Periaqueductal Grey Flashcards
(13 cards)
The PAG is involved in…
- behavioral expression of survival-related, defensive responses during threat and stress
(flight/fight/freezing behavior); - modulation of the expression of predatory behavior;
- autonomic control; modulation of nociceptive sensory
- information and analgesia (connections with ACC)
emotional coping strategies
Animals, including humans, react with distinct emotional coping strategies to different sets of
environmental demands. These strategies include the capacity to affect appropriate responses to escapable or inescapable stressors
What’s the difference between active and passive emotional coping strategies?
Active emotional coping strategies are particularly adaptive if the threat/stress is escapable; on the other hand, passive emotional coping strategies (quiescence, immobility, decreased responsiveness to the environment) are useful when the threat/stress is inescapable.
Active emotional coping strategies lead to “engagement with” the environment (e.g., fight or flight)
Characterized by increased somatomotor activity, coupled with cardiovascular changes which include hypertension, tachycardia and alterations in regional perfusion patterns to favor redistribution of blood flow to vascular beds with increased metabolic needs
Passive emotional coping leads to “disengagement from” the environment
Characterized by reduced somatomotor activity (i.e., quiescence or immobility), decreased reactivity to the environment and sometimes hypotension and bradycardia
The PAG has been identified as a region containing distinct neural substrates which initiate passive or active emotional coping strategies
PAG organization
The PAG is organized into columnar subregions with distinct ascending and descending
connections, that coordinate different survival-related responses during threat and stress:
- passive coping strategies are evoked from ventrolateral PAG
- active coping strategies are evoked from dorsolateral PAG and lateral PAG
- anxiety-like behavior evoked from dorsomedial PAG
The dl/lPAG receives inputs from sensory systems, the amygdala, the ventromedial hypothalamus, and the medial prefrontal cortex (mPFC) and innervates the sympathetic nervous system →facilitate threat and confrontational defense, fight, flight, and other active coping responses
with significant autonomic activation
The vlPAG is innervated by the anterior insula and medial and dorsomedial prefrontal
cortices and innervates the parasympathetic nervous system→ mediate passive
coping behaviors, characterized by quiescence, hyporeactivity, hypotension, bradycardia
PAG lesions
- vPAG lesion diminishes freezing, indicating that the ventral PAG is necessary for defensive freezing behavior
- dlPAG lesion enhances freezing, indicating that the dorsolateral PAG exerts tonic inhibition over the ventral PAG
Afferents and reciprocal connections of PAG
The PAG has reciprocal connections to the prefrontal cortex, basal ganglia and VTA,
hypothalamus, hippocampus, amygdala, and spinal cord
Afferents to the PAG without reciprocal connection include ones from the orbitofrontal cortex
(OFC) and insula
PAG substructures in human
PAG substructures in humans appear to conform to the animal model of four longitudinal columns
either side of the aqueduct, with possible differences in the size and shape of these columns
Tractography demonstrates differential connectivity patterns arising from the four divisions of the
human PAG
The human defense cascade
- Freeze (attentive immobility, orienting response)
“Uproar” sympathetic activation:
- Flight
- Fight
dizziness, lightheaded, palpitation, dry mouth, numbling, muscle tension, feelings of irreality, reduced pain perception
- Fright (tonic immobility, unresponsive immobility): tachycardia, vasoconstriction, hypertension, hyperalertness, high emotional arousal, fear largely repressing anger, assaultive breakout followed by immobility
“Shut-down” parasympathetic activation:
- Flag
- Faint
bradycardia, vasodilatation, hypotension, drop in arousal, surrender, cognitive failure, numbling of all emotions
Is the PAG involved in defensive behavior in humans?
PAG response is greater in response to negative than neutral pictures
Activity in the PAG (exp. ventral) correlates with heart rate decrease (“fear bradycardia”)
Activation of the human PAG is linked to a parasympathetically dominated autonomic response that is characteristic of freezing behavior in both animals and humans →passive defense mode that subserves a state of attentive immobility
Active avoidance of a virtual predator that can chase, capture, and inflict pain: what’s the neural response to distal and proximal threat in humans
When threat is detected (“cue phase”): activity in the PAG and rACC is greater for the predator cue than for the neutral cue (rACC activity → response conflict between fleeing or staying; anticipatory anxiety that promotes avoidance; fear of pain)
The “imminence effect” in the predator condition (“chase phase”):
- for distal threat, activity is greater in vmPFC (different alternative goal-directed behaviors are compared in order to choose the most effective strategy to avoid the threat or distress)
- for proximal threat, activity is greater in the PAG (fast and obligatory response is required, preparing the organism for survival and possible tissue damage
PAG, dread rating and confidence of escape
Activity in the PAG is positively correlated with dread ratings and negatively correlated with confidence of escape.
Patients with panic disorder and chronic anxiety show decreased vmPFC and increased gray matter volume and activity in the midbrain, encompassing the PAG
PAG and anticipation of pain
The PAG is activated when receiving, but also when anticipating pain —> anticipation of a painful
stimulus allows the organism to “tune” its nociceptive system to better cope with the upcoming aversive stimulation (increased anticipation of pain was associated with higher pain intensity ratings→increased sensitivity)
PAG’s role in pain regulation
The PAG plays a bi-directional role in both upward and downward projections, and is involved in pain transduction and regulation through several analgesic pathways, including:
1) The brainstem downward inhibitory system, i.e., the anterior cingulate cortex -PAG-rostral ventral medulla-spinal cord dorsal horn/spinal tract nucleus of the trigeminal nerve pathway; 2)Midbrain limbic analgesic circuit, i.e., nucleus accumbens-amygdala-habenular nucleus-PAG- rostral ventral medulla;
3) arcuate nucleus - nucleus raphe medius-locus coeruleus–PAG–spinal cord dorsal horn pathway; and
4) Thalamic nucleus submedius-Ventrolateral orbital cortex -PAG-spinal cord loop
