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Theme 3 Modulatory Systems in Psychiatry > L1 Neurobiology and neurochemistry of reward and addictive behaviours. > Flashcards

L1 Neurobiology and neurochemistry of reward and addictive behaviours. Flashcards

1
Q

What is addiction

A

A persistent disorder of brain function in which compulsive drug use occurs despite serious negative consequences for the afflicted individual.
due to changes in synaptic plasticity

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2
Q

What is withdrawal

A

Negative physiological and emotional features that occurs when the drug is not taken
generally opposite to positive experience induced by the drug.

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3
Q

What is Tolerance

A

diminishing effect of drug after repeated administration

-need more drug to get the same effect

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4
Q

Which regions of the brain are involved with Natural reward system?

A

Mesocorticolimbic system

PFC

Amygdala

Hippocampus

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5
Q

Evidence that Dopamine can act as error or learning signal

A

When given a reward with no stimulus
- There is a spike in activity after the reward

When given a stimulus prior to the reward

  • Spike in activity before reward
  • Anticipation of the reward is more pleasurable than receiving the reward

When reward does not come-

  • Anticipation still spikes
  • Fall in dopaminergic effect
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6
Q

Predicted vs unpredicted stimulus and learning

A

Unpredicted reward
increased activity in the Nucleus Accumbens – ‘tells’ our brain that there is something we should be learning

Predicted= response in temporal lobe
-indicating learning has taken place

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7
Q

Functions of the Reinforcement System

A

Detect reinforcing stimulus

  • Recognise something good has just happened
  • Time to learn

Strengthen neural connections

  • Between neurons that detect the stimulus and the neurons that produce the instrumental response
  • Long term potentiation
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8
Q

Natural Reinforces for reward

A

Food
Sex

Causes extracellular dopamine release in nucleus accumbens

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9
Q

What are the effects Pscychostimulants on dopaminergic system?

A

Direct action on Daergic neurons in NAcc

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10
Q

What are the effects Opiates on dopaminergic system?

A

Indirectly – inhibit GABAergic interneurons in VTA

causing disinhibition of VTA DA neurons

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11
Q

What are the effects Alcohol on dopaminergic system?

A

Disinhibition of VTA DA neurons

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12
Q

What are the effects Nicotine on dopaminergic system?

A

Increases Nacc DA directly and indirectly

stimulates nicotinic cholinergic receptors on mesocortiolimbic DA neurons

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13
Q

What is Dependence

A
  • homeostatic response to repeated drug administration - unmasked by withdrawal
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14
Q

Sensitization

A

repeated administration elicits escalating effects

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15
Q

Cocaine and amphetamine

overview

A

inhibition of dopamine (DA), serotonin (5-HT) and norepinephrine (NE) reuptake transporters

Cocaine inhibits transporters prolonging pool of DA
Amphetamine reverses transporter- increase DA

MOA- increase extracellular DA in NAcc by action on DAT

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16
Q

Effects of cocaine and amphetamine

A

Psychosis

Long term effects

  • decreases DA transporters
  • increased cellular and molecular changes that protmote dysregulation

Hyperfrontality [decreased blood flow to prefrontal cortex]

17
Q

How does Cocaine work

A

inhibits transporter to prolong pool of extracellular DA

18
Q

How does Amphetamine work

A

reverses transporter to increase extracellular DA levels

psychostimulant

19
Q

How do drugs of abuse work [3]

A
  • increase AMPA/NMDA ratio
    -increases basal excitatory
    synaptic strength.
    -Neuronal basis of many forms of learning
20
Q

Dopamine receptors in addiction

A

Decreased D2 receptors in cocaine addiction which normally causes inhibition and suppresses behaviour

The dopamine system central to conditioning and motivation

Changes likely responsible for reduced sensitivity to natural
rewards that develops with addiction.

21
Q

Molecular activity of emotional dependence

A

Compensatory changes in VTA / NAcc to lower DA transmission:

Increased activity at D1 receptors (Gs coupled) in NAcc

Adenylyl cyclase - cAMP - PKA - downstream events

increased dynorphin (DYN) synthesis (endogenous opioid)

dynorphin released in VTA

acts at K opioid receptor

Inhibits VTA neuron firing
and NAcc DA release

Less DA release in NAcc

22
Q

Associative learning and addiction

A

Coincident firing between sensory pathways and the mesocorticolimbic pathway will induce LTP and strengthen synaptic connections

23
Q

Potential site for LTP

A

Glutamatergic synapses on reciprocal connections between

NAcc, VTA, cortex, hippocampus and amygdala

24
Q

DA and LTP

A

DA enhances LTP
-modifies glutamatergic transmission allowing LTP

  • CREB mediated gene transcription and new protein synthesis
  • synaptic remodelling - increased spines and dendritic branches

-long term molecular and
cellular changes remain
months after abstinence

  • memories in these
    pathways may trigger
    relapse years later
25
Q

Opiates

  • Examples
  • Action
  • Reward and Reinforcement
A

E.g morphine, heroin

Inhibitory

  • decrease adenylyl cyclase activity
  • lead to opening of K+ channels, close Ca2+ channels

Disinhibition of DA neurons in VTA by blocking GABA which normally inhibits DA release (mu receptor)
Action at opiate receptors in the NAcc - independent of DA release

26
Q

Alcohol

-receptor type

A

GABA a agonist (inhibitory)

NMDA antagonist (blocks excitation)

27
Q

How does alcohol produce rewarding effects?

A

NMDA antagonism of cortical inputs to VTA disinhibits VTA DA neurons so increases DA release in NAcc

28
Q

Naltrexone

A

An opiate antagonist

aid smoking cessation and associated weight gain, encouraging preliminary results

29
Q

Nicotine

A

DIRECTLY BY
Acts at nicotinic acetylcholine receptors (nAChRs)

Nicotine treatment increases DA release in the NAcc
Due to:
a) activation of receptors on cell body in the VTA (increasing cell firing)
AND INDIRECTLY BY
b) facilitation of DA release by pre-synaptic receptors in NAcc

30
Q

Physical dependence to opiates

A

Chronic activation of opiate receptors leads to homeostatic mechanism that compensates for the functional changes leading to tolerance and physical dependence

Acute morphine- acutely inhibits firing of LC
Chronic treatment- normal firing rates
Withdrawal- increase in LC firing

31
Q

Physical dependence to alcohol

A

Acute effects of alcohol
-agonist at GABAa receptor
-antagonist at NMDA receptor
Cells inhibited from firing

Chronic alcohol
Down regulation of GABAA receptors
Upregulation of NMDA receptors
In presence of alcohol firing rates return to normal

Withdrawal 
in absence of alcohol
balance shifts to excitation
physical symptoms 
- agitation, tremors, hypertension, seizures

Theme 3 Modulatory Systems in Psychiatry (10 decks)

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