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ALASTAIR DOBBIN ET AL.
active on functional magnetic resonance imaging (fMRI) when subjects
compare very similar objects but is completely inactive comparing
identical objects (Bakker, Kirwan, Miller, & Stark, 2008); animals with
damage to the DG are unable to discriminate correct and incorrect
food wells when their locations are close together (Gilbert, Kesner, &
Lee 2001); the pattern-separation function of the dentate gyrus appears
to maintain access to distinct representations of temporally and spa-
tially separated memories, particularly those from a closely similar
context . Rats reaching a junction in a maze replay previous experi-
ences from each subsequent pathway in their hippocampus (Redish &
Johnson, 2007); any dysfunction at this point will compromise effective
choices. There is an animal model of depression where removal
(Knock Out) of a serotonin 1a receptor—Ht1a, a widely expressed
marker for anxiety and depression in humans (Parsey et al., 2006)—
creates transgenic mice (Ht1a
KO
) that have excessive fear to ambiguous
cues, that is, cues that are only partially predictive of noxious stimuli,
as opposed to their “wild” littermates (normal mice) who show behav-
ioral responses consistent with the threat contingencies (and can get
the cheese in a partial threat situation) (Tsetsenis, Ma, Lo Iacono,
Beck, & Gross, 2007). In this latter study they found that subsequent
restoration of function to the amygdala in the knockout mouse does
not change this inappropriate fear of the ambiguous cues, but restora-
tion of DG function does, so the conclusion is that the DG of the hip-
pocampus modulates the amygdala, a finding confirmed by Maren and
Hobin (2007) who found “hippocampal processes influencing amygdala
neuronal activity during the retrieval of extinction memories” (p. 322).
These studies could explain why overgeneralization (as opposed to sep-
arate distinct memories that require effective DG function) outperforms
other predictive indices in depression (Hermans et al., 2008). Neurogen-
esis continues throughout adult life in the dentate gyrus of the hippoc-
ampus, where new cells are added continuously (Imayoshi et al., 2008),
but learned helplessness (via an inescapable stress) reduces neurogene-
sis (Gould, McEwen, Tanapat, Galea, & Fuchs, 1997), which may explain
the direct correlation between reduction of size of the hippocampus in
and time spent depressed (Sheline, Sanghavi, Mintun, & Gado, 1999).
One month after the specific destruction of new cells in the dentate gyrus,
mice showed significantly poorer performance on a maze-learning test
(Imayoshi et al., 2008).
How do these neurobiological understandings and thinking styles
relate to hypnosis, particularly in depression? There are many insights
that these areas of research can bring to the fields of hypnosis and hyp-
notherapy.
Rainville, Hofbauer, Bushnell, Duncan, and Price, (2002), examining
brain activity by positron emission tomography (PET), noted that hyp-
nosis involves
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