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202: Theme 3, Modulatory systems in psychiatry > Neurobiology and neurochemistry or reward based behaviours > Flashcards

Neurobiology and neurochemistry or reward based behaviours Flashcards

1
Q

Addiction

A

Persistent disorder of brain function where compulsive drug use occurs despite serious negative consequences in afflicted individual
- Due to changes in synaptic plasticity

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2
Q

Withdrawal symptoms

A

Negative physiological and emotional features that occurs when a drug is not taken.

Usually opposite to positive experience induced by the drug

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3
Q

Tolerance

A

Diminished response to the effects of a given amount of drug
- Due to repeated exposure to the drug

Increasing larger dosage is required to have the same effect

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4
Q

Regions in the brain for the natural reward system/ addicition

A

Mesocorticolimbic system

Prefrontal cortex

Amygdala

Hippocampus

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5
Q

Dopamine error / 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 nucleus accumbens
- Tells the brain they should be something being learned

Predictable = response in temporal lobe
- Indicates 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 reinforcers for reward

A

Food
Sex

Causes extracellular dopamine release in nucleus accumbens

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9
Q

Psychostimulants

- Effects on dopaminergic system

A

Directly affects dopaminergic neurones in the nucleus accumbens

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10
Q

Opiates

- Effects on dopaminergic system

A

Indirectly – inhibit GABAergic interneurons in VTA

- Disinhibition of VTA DA neurons

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11
Q

Alcohol

- Effects on dopaminergic system

A

Disinhibition of dopamine neurones

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12
Q

Nicotine

- Action

A

Increases Nacc DA directly and indirectly

Stimulates nicotinic cholinergic receptors on mesocortiolimbic DA neurons

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13
Q

Dependance

A

Homeostatic response to repeated drug administration

Unmasked by withdrawal

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14
Q

Sensitisation

A

Repeated administrating of drug = escalating effects

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15
Q

Cocaine and amphetamine

  • Mechanism
  • Role in reinforcement
A

Inhibits dopamine, serotonin and noradrenaline reuptake transporters

  • Cocaine inhibits
  • Amphetamine reverses transporters

= Increased synaptic DA

Reinforcement
- Action on dopamine transporter on plasma membrane

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16
Q

Cocaine and amphetamine

- Effects

A

Psychosis

Long term

  • Decreases dopamine transporters and terminals
  • Increased cellular and molecular changes that promote dysregulation

Hypofrontality [decreased blood flow to prefrontal cortex]

17
Q

Increased excitatory strength and drug abuse

A

Drug abuse shows significant increase in AMPA/NMDA ratio

= Increased basal excitatory synaptic strength

18
Q

Dopamine receptors in addiction

A

Fewer D2 receptors

- Reduces sensitivity to natural rewards that develops with addicition

19
Q

Molecular activity of emotional dependence

A

Compensatory changes in the VTA or Nucleus accumbens = lower DA transmission

At first;
- Increased D1 receptor activity in NAcc sets off Gs protein signalling

PKA and cAMP release =

VTA

  • dynorphin synthesis and release is inhibited
  • Acts on K opiod receptor

Nucleus accumbens
- Less DA release

20
Q

Associative learning and addiction

A

Coincident firing in sensory and mesocorticolimbic pathways
= LTP induction = strengthened synaptic connections

Glutaminergic synapses form on reciprocal connections in:
- NAcc
- VTA
- Cortex
- Hippocampus
- Amygdala
= Potential sites for LTP

Information present at the time of drug induced DA release —–> associated with drug taking

21
Q

Dopamine and LTP

A

DA acts on D1 receptor [Gs protein]
- Increase in PKA = gulatamatergic transmssion = LTP

Late phase LTP
- CREB protein mediation and protein synthesis

Synaptic remodelling
- Increased spines and dendrite branches
- long term molecular and 
cellular changes remain
months after abstinence
- Memories in these 
pathways may trigger 
relapse years later
22
Q

Opiates

  • Action
  • Reward and reinforcement
A

Acts on endogenous opioid receptors (Gi coupled)

Morphine mainly acts on gamma receptors

Reward and reinforcement
- Disinhibition of DA neurons in VTA

  • Action at opiate receptors in the NAcc - independent of DA release (μ or δ)
23
Q

Alcohol

- Mechanisms

A
  1. GABA-alpha agonist
  2. NMDA antagonist
    - In the VTA cortical inputs = disinhibits VTA DA neurones
    - Increases Dopamine release in the nucleus accumbens

Rewarding effects blocked by DA receptor antagonists in NAcc

24
Q

Naltrexone and alcohol

A

Opiate antagonist
- Reduces alcohol self administration in animals

  • Used to reduce alcohol consumption, relapse and craving
25
Q

Nicotine

- Mechanism

A

Acts on nicotinic Ach receptors

Nicotine = release of dopamine in nucleus accumbens due to:

  • Activation of receptors on cell body in the VTA
  • Facilitated DA release by pre-synaptic receptors in NAcc
26
Q

Opiates and nicotine

A

Opiates block nicotine induced behaviours and self administration
- I.e Naltrexone used to add smoking cessation

27
Q

Physical dependancy on opiates

A

Locus coeruleus

  • Contains opiate receptors
  • Nucleus involved in attention, arousal and vigilance [NADR]

Chronic activation of opiate receptors = homeostatic compensation = tolerance and physical dependance

28
Q

Morphine and locus coeruleus

A

Acute morphine = inhibits LC neurones

Chronic morphine = LC neurones return to firing state

Withdrawal = Dramatic increase in LC neurones firing
- Over activation of ANS

29
Q

Clonidine

A

Alpha-2 agonist that blocks the over activation of ANS seen in physical withdrawal of opiates

30
Q

Physical dependance to alcohol

A

Acute effects
- GABA-alpha agonist
- NMDA antagonist
= Cell firing inhibited

Chronic

  • Downregulation of GABA-alpha
  • Upregulation of NMDA
  • Firing rates normal in presence of alcohol

Withdrawal

  • In alcohol absence= excitation
  • Physical symptoms
31
Q

Reward pathway in the brain

A

Release of dopamine in mesocorticolimbic system.

DA released from the VTA to multiple areas when a rewarding stimulus is experienced:

  • Prefrontal cortex
  • Nucleus Accumbens
  • VTA
  • Amygdala
  • Hippocampus

Release of DA stimulates the desire for the stimulus again

32
Q

Mechanism of emotional dependance

A

Due to compensatory control to decrease Dopamine release in the VTA and NAcc

  1. Drugs act on D1 receptors [Gs] in NAcc
    - Triggers downstream events [cAMP, PKA]
  2. Downstream events trigger release of Dynorphin from NAcc to VTA
    - Dynorphin acts on Kappa receptors on VTA DA neurones.
  3. Activation of K receptors reduces VTA DA neuronal firing= less release of DA into NAcc

As a result–> Less DA is released in the event of the drug not being there
- Naturally rewarding stimuli cannot produce enough DA

202: Theme 3, Modulatory systems in psychiatry (7 decks)

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