Stress/PTSD is Contagious at Molecular Level, Quickly

Stress can trigger enduring changes in neural circuits and synapses.  The behavioral and hormonal consequences of stress can also be transmitted to others,

  • In female mice that were subjected to authentic stress, this metaplasticity was diminished following interactions with a naive partner.
  • metaplasticity could be transmitted sequentially from the stressed subject to multiple partners.

Even a brief exposure to a stressor leaves a lasting imprint on the brain.  These imprints can be overt, manifesting as changes in intrinsic activity, activation of specific cell ensembles or changes in the strength of synapses..  Stress also primes neural networks, resulting in metaplasticity that is evident at synapses.. during a subsequent challenge.

Our findings demonstrate that transmitted stress has the same lasting effects on glutamate synapses as authentic stress…In mammals, an immediate threat activates multiple, interconnected neural networks to launch an innate behavioral program that maximizes the probability of survival. These networks also drive CRH neurons…to release hormones that allow the animal to cope in the face of challenge and restore homeostasis.

In social species such as humans, primates and rodents, distressed individuals benefit from consolation behaviors provided by others.  These interactions, however, can also transmit stress to the naive individual Indeed, behavioral and endocrine changes in partners of stressed individuals offer proof that some parameters associated with stress map from one individual to others in the group.

social interactions may also transmit persistent synaptic changes, or metaplasticity, from one individual to another….These inputs, which originate in key stress-sensitive brain regions, including the brainstem, the medial amygdala and local cell populations in the hypothalamus, are primed by acute stress.  This priming enables these synapses to undergo short-term potentiation (STP) in response to high-frequency afferent stimulation. STP following a single stress persists for days, providing a robust readout of the lasting effect of acute stress on this system.

The behaviors that transmit stress from one individual to another also buffered the synaptic consequences of stress in females, but not males.

Acute stress primes glutamate synapses.  Priming and sex-specific buffering of synaptic changes following interactions with others.  Stress transmission requires investigative behavior and a pheromone signal… stress-naive individuals initiate unreciprocated, investigative behaviors when exposed to distressed individuals.  These behaviors may allow the unstressed

partners to detect alarm signals from stressed individuals.  Studies have shown that stressed individuals alert naive partners by releasing volatile chemical signals from the anogenital region and face that are only detected when partners are in close contact.

The pheromone from the anogenital region activates stress-responsive centers in the brain and is structurally similar to predator odor.   Exposure to predator odor activates a neural circuit that links the olfactory bulb.

“in females, but not males, the partner buffered the synaptic load in stressed individuals...Abnormalities in the CRH system are evident in post-traumatic stress disorder (PTSD) and other stress-related affective disorders, such as anxiety and depression, and recent work has implicated PVN CRH neurons as drivers of anxiety-like behaviors.”

…the consequence of stress on synapses is both graded and sex dependent and is consistent with our previous findings that relatively mild stressors have profound consequences for CRH neurons in females.  Although we have not explored the mechanisms responsible for this differential sensitivity, they may result from previously described sex differences in CRHR1 signaling…not only is stress transmitted from a stressed subject to partners, as previously reported in rodents and humans, but the enduring synaptic consequence of stress, or the synaptic load, is also transmitted from subject to partners.  These findings suggest that, in addition to consoling the stressed individual, affiliative behaviors in humans, primates and rodents may serve a strategic purpose by communicating information about a stressful event. Social interaction also modifies synaptic load in female subjects… females, through a ‘tend and befriend’ strategy, may buffer the effects of stress more effectively than males…

This suggests that social context and environment…From an ethological perspective, the ability to buffer the effects of stress while simultaneously extracting experiential information from the distressed individual has clear adaptive benefits.  This information may promote coalition formation during times of stress while editing neural circuits to prepare for subsequent challenges without subjecting all group members to danger directly.

In humans, buffering or consolation behavior is nearly universal, yet our findings suggest that the partner, or consoling individual, may experience long-term synaptic consequences similar to those of the distressed individual.  This may, for example, offer a potential explanation for why individuals who have themselves not experienced a trauma develop PTSD symptoms after learning of the trauma of others.


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