L9 based on Giulia's notes Flashcards

1
Q

Three important neural networks

A

the Default Mode Network (DMN), the Central Executive Network (CEN), and the Salience Network (SN).

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2
Q

What is the Default Mode Network (DMN) and when is it active?

A

The DMN is a brain network active when the brain is at rest and not focused on external tasks.

It governs self-relevant cognitive processes such as daydreaming, mind-wandering, and emotional regulation.

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3
Q

Is the DMN involved in stress responses?

A

While not directly involved in stress responses, the DMN activates during stress and interacts with other brain networks like the Salience Network (SN).

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4
Q

How does the DMN interact with the Salience Network (SN)?

A

The Salience Network helps determine when to switch brain activity between the DMN and other networks engaged in external tasks or attention.

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5
Q

What disorders show disruptions in DMN connectivity?

A

Disorders with DMN disruptions include:
Alzheimer’s disease: Altered connectivity and activity.
Autism: Connectivity irregularities linked to social and cognitive processing challenges.

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6
Q

How does psilocybin affect the DMN?

A

Psilocybin (found in psychedelic drugs) modulates DMN activity, showing potential therapeutic effects for certain disorders by altering brain connectivity and reducing rigid thought patterns.

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7
Q

What is the Salience Network (SN) and its primary components?

A
  1. The SN identifies and filters relevant or “salient” stimuli from incoming information.
  2. It primarily consists of the dorsal anterior cingulate cortex (dACC) and anterior insula (AI).
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8
Q

How does the Salience Network (SN) function in task switching?

A
  1. The SN mediates switching between:
    - The Default Mode Network (DMN) for introspective tasks.
    - The Central Executive Network (CEN) for goal-directed tasks.

2.Ensures the brain focuses on the appropriate task for the situation.

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9
Q

What role does the SN play during stress?

A
  1. Integrates emotional and sensory information, essential for:
    - Threat detection
    - Stress response coordination
  2. Relays signals to the amygdala, triggering norepinephrine (NE) release to heighten alertness and excitability.
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10
Q

How is the Salience Network (SN) linked to psychiatric disorders?

A

Depression: Enlarged frontostriatal network may overemphasize negative stimuli.

Anxiety: Hyperactive anterior insula (AI) predicts excessive bodily states, leading to worry and heightened anxiety.

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11
Q

How does the SN influence physiological responses during stress?

A

Through its connection to the brainstem, the SN can:
1. Increase blood pressure
2. Prepare the body for perceived threats.

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12
Q

What is Central Executive Network (CEN) responsible for?

A

Also known as the frontoparietal network, the CEN is responsible for goal-oriented, cognitively demanding tasks such as problem-solving, attention, and learning.

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13
Q

How does the Central Executive Network (CEN) function under stress?

A

Role in Stress: Acute stress can impair CEN functioning by reducing activity in the dorsolateral prefrontal cortex (dlPFC), which diminishes performance on cognitive tasks. Too much stress leads to a failure to suppress DMN activity, causing difficulty focusing on external demands.

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14
Q

How is the CEN involved in psychiatric disorders?

A

The CEN is disrupted in almost every major psychiatric disorder, from depression to schizophrenia, where goal-directed behavior and executive functioning are impaired

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15
Q

Effects of Acute Stress on Salience Network (SN)

A
  1. Stress triggers activation of the amygdala, which is part of the SN, resulting in the release of catecholamines (e.g., norepinephrine) from the locus coeruleus (LC). This increases physiological reactivity (e.g., heightened heart rate, vigilance).
  2. The SN, which mediates switching between the DMN and CEN, becomes more active, prioritizing attention to stress-related stimuli.
  3. Increased SN activity drives focus on immediate threats but can lead to subjective anxiety and over-reliance on stress-focused processing.
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16
Q

Effects of Acute Stress on Default Mode Network (DMN):

A

During acute stress, the DMN, typically associated with mind-wandering and self-referential thinking, fails to deactivate. This inability to suppress DMN activity during cognitive tasks contributes to fatigue and cognitive burden.
Stress increases connectivity between the DMN and SN, which can amplify rumination and emotional dysregulation.

17
Q

Effects of Acute Stress on Central Executive Network (CEN):

A

Stress attenuates activity in the dorsolateral prefrontal cortex (dlPFC), impairing working memory and cognitive flexibility (e.g., adaptability to changing situations).

High cortisol levels during acute stress temporarily accentuate this impairment, although cortisol’s long-term effects may help restore balance after the stressor is resolved.

18
Q

After a Stressor: Network-Specific Responses - Default Mode Network (DMN):

A

After stress, the DMN shows consistent increased activation even during tasks requiring attention, reflecting a lack of deactivation and difficulty shifting focus.

Increased connectivity within the DMN nodes (e.g., medial prefrontal cortex [mPFC] and posterior cingulate cortex [PCC]) and between the DMN and SN is observed. This may contribute to excessive rumination and difficulty disengaging from self-referential thoughts.

19
Q

After a Stressor: Network-Specific Responses - Central Executive Network (CEN):

A

The CEN’s response depends on the intensity of the stressor and the time elapsed since stress onset:

Moderate stress may transiently enhance CEN function due to heightened focus.

Excessive stress, however, leads to reduced activation and a failure to suppress the DMN, impairing goal-directed behaviors.

The CEN often shows an inverted U-shaped response, where mild stress enhances function, but extreme stress impairs it.

20
Q

After a Stressor: Network-Specific Responses - Salience Network (SN):

A

The SN remains hyperactive, maintaining focus on threat-related stimuli even after the stressor has passed. This overactivation is linked to increased anxiety and prolonged stress-related processing.

Its connectivity with the DMN increases, further amplifying emotional responses and preventing cognitive recovery.

21
Q

NEUROMODULATION is

A

Neuromodulation refers to the process of altering neural activity through targeted delivery of a stimulus (chemical, electrical, or mechanical) to specific areas of the nervous system.

22
Q

How Neuromodulation Can Shape the Future of Mental Health Care?

A

Alternative to Medication: Neuromodulation offers a way forward for individuals who do not respond to medications, which is common in treatment-resistant depression or chronic anxiety.

Targeted Approach: Unlike medications, which affect the entire brain or body, neuromodulation can focus on specific brain areas or networks responsible for mental health issues, reducing unwanted side effects.

Addressing Multiple Problems: Depending on the brain region targeted, neuromodulation can simultaneously improve multiple symptoms. For example, targeting the prefrontal cortex might improve both depression and cognitive deficits.

23
Q

Transcranial Magnetic Stimulation (TMS) is

A

TMS is a non-invasive neuromodulation technique that uses magnetic fields to modulate brain activity. It’s like using a magnetic tool to “wake up” or “calm down” specific areas of the brain, depending on what’s needed.

24
Q

Transcranial Direct Current Stimulation is

A

tDCS is a non-invasive brain stimulation technique that uses constant, low electrical currents applied through electrodes on the scalp to modulate brain activity. It can either increase or decrease the excitability of neurons in targeted brain regions depending on how it is applied.

25
Q

Applications and Benefits of tDCS:

A
  1. Affecting Neurotransmitter Systems:
    tDCS can influence neurotransmitter activity (like dopamine, serotonin, and glutamate) in specific brain circuits.
  2. Long-Lasting Effects:
    tDCS can create changes in synaptic strength, which means the effects can persist after the stimulation session ends.
  3. Rehabilitation:
    Anodal stimulation is often used in rehabilitation to increase the excitability of the motor cortex, helping patients recover motor function after a stroke or injury.
  4. Cognitive and Stress Regulation:
    Stimulating areas like the DLPFC can help lower stress by reducing HPA axis activity (leading to less cortisol release) and promoting relaxation through better parasympathetic control.

or

  1. tDCS is a flexible tool: By adjusting the placement of electrodes and the type of stimulation (anodal or cathodal), it can be used to either enhance or suppress brain activity in specific regions.
  2. Practical uses: tDCS is being explored for treating depression, anxiety, chronic pain, and motor impairments.
  3. Non-invasive and low-risk: tDCS is easy to use and causes minimal side effects, making it suitable for home-based or clinical treatments.
26
Q

Key Brain Regions and Their Roles:

A

Anterior Cingulate Cortex (ACC):
The ACC calibrates and regulates the magnitude and duration of cardiovascular reactions to stress.
It ensures the response is proportional to the psychological stressor. If the ACC fails to regulate properly, it can lead to miscalibrations such as exaggerated or blunted reactions, which are metabolically inappropriate and potentially harmful.
Insula (Integration Center):
The insula integrates interoceptive signals (sensory information from the body about its internal state) and connects these signals to emotional and cognitive processes.
Dysfunction in the insula may contribute to conditions like arrhythmias or “broken heart syndrome”, where extreme emotional stress triggers acute heart failure.
Amygdala (Rostral Forebrain Interaction):
The amygdala processes psychological stressors and modulates the stress response.
Dysregulation in the amygdala can disrupt the homeostatic balance between heart rate and blood pressure. This leads to simultaneous increases in both, making the system less responsive to sensory feedback from the body and increasing cardiovascular risk.