A Single Gene Controls Emotional Recall!
And the neurotransmitter norepinephrine (NE), which has been in the
news lately, plays a key role in the overstated headline of the day:
Emotional recall is in your genes
18:00 29 July 2007
Paul Marks
Image from Fig. 1A of Depue et al. (2007)
Your ability to recall emotional events - such as meeting the love
of your life, or the trauma of a painful car crash - is governed by
a common variation in a single gene, according to a new study.
[NOTE: As if variations in many other genes were tested.]
. . .
Highly emotive incidents trigger the brain to release the hormone
and neurotransmitter noradrenaline. This stimulates the amygdala -
part of the brain involved with processing emotional reactions - to
store memories in the hippocampus and other parts of the brain,
says Dominique de Quervain, a neuroscientist at the University of
Zurich in Switzerland.
Yet for some reason, recall of emotional events varies a great deal
from person to person. So de Quervain wondered if common variations
in a gene called ADRA2B, which codes for [one of the subtypes of
the alpha-2] noradrenaline receptor, could be responsible. Some 30
per cent of Caucasians and 12 per cent of Africans possess this
variant, he says.
So this is the alpha-2 receptor, which responds to clonidine (agonist)
and yohimbine (antagonist), rather than the beta-2 receptor, which is
antagonized by our old friend, propranolol. According to the NCBI
Sequence Viewer v2.0 Summary on ADRA2B adrenergic, alpha-2B-, receptor
[Homo sapiens]:
Alpha-2-adrenergic receptors are members of the G protein-coupled
receptor superfamily. They include 3 highly homologous subtypes:
alpha2A, alpha2B, and alpha2C. These receptors have a critical role
in regulating neurotransmitter release from sympathetic nerves and
from adrenergic neurons in the central nervous system. This gene
encodes the alpha2B subtype, which was observed to associate with
eIF-2B, a guanine nucleotide exchange protein that functions in
regulation of translation. A polymorphic variant of the alpha2B
subtype, which lacks 3 glutamic acids from a glutamic acid repeat
element, was identified to have decreased G protein-coupled
receptor kinase-mediated phosphorylation and desensitization; this
polymorphic form is also associated with reduced basal metabolic
rate in obese subjects and may therefore contribute to the
pathogenesis of obesity. This gene contains no introns in either
its coding or untranslated sequences.
Let's return to the New Scientist article.
One group comprised healthy Swiss citizens and the other comprised
traumatised survivors of the Rwandan genocide - who were living in
a refugee camp in Uganda.
The researchers found that, in both groups, people carrying the
ADRA2B gene variant were "substantially more likely" to remember
both positive and negative pictures than people with other forms of
the gene. Neutral images were recalled to the same degree by people
with and without the variant.
However, Rwandans with the variant had far higher recall of
negative emotional events than the Europeans who carried it - and
this was unrelated to whether or not they suffered from post
traumatic stress disorder.
"The genetic variant is related to enhanced emotional memory,"
concludes de Quervain. "But it also appears to predispose people to
stronger traumatic memories when something terrible happens."
Is that the same as saying that a single gene governs your ability to
recall emotional events? It certainly appears to influence one's
ability to recall emotional events, whether pleasant, unpleasant, or
traumatic. That's not to say, however, that other genes do not have
any influence over such complicated cognitive and affective processes.
In the paper (de Quervain et al., 2007), a large group of normal Swiss
participants (n=435) was shown a series of photographs from the
International Affective Picture Set (10 each positive, negative, and
neutral in emotional content) and asked to rate them on valence and
arousal. Ten minutes later, they were asked to recall the words.
Overall, the participants showed an advantage in recalling emotional
words relative to neutral words: 57% better for positive and 55% for
negative. The breakdown for carriers and noncarriers of the variant
are shown in the table below, which illustrates that the carriers
showed a significantly greater enhancement in emotional recall.
SWISS
All emotional pictures
carriers (N = 214) 78% +/- 7%
noncarriers (N = 221) 43% +/- 6%
Positive
carriers 77% +/- 8%
noncarriers 43% +/- 7%
Negative
carriers 79% +/- 7%
noncarriers 43% +/- 6%
The second group of participants had survived one of the most horrific
events of the 20th century: the 1994 genocide of 1,000,000 human
beings in Rwanda over the course of only 100 days (Survivors Fund,
SURF). These individuals were in a refugee camp and were recruited to
participate not in the trivial picture recall task, but to report
their experiences in a clinical setting. At this point, it's best to
quote the paper directly:
We hypothesized that deletion carriers would have increased
emotional memory for traumatic events reflected in increased
re-experiencing symptoms. We tested this hypothesis in 202 refugees
who had fled from the Rwandan civil war and were living in the
Nakivale refugee camp in Uganda at the time of investigation (100
females, 102 males; median age, 34 years...). All subjects had
experienced multiple, highly aversive situations and were examined
by trained experts with a structured interview based on the
Post-traumatic Diagnostic Scale with the help of trained
interviewers chosen from the refugee community. Traumatic events
were assessed using a checklist of 31 war- and nonwar-related
traumatic-event types (for example, injury by a weapon, rape,
accidents). The population consisted of 133 subjects fulfilling the
diagnostic criteria of DSM-IV for post-traumatic stress disorder
(PTSD) and 69 subjects without PTSD or a history of PTSD. Deletion
carriers had a significantly higher score for re-experiencing
symptoms per traumatic-event type than did noncarriers (carriers,
N=42, 0.47 +/- 0.05; noncarriers, N=160, 0.31 +/- 0.03), whereas
the deletion was not significantly associated with hyperarousal or
avoidance symptoms. The association of the deletion with increased
traumatic memory was independent of the presence of PTSD ... and
the genotype was equally distributed across the diagnostic groups.
Correcting for gender did not influence the genotype effect on
traumatic memory.
Fig. 3 (de Quervain et al., 2007)
The authors' conclusion:
Taken together, we show that a genetically anchored alteration in
the noradrenergic system is related to enhanced emotional memory in
healthy young Swiss subjects. Furthermore, we found that the same
genetic alteration is related to increased traumatic memory in a
Sub-Saharan African population of civil war refugees who
experienced multiple and highly aversive emotional situations. The
present findings suggest that the price for the deletion-related
enhancement of emotional memory may be enhanced intrusive and
distressing emotional memory for traumatic events.
Reference
de Quervain DJ, Kolassa IT, Ertl V, Onyut PL, Neuner F, Elbert T,
Papassotiropoulos A. (2007). A deletion variant of the alpha
2b-adrenoceptor is related to emotional memory in Europeans and
Africans. Nature Neurosci. Published online: 29 July 2007.
Emotionally arousing events are recalled better than neutral events.
This phenomenon, which helps us to remember important and potentially
vital information, depends on the activation of noradrenergic
transmission in the brain. Here we show that a deletion variant of
ADRA2B, the gene encoding the alpha2b-adrenergic receptor, is related
to enhanced emotional memory in healthy Swiss subjects and in
survivors of the Rwandan civil war who experienced highly aversive
emotional situations.
Symbol Report: ADRA2B
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