Systems Neuroscience Flashcards

1
Q

Give some examples of teh level of description and understanding that encompasses Systems Neuroscience

A

Basal ganglia thalamocortical system

Visual system

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2
Q

What what systems neuroscience can be quoted from Zeki 2003?

A

No evidence that single cells/molecules are a ‘neural correlate of consciousness

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3
Q

Describe the predicate of systems neuroscience

A

Abnormal behaviour and sybjective experiences linked to abnormal functioning of brain systems

There are direct correlations, and can in some cases predict subjective experience

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4
Q

Describe the predicate of biological psychiatry

A

The brain is the organ that generates, sustains and supports mental function, and modern psychiatry seeks the biological basis of mental illness

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5
Q

Systems neurosciene generates models fo brain function to link with descision making

Give two examples of how this is achieved

A

(1) Computational Neuroscience
- Computational psychiatry - Montague 2012
- Neuroeconomics in psychiatry - Hasler 2012
(2) Animal Model
- 5-HT and mechanisms of defence - Deaken & Graeff 2013
- Drug addiction, allostasis and reward, neurobiology of addiction (Koob & Volkow 2010)

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6
Q

Describe Koob’s Allostasis theory of addicition

A

Brain changes that occur in the development of addiction explain the persistence of vulnerability to relapse

Addiction is a spiralling dysregulation of brain reward systems

Progressively increasing to cause loss of control

Counteradaptive processes (such as opponent-process) fail to return to normal homeostatic state, forming an allostatic state

Allostasis represents a chronic deviation from reward set point norms

Driven by dysregulation of reward circuits and endocrine stress responses

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7
Q

Describe the spiral progression of the stages in Koob’s Allostasis model of addicition (3)

A

Binge Intoxication

Withdrawal/ Negative affect

Proccupation / Anticipation

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8
Q

Who proposed the ‘opponent process’ model of addiction, which Koob extended into allostasis?

A

Solomon & Corbit 1974

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9
Q

Describe the evidence for 5-HT function in depression which pre-dated Deakin’s theory

A

Evidence that dopamine was involved in reward

Serotonin thought to have a complementary role

5-HT had an inhibitory effect on behaviour and may have anxiogenic properties

5-HT neurones mediate the effects of punishment behaviour

(still debated whether 5-HT mediates aversive motivational state)

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10
Q

What did Deakin and Graeff propose?

A

DRN neurones fucntion in opposite to dopaminergic neurones

Function as a ‘stop’ or negative reinforcement signal, guiding away from threatsm, toward dopamine cues

MRN neurones mediate an ‘unlearning’ function during punishment or instrumental learning.

Linked to evidence on 5-HT1a agonists impairing memory and projections to hippocampus

Suggested that MRN neruones prevent consolidation of aversive memories, tolerating adversity (resilience)

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11
Q

According to Deakin’s theory, what two roless does 5-HT appear to have in anxiety?

A

Aversion toProximal threats

Aversion to Distal threats

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12
Q

In Deakin’s theory, what role does the brainstem play in the Depression and anxiety?

A

Brain stem - responding to aversive threats

Amygdala - m, hypothalamus - PAG

This system is modulated in different ways be 5-HT

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13
Q

In Deakin’s theory, what role does the Amygdala play in Anxiety and Depression?

A

Amygdala - distal threats

Receives cortical afferents with complex stimuli information

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14
Q

In Deakin’s theory, what role does the PAG play?

A

PAG - Proximal threats

Mediates flight/fight behaviour

Hard-wired, unconditioned reflexive response to proximal threat (imminent death!)

Touch / pain / suffocation (hypoxia)

‘Painic attacks’ can be triggered by CO2

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15
Q

Why might 5-HT be activated in punishment, yet inhibit PAG fight / flight mechanism?

A

When threats perceived at a distance by amygdala, PAG outputs for autonomic and respiratory function activated

Fight / flight component is inhibited from premature activation by 5-HT release from DRN neurones

This enables learned avoidance strategies to guide away from threat

Implies that anticipatory anxiety inhibits panic attacks (clinical evidence: pain attacks made worse by relaxation therapy)

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16
Q

Deakin’s theory has numerous implications. How does it explain ‘learned helplessness’? (animal model of depressive illness)

A

-Increased anxiety and impaired escape behaviour

Both mediated by profound activation of DRN (fMRI)

Medial frontal cortex detects when punishment is controllable and inhibits DRN

17
Q

Deakin’s theory has numerous implications. How does it explain fear processing?

A

Proposed that effects of the DRN on amygdala and in dopaminergic structures, are mediated by high concentrations of 5-HT2c receptors

18
Q

Deakin’s theory has numerous implications. How does it explain depression and resilience?

A

MRN projection to the hippocampus mediate behavioural adaption to chronic or repeated aversive experiences

  • systemic/hippocampal 5HT1a agonist/anti-depessants prevent anxiety
  • SSRIs may correct an ipairment of 5HT1a neurotransmission

Predicts that recovery from depression associated with increased MRN activity, and reduced hippocampal activity