Brain Influence on Addiction Flashcards

1
Q

What is addiction defined as in the DSM-IV?

A

Substance dependence.

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2
Q

Which symptoms must a person have in the past 12 months to be diagnosed with substance dependence?

A

1) Tolerance
2) Withdrawal symptoms
3) Increasing doses
4) Inability to reduce intake
5) Considerable amount of time spend obtaining substance
6) Interferes with lifestyle
7) Continues to use substance despite consequences

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3
Q

What is Pavlovian conditioned place preference?

A

Associating the drug (US) with a context or setting (CS), resulting in drug-takers to approach the assocated context (CR).

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4
Q

Explain Instrumental Learning self-administration experiments.

A

Animals press do an action such as a level press resulting in the outcome of a drug, developing an association between the lever press and access to drugs.

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5
Q

Define the Mesolimbic Dopamine System.

A

The system in the midbrain that synthesizes and releases transmitted dopamine to the limbic system. It is important for mediating the impact of drugs and drug abuse.

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6
Q

What is the brain pathway of the Ventral Tegmental Area (VTA)?

A

The VTA’s neurons and axons project up through the brain to form a synapse at the Nucleus Accumbens and Prefrontal Cortex.

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7
Q

Where is the VTA located in the brain?

A

Directly below the midbrain.

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8
Q

What machines do researchers use to measure changes in the brain?

A

Functional Magnetic Resonance Imaging (fMRI)

Positron Emission Tomography (PET)

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9
Q

What affect does dopamine have on drug use in rats’ nucleus accumbens?

A

Dopamine signficantly influences drug addiction behaviour.
Injection of dopamine causes rats to rapidly consume nicotine. Additionally, large self-administration of cocaine or amphetamine causes a rapid increase of dopamine in the nucleus accumbens of rats.

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10
Q

Explain the process of Dopaminergic Neurotransmission.

A

1) Neurotransmitter dopamine is synthesised in VTA and stored in vesicles of the pre-synaptic neuron.
2) Amino acid Tyrosine is converted into L-DOPA, driven by the enzyme Tyrosine Hydroxlyase.
3) DOPA Decarboxylase acts on L-DOPA to produce Dopamine.
4) Dopamine is packaged into vesicles in the terminal button.
5) Arrival of an action potential causes dopamine vesicles to fuse with the membrane of the pre-synaptic terminal, releasing dopamine into Synaptic Cleft.

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11
Q

What are the two dopamine receptors?

A

D1 Dopamine Receptor - when on a post-synaptic neuron it raises the concentrations of cAMP which is often a rewarding action.
D2 Dopamine Receptor - when on a pre-synaptic neuron, it reduces levels of cAMP in the terminal and reduces further dopamine release, which is an aversive (punishing) action.

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12
Q

What is the purpose of Cyclic Adenosine Monophosphate (cAMP)?

A

A second messenger used for intracellular signal transduction (introduction of new DNA).

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13
Q

Explain the transportation and deactivation of dopamine in the brain system.

A

1) Dopamine is removed from the synaptic cleft to a pre-synaptic terminal by a dopamine transporter.
2) Inside the pre-synaptic terminal, degrading monoamine oxidase (MAO) enzymes deactivate dopamine
3) Dopamine remaining in the synaptic cleft are also deactivated.

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14
Q

Explain the effect of cocaine on the dopamine system.

A

Cocaine binds and deactivates dopamine transporters, resulting in the inability to remove dopamine from the synapse quickly. Whenever the cell releases dopamine, increasing amounts are stuck in the synpase ready to bind a receptor, resulting a large dopamine effect.

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15
Q

What is the effect of opiates on the dopamine system?

A

Opiates such as heroin or morphine act to remove the endogenous (origin) break on the dopamine system. They bind to GABA receptors, which inhibit the actions of dopamine neurons, and inhibit the GABA neurons. This results in an excitatory impact of dopamine neurons.

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16
Q

How do GABA neurons mediate the dopamine system?

A

Dopamine neurons are tightly regulated by GABA neurons in the VTA. The GABA neurons release inhibitory receptors, reducing the effect of dopamine.