested to involve cortex more so than reinforcement systems
• Low doses of ethanol can block nicotine discrimination in rats but not humans; caffeine potentiates nicotine discrimination in rats
• Humans can discriminate different doses in an identical cigarette; detect nicotine in nasal spray

48
Q

What is the tolerance of nicotine?

A

• Develops to nausea produced by stimulating the vomit centre of the brain

49
Q

What are the withdrawal symptoms of nicotine?

A

• Symptoms: Decrease HR; increased eating; decreased concentration; increased waking during sleep; cravings; anxiety; depression; aggression; depression; nervousness; headaches; nausea

50
Q

When do withdrawal symptoms develop, how long do they last?

A
  • Develop over 1st 3 days abstinence, peak – 1 wk then decrease
  • Most symptoms disappear > 1 month; cravings may persist & triggered by cue exposure
51
Q

What regulates the severity of withdrawal?

A

• Severity not related to dose, length of smoking, previous attempts to quite, age, gender, alcohol or caffeine
Fast metabolizers; more severe withdrawal

52
Q

What is the treatment for nicotine addiction?

A 
•	2/3 adult smokers want to quit; only 1/10 attempters succeed 
•	Nicotine replacement therapy 
o	Patches 
o	Gum 
o	Nasal spray 
•	Pharmacotherapies 
o	Buproprion (Zyban) 
o	Varenicline (Champix0 
•	The future: nicotine vaccination? 
o	TA-NIC &amp; NicVAS clinical trials

PYB260 (9 decks)

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