Let’s take a closer look at tonic immobility. When does it happen? How does it affect the animal? How does it affect the predator? And, perhaps most importantly for our purposes, “Does tonic immobility have after-effects?” As we will see, it does indeed.
To preview: The after-effects of tonic immobility are determined by what caused the tonic immobility in the first place, what happened during the time that the animal was immobile, the manner in which the animal emerged from its immobility, and what happened to the animal afterward.
When Psychologists Take Away All Safety
As you remember, the autonomic nervous system has two branches: (1) the sympathetic, emergency, fight-or-flight system, and (2) the parasympathetic, withdrawal/immobility system. As Porges (1995a) has emphasized, the parasympathetic nervous system has two very different functions. Mostly, this system becomes active when the environment does not need to be dealt with; at those times, the parasympathetic nervous system facilitates homeostatic functions such as digestion, growth, healing, and conservation of energy. The parasympathetic nervous system’s second function is triggered when the sympathetic nervous system’s fight-or-flight operations fail. Then, there is a sudden, massive parasympathetic innervation of the heart and the animal may collapse into immobility.
The noted fear researcher, Joseph LeDeux, conditioned rats to fear a tone that occurred whenever they were shocked. Later, something very interesting happened (Iwata & LeDeux, 1988). If the conditioned rats heard the tone while they were roving freely about their cage, their heart rate and blood pressure increased (i.e., fear and sympathetic innervation). On the other hand, if they heard the tone while they were restrained, their heart rate and blood pressure decreased (i.e., inability to flee and parasympathetic innervation): So:
Signal of pain when they could flee ==> Sympathetic Activation
Signal of pain when they could not flee ==> Parasympathetic Activation.
This same duality of response occurs naturalistically. If free-ranging woodchucks are approached in the open by a human, their heart rate accelerates and they flee (i.e., sympathetic activation). On the other hand, if woodchucks are approached when they are near or in their burrow, their heart rate slows (i.e., parasympathetic activation). The woodchucks’ bradycardia was greatest when their danger and helplessness was greatest — namely, when a dog was digging into their burrow (Smith and Woodruff, 1980).
Bottom line: An animal’s parasympathetic innervation is greatest when it is approached in its place of safety by a potential predator. Remember: Submerged alligators (submergence is their place of safety) dropped their heart rate from 30 bpm to 2-5 bpm when approached by a canoe. The alligator then remained submerged for 30 minutes (instead surfacing every 5-7 minutes as alligators normally do).
What does this have to do tonic immobility? Quite simply, parasympathetic innervation may culminate in full-blown tonic immobility if the experimenter continues to restrain the animal (thereby increasing the animal’s helplessness in the face of pain and danger).
Restraint and Inescapable Danger
One of the most dramatic examples of inescapable restraint and utter loss of safety is the series of studies that were conducted by Curt Richter. Richter (1957, 1958) dropped domestic rats into a vat of water where they were harassed by a jet of water that produced turbulence in the water. Nevertheless, these rats swam for about 60 hours — until they became exhausted and drowned. Then, Richter performed the same experiment with rats who had been shorn of their vibrissae (whiskers). This was not an inconsequential thing to do; a rats’ vibrissae are a major sensory organ. To Richter’s surprise 2 of these whiskerless domestic rats drowned within minutes; the other 10 continued to swim strongly for a long time.
Curious about this mysterious “death response,” Richter launched a new series experiments — this time with 34 brown, sewer rats (Rattus norvegicus). Norway rats are incredibly fierce and suspicious. In fact, they are so fierce that, in order to avoid being severely bitten, Richter was forced to concoct a special device to pick them up and restrain them. He then trimmed their vibrissae and dropped them into the vat of water. All 34 of these fierce rats died in 2 to 8 minutes!
Despite the influence at that time of Walter Cannon’s writings about the fight-or-flight function of the sympathetic nervous system, Richter noticed, to his surprise, that his rats’ deaths were preceded by their hearts slowing (rather than accelerating from sympathetic activation). Autopsies confirmed his observation. Their hearts were found to be in a state of diastole, engorged with blood. They had died ‘a vagus death.’ [The vagus is the major nerve in the parasympathetic nervous system that controls heart rate.]
Richter then did something very strange. He wrote that the rats had become “hopeless” — that they had just ‘given up’ and died. I cannot convey adequately how strange it was for Richter to say this. His comment about hopelessness was a very ‘un-rat-psychologist’ thing to say. Academic psychology in the late 1950s was profoundly behavioristic. Everything was behavior. And there was no room in behaviorism for things like ‘hopelessness’ or ‘giving up.’
Richter was especially taken aback by the fact that some of his fierce Norway rats ‘gave up’ even before they were dropped into the vat of water!
“a reaction of hopelessness is shown by some wild rats very soon after being grasped in the hand and prevented from moving. They seem literally to give up.” (Richter, 1958, p. 120)
This mysterious ‘giving-up’ “death response” was so striking to him that he sought to ‘cure’ it. [He may also have wanted to justify his ‘heretical’ comments about hopelessness.] :-)
Richter intuitively sought to teach the rats that ‘all was not hopeless’:
“Support for the assumption that the sudden death phenomenon depends largely on emotional reactions to restraint or immersion comes from the observation that after elimination of the hopelessness the rats do not die. This is achieved by repeatedly holding the rats briefly and then freeing them, and by immersing them in the water for a few minutes on several occasions. In this way the rats quickly learn that the situation is not actually hopeless; thereafter they again become aggressive, try to escape, and show no signs of giving up. Wild rats so conditioned swim just as long as domestic rats or longer.” (Richter, 1957, p. 196, emphasis added)
Martin Seligman, one of the fathers of learned helplessness, was fascinated by Richter’s experiments. Not surprisingly, Seligman referred to Richter’s rats as “helpless.” Seligman described a Richter-related, unpublished study about tonic immobility in baby chicks (Seligman, 1975).
H. J. Ginsberg induced tonic immobility in baby chicks by restraining them [Note: Restraint is the classic procedure that psychologists use to induce tonic immobility.]. Ginsberg allowed half of these chicks to come out of tonic immobility at their own pace. He forced the other half to come out of their state of tonic immobility prematurely — by repeatedly prodding their breast with his finger.
Ginsberg then dropped the chicks into vats of water where they swam until they drowned. He compared their time-to-drowning with a third group of chicks that had never experienced tonic immobility. The chicks who had been forced to come out of tonic immobility prematurely died the fastest. The control group of chicks who had never experienced tonic immobility swam the next longest. Finally, the group of chicks that been allowed to come out of tonic immobility at their own pace swam the longest.
Seligman interpreted these results in terms of helplessness vs. control. The more control that a chick had experienced over its own fate, the longer it resisted drowning.
Why Did Evolution Select For This Automatic Response of Tonic Immobility?
The survival value of tonic immobility presumably lies in the fact that immobility causes the predator to lose interest in its prey. The Internet, in fact, provides a plethora of news reports and advice articles about the survival value of ‘playing dead’ when attacked by a predator.
For example, a woman described a bear attack that happened a few months ago when she was camping in Yellowstone Park (The Early Show, CBS, 7-29-10):
“Next thing I know, this bear is chewing on my arm. I screamed. He bit harder. I screamed harder.” She then realized that “screaming was not working… I don’t know if you call it instinct, but something inside me just said… ‘I want to live.’ And I just told myself, ‘Play dead.’ …As soon as I went limp, I feel his jaws get loose and then let me go and he went away.”
Notice the difference between (1) this woman who ‘played dead’ and (2) the chicks that Ginsberg forced to come out of tonic immobility prematurely (and then dropped into a vat of water). The woman was delighted and empowered. The chicks were defeated and helpless. And they died quickly.
‘Playing dead’ worked exactly the way Nature designed tonic immobility to function — when the predator was a bear. The chick’s immobility also worked the way Nature had designed it to function, but the experimenter was not a bear. Human predators behave differently. Tonic immobility usually does not cause a human predator to lose interest.