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PTSD - Effects Of Stress On The Brain
January 21, 2002

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PTSD - Effects Of Stress On The Brain
January 21, 2002

Study: Stress Takes Toll on Brain

Stress - Long-term Biopsychosocial Effects

Study: Stress Takes Toll on Brain

By LAURAN NEERGAARD
Associated Press Medical Writer 
January 18, 2002

WASHINGTON (AP) — Short bouts of stress caused the brain cells of mice to become hypersensitive for weeks, says a new report seeking to uncover the molecular root of post-traumatic stress disorder.

It's not clear if human brain cells react the same way. But the research, by Israeli scientists, is generating interest among scientists struggling to unravel traumatic stress in the aftermath of terrorism.

``It's a tantalizing new lead,'' said Rockefeller University professor Bruce McEwen, who researches stress effects on the brain. 

Anyone who has ever experienced trauma knows such experiences can leave you nervous, easily startled. It's one way the body protects itself from future harm, by learning from a bad experience. But in some people, this protective mechanism goes too far, leading to high anxiety, nightmares and flashbacks known as post-traumatic stress disorder.

No one knows just what happens to switch a normal stress response to an abnormal, hyper response.

But in Friday's edition of the journal Science, Hermona Soreq and colleagues at Hebrew University argue a key player is a brain protein called acetylcholinesterase, or AChE, that is important in helping messages jump from one neuron to the next.  

Soreq exposed mouse brain cells to AChE-affecting chemicals, including the stress hormone cortisol, and examined the brain tissue of mice stressed in such ways as forcing them to swim. 

Within minutes, relatively short periods of stress caused the mice to produce a usually rare, abnormal version of AChE that doesn't provide the same help in neuronal signaling.

That somehow left the mice's neurons hypersensitive. Brain scans found higher levels of electrical activity that lasted for weeks, a lengthy effect Soreq called surprising.

Soreq also works for an Israeli drug company attempting to create an AChE-targeting treatment for traumatic stress. One of the mouse cell studies suggested a chemical called EN101 could be a candidate for further study.

Sometimes, ``we need stress responses. ... We need to be more alert, we need neurons to be active when the situation calls for that,'' Soreq said. But, ``our findings show that traumatic experiences as well as certain chemicals do have long-lasting effects, and that repeated stress may cause cumulative effects.'' 

Soreq cites similarities in symptoms between patients with post-traumatic stress disorder and people poisoned by agricultural chemicals that target the cholinergic system. That system is involved in how the brain stays vigilant. AChE interactions with other brain chemicals have also been associated with memory and behavior.

But it's far from the only theory behind post-traumatic stress disorder, cautioned Rockefeller's McEwen. On Jan. 29, he is hosting a special lecture in New York City for people worried about the effects of the Sept. 11 terrorist attack, where scientists from five universities will put into laymen's terms all that is known about stressing the brain.

Based on a study that blocking certain cell receptors inhibits the formation of bad memories, some researchers are exploring whether beta-blocking drugs might prove stress-protective, McEwen said.

Other research shows the actual brain circuitry in a region called the amygdala changes after an animal is stressed, findings generating intense interest.

Even newer studies suggest trauma victims whose bodies produced less of the stress-related hormone cortisol in the aftermath were more likely to develop post-traumatic stress disorder.

The disorder ``is a very complicated phenomenon in which various hormones in the body and various systems in the brain may all be involved,'' McEwen notes. While Soreq's abnormal AChE may indeed play a role, ``it's far from clear exactly how and where.'

But regardless of what causes post-traumatic stress, the good news is ``the brain is very resilient. Many of these changes are not irreversible,'' he said.

Stress - Long-term Biopsychosocial Effects

1.    Beliefs, perceptions, thoughts, feelings, behaviors, and social reactions all have biological consequences in terms of the functioning of the brain and central nervous system.  

2.    Science now knows that even the small and seemingly insignificant attitudes such as a need for control affects cortisol release and triggers the HPA axis (Croes, Merz & Netter, 1993).  

3.    More recent research indicates that stress alters the immune system and the endocrine system (Rossi, 1993). Obviously, performing artists have immune and endocrine systems, but how could altered immunity, for example, affect performing? 

4.    Long-term maladaptive stress responding leads to a condition known as allostatic load. 

5.    When stressed, our bodies react with an innate response known as the stress response, whereby we "turn on" the ability to shift important resources toward the organ systems which are most likely to enable us to deal directly with the stressor. 

6.    Some (not all) of the effects of the stress response are increased heart rate, blood pressure, muscle tension, hyper-alertness and increased blood sugar levels. 

7.    In a healthy person who is in a healthy situation, stress responding is transient and the person returns to normal quickly.   In other words, when the stressor is is no longer present, the stress response is supposed to abate and our bodies are supposed to return to "normal." 

8.    For some, however, these responses remain high ("red-alert" status) and our organ systems stay in "red alert" too long and/or turn "on" too often. 

9.    According to Dr. McEwen, the "red alert" status, in chronic, stress-related disease, does one of four things: 

(1)   It may come on too often (repeated "hits"), 

(2)   It may fail to adapt to the same stressor over time (such as never getting used to doing something stressful), 

(3)   It may turn on and stay on even though the stressor is passed, or 

(4)   It may cause some organ systems to stop reacting, requiring an overreaction in other systems (McEwen, 1998) in an attempt to preserve homeostasis. 

10.  The cognitive components are equally problematic because the stress response causes inflexible thought and interrupts transfer of long-term memory to working memory, contributing to memory error in performance.

References:

Croes, S., Merz, P. & Netter, P. (1993). Cortisol reaction in success and failure condition in endogenous depressed patients and controls. Psyconeuroendocrinology, 18(1), 23-35.

McEwen, B. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338(3), 171-179.

Rossi, L. E. (1993). The Psychobiology of Mind-Body Healing. New York: Norton.

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