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LEARNED HELPLESSNESS

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LEARNED HELPLESSNESS


Seligman, Maier, & Overmier’ s [late 1960’s] boss
dog studies.

Stage 1: Boss dog in hammock can control shock to
foot with head swing while deputy dog cannot.
Yoked control=
Ncell= 8; 6 milliamps for 30 sec’s each X 64. Note
nisbett and S = 350-1450 milliaamps.

Stage 2 – 24 hrs later: Dogs in shuttle box with one
side electrified on floor [foot shock for 60 sec’s over
ten trials] but escape possible-jump low wall. Boss
dog learns fast. Deputy dog does not escape [6 of 8
dogs 75% tolerate 9 –10 shocks. If tested 7 days later
a new batch of deputies also escapes poorly= 60 %
tolerate all ten.

Generality and variations:
 many species [rats, dogs, cats, people]; many
stressors-noise, crowding, cold, defeat, restraint, pain.
True when stage 1 done under curare for helpless
animal.
     Target behaviors:  escape,  shock elicited
aggression,  competition for food,  immune
function and health.
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 e.g. Cohen et. al. 1992 Inescapable changes in social
structure drops immunity in chimps.

Sklar & Anderson 91 more tumors in cancer prone
rats after L.H.

Why?:
Seligman and Maier’s preferred answer:
A) Yoked animal has learned an idea = “I cannot
    prevent pain [or at least foot shock] . My actions
    have no impact [here?].” or Outcomes are not
    CONTINGENT on my behaviors. This represents
    a cognitive deficit = a mental block to seeing that
    escape IS possible in new setting. The animal
    has LEARNED HE/SHE IS HELPLESS.
B) Animal is so bummed that he/she is not motivated
    to try new behaviors. Lost hope>no behavioral
    juice a la drive theory.
Note: animals have ideas. The ideas are not tied to
specific settings [new stim are eliciting helpless r].
It’s not S(1) > R(1).

Opposing views:
L.H.> analgesia. Escape less cause it hurts less.
Tested with tail flick to shock. Yes. Release of
endorphins??? But rat work mainly and doesn’t
disprove that L.H. idea> analgesia.
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Weiss and friends: a two “flavors” view.

Most rat studies test for Lh 30 min later.
No Lh in dogs 48 hours later in O & S 67 but in
another [S & M 67] Lh 7 days later. Learning is
supposed to be permanent so why not 48 hours
later?? And whats with the inconsistancy??

Flavor # 1: Rat work and Overmier & Seligman 67
used short, intense shock. Might this deplete nt’s
such as Epin and nor ep so much that action stops??
If so, it would be only temporary until nt’s bounce
back-like an hour later and certainly by 48 hours
later. So most rat Lh of this type could be due to
shortage of nt juice.

Flavor #2: Long, moderate [1 milliamp] shock >
initial stuggle and action then waiting and then shock
offset = neg Sr. for what??? Inaction. This form of
LH should last.
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Data: Flavor #1- Weiss, Stone and Harrell 1970. Rats
given Lh. Trt over 14 days of one trial with strong,
short shock. Control rats get no days. Then on day
15, all get one strong short unavoidable shock, and
then given a second avoidable shuttle box shock.
Who escapes??

Rats should adapt to stress with less nt loss over time.
If so, 14 day rats should show LESS LH than controls
if Weiss is correct. If its learned H. if anything 14 day
rats should show MORE LH than controls.

Only Naïve Controls show poor escape and also less
brain noreph.

Flavor #2-Glazer and Weiss 1976 The Nosing study.
Rats receive long weak shock
     Day 1: Rats-60 inescapable tail shocks of 1
milliamp for 6 sec . Controls get no shock

72 hours later given chance to escape in one of
several settings. Some require high activity such as
FR 3 Bar Press; FR 2 shuttle box. While one required
stillness = nosing a target.
Lh helped nosing and hurt high activity escape beh.
[repl with yoked design].
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Other data: Weiss, Stone and Harrell 1970
Autopsies of rat brains show less noreph in Lh.
Animals.
Glazer, Weiss, Poherecky and Miller 1975
Admin tetrabenzamine to naïve rats. This depletes
noreph chemically. These drugged animals do worse
at high activity escape but are ok on nosing escape.

Then give rats MAO inhibitor that elevates noreph in
brain. They are immune to Lh manip.

This manipulative work shows that in rats, nt
depletion plays a key role in “Lh” triggered by
intense sudden stressors and suggests that some
forms of freezing under stress could be due to same
type of mech.

But in human research a good deal of belief that Lh is
a cog/motiv problem as orig. stated by Seligman.

Extended as one explanation for depression

Lynn Abrahamson, Seligman and Teasdale. Neg
events attributed to Global, Stable & internal causes=
depressive attributional style. Stable/External>Anger;
[note: orig uncontrollable pos events also>Lh.}
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Optional:
Strategy 1: does Lh manip create bad mood and or
depressed feelings in normals. Sort of but is it the
same intensity??
Strategy 2. Compare depressed to normals after Lh.
Manip on such things as expected future success; task
persistance; escape beh. [correl strategy]
Strategy 3. Compare attrib made by depressed and
normals following Lh
Strategy 4 compare attrib for real bummers for Dep
and normals and does it correl with meas of attrib
style...Data confused
Strategy 5 Manip attrib style among depressives and
look for depr change. Style manips not so powerful
but manipulation of specific depressive thoughts is
more effective [Beck].
Cognitions and attrib clearly do play a role in
maintaining depression and can be used to control it
but in many cases the core cause is physiological.

Nevertheless, Lh has become a core perspective in
thinking about human responses to stress. Generally
accepted that in stressful settings it is beneficial to
decrease helplessness by upping perceived control
and self efficacy. Seen more in following sections.

				
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