Answer the following 8 questions:
What is the research problem that is being investigated? What is the purpose of the
research being conducted?
What is the research question?
What are 2 or more theories that are discussed in the Introduction? How are they used to
motivate (or set up) the research question? Do the authors agree or disagree with these
theories?
How is the research question operationalized? First, identify the abstract constructs being
studied. Next, identify the concrete way these are being observed or measured. This
should include your IV and DV.
What is the research design (i.e. between or within subjects, what type of statistical tests
were used, what were the levels of each variable)?
Describe the results (but not their broader implications). Were the results significant?
Which ones? Do these support or not support the hypothesis?
What limitations are mentioned? Why are these limitations theoretically interesting?
PSYC 575
JOURNAL ARTICLE SUMMARY ASSIGNMENT INSTRUCTIONS
OVERVIEW
For each Journal Article Summary, you will choose an article to review and use the Journal
Article Summary Form to complete the assignment. The article you select must be a peer-
reviewed journal article in the field of cognitive psychology. The article must also be a primary
source, meaning that the authors are discussing their own research, not others’ research (e.g.
review articles). Do not use an article that conducted a meta-analysis. It is ideal to select an
article that you will be using in your paper; however, this is not a requirement. If you use an
article that does not meet these criteria, you will not receive credit for this assignment. See the
example below for detailed explanation of the required material for each question. Submit the
completed form and a PDF of the article being reviewed. All material must be in current APA
format.
INSTRUCTIONS
1. APA reference of article being reviewed
Write the reference for the article as if it were in the reference section of your paper.
2. What is the research problem that is being investigated? What is the purpose of the
research being conducted?
Provide the “why” behind the paper. Why have they conducted this experiment? For
example: “These experiments were designed to explore the role of second order
conditioning in anxiety disorders.”
3. What is the research question?
The research question is more specific. What is the specific question or questions the
article will answer as a result of the study or experiment? For example: “Are adolescents
more sensitive to the memory imparting effects of alcohol?”
4. What are 2 or more theories that are discussed in the Introduction? How are they used to
motivate (or set up) the research question? Do the authors agree or disagree with these
theories?
Simply restate the theories discussed in the introduction in your own words. State how
these theories are driving the research questions. If the authors’ hypothesis is correct,
will it support the theory or be inconsistent with the theory? You should have good idea
of where the authors stand based on the evidence presented and the arguments they are
making.!
5. How is the research question operationalized? First, identify the abstract constructs being
studied. Next identify the concrete way these are being observed or measured. This
should include your IV and DV.
PSYC 575
A construct is an abstract explanatory variable that this not directly observable (e.g.
memory). The concrete way the construct is measured will point you to the dependent
variable (DV). For example, if the paper is concerned with memory, the DV may be the
number of items recalled. The independent variable (IV) could be the amount of sleep
each participant was allowed the night before the test. Remember that we cannot directly
measure many of the constructs that are studied in psychology, so it is important that we
identify how they are being operationalize in each research study.
6. What is the research design (i.e. between or within subjects, what type of statistical tests
were used, what were the levels of each variable)?
This information will be in the methods section of your paper. Be sure to provide enough
detail to describe how the study was designed.
7. Describe the results (but not their broader implications). Were the results significant?
Which ones? Do these support or not support the hypothesis?
Describe the result in your own words. For example: Group X were able to recall
significantly more words than Group Y. This finding supports the hypothesis that
manipulation Y would reduce recall. !
8. What limitations are mentioned? Why are these limitations theoretically interesting?
Limitations can be found in the discussion section of the paper. If a limitation is that they
didn’t have X control group, then explain in your own words why that is important. Does
it change the interpretation of the findings?
Note: Your assignment will be checked for originality via the SafeAssign plagiarism tool.
Stress and memory retrieval: mechanisms and
consequences
Oliver T Wolf
Stress impairs memory retrieval. Recent findings illustrate the
temporal dynamics and the underlying mechanisms of this
effect. The effect appears to occur in multiple memory
systems, ranging from striatal-based stimulus-response
memory to prefrontal-based extinction memory. The effects of
stress on memory retrieval might have long-term
consequences due to their impact on re-encoding and re-
consolidation. These properties could be of interest for future
intervention studies.
Address
Department of Cognitive Psychology, Institute of Cognitive
Neuroscience, Faculty of Psychology, Ruhr University Bochum,
44801 Bochum, Germany
Corresponding author: Wolf, Oliver T
Current Opinion in Behavioral Sciences 2016, 14:40–46
This review comes from a themed issue on Stress and behavior
Edited by David A Morilak and Carmen Sandi
For a complete overview see the Issue and the Editorial
Available online 24th December 2016
http://dx.doi.org/10.1016/j.cobeha.2016.12.001
2352-1546/#2016 Elsevier Ltd. All rights reserved.
Introduction
Our memories are influenced by stress and its associated
neuroendocrine responses. A frightening encounter with
a robber or an especially poor performance during a job
interview may be vividly remembered for a life time.
These are examples of the enhancing effects stress can
have on memory encoding and consolidation. At the
same time, we might forget our wedding anniversary
because we are stressed at work, or we might be unable
to retrieve the name of a specific brain region during a
stressful neurobiology exam. The latter two are exam-
ples for the impairing effects stress can have on memory
retrieval. This phenomenon in particular is the focus
of the present brief and selective review, which will
address the following main points: the temporal devel-
opment and underlying mechanisms of retrieval im-
pairment, its occurrence outside of the domain of
hippocampus-based memories, long-term consequences
of this retrieval impairment, and its relevance for mental
disorders (see Box 1).
When faced with a real or anticipated threat, the organism
responds with a complex and well-orchestrated neuroen-
docrine stress response [1
]. The rapid activation of the
sympathetic nervous system (SNS) leads to the release of
(nor)adrenalin (NA) from the adrenal medulla. This ini-
tial response causes hypervigilance at the expense of
selective attention and other top-down control processes
[2,3
], and, with respect to memory, leads to enhanced
encoding of salient and relevant features of the environ-
ment [4,5]. In parallel, the hypothalamic–pituitary–adre-
nal (HPA) axis is activated. Corticotrophin-releasing
hormone (CRH), secreted from the paraventricular nu-
cleus of the hypothalamus, stimulates the anterior pitui-
tary to release adrenocorticotrophin (ACTH). This
messenger, in turn, causes the adrenal cortex to release
glucocorticoids (GCs; mostly cortisol in humans, and
corticosterone in most laboratory rodents). These stress
hormones first increase 5–10 min after stress onset and
typically reach their peak 20–30 min post-onset [6]. Glu-
cocorticoids exert their action via mineralocorticoid
(MRs) and glucocorticoid receptors (GRs). These two
receptor types differ in their localization (MRs are more
restricted to limbic regions, GRs are expressed more
widespread in the brain) and affinity. It was initially
assumed that these receptors exist exclusively within
the cell and exert slow but potentially long-lasting action
by directly influencing the genome (genomic GC effects)
[7
]. More recently, however, convincing evidence has
shown rapid, non-genomic GC effects mediated via mem-
brane-bound (as opposed to intracellular) versions of
these receptors [7
,8]. Three interacting and partially
overlapping stress response signals must thus be consid-
ered: (1) The initial arousal response mediated by NA and
CRH, (2) the slightly delayed non-genomic GC signal
with mostly excitatory properties, which occurs in inter-
action with the initial NA signal, and (3) the further
delayed genomic GC signal, which, mostly mediated
by intracellular GRs, reduces neuronal excitability and
promotes normalization of the system [1,9,10,11
]. These
three response waves are illustrated in Figure 1. The time
frames mentioned represent rough estimates, as they are
likely to differ depending on the intensity of the stressor
and/or the investigated brain region.
Stress and episodic memory retrieval:
temporal development and underlying
mechanisms
Initial findings on the enhancing effects of stress and GC
treatment on memory consolidation were already de-
scribed in the 1960s (e.g., [12]). Since then research
Available online at www.sciencedirect.com
ScienceDirect
Current Opinion in Behavioral Sciences 2017, 14:40–46 www.sciencedirect.com
has established that the stress-induced activation of the
SNS and HPA axis leads to enhanced memories of the
stressful episode [13], especially regarding its central
aspects [5]. The two stress mediators achieve this by
interacting in the basolateral amygdala (BLA), thereby
boosting memory consolidation in the hippocampus
(for recent reviews, see [4,9,14,15]). The impairing effect
of stress on memory retrieval was first thoroughly charac-
terized in 1998 by de Quervain and colleagues in rats. By
separating the initial acquisition phase from the retrieval
test by a day, they were able to show that stress prior to
long-term memory retrieval substantially impaired spatial
memory retrieval [16
]. Importantly, this effect was
apparent 30 min, but not two minutes or four hours, after
stress induction. This temporal profile is well in line with
a presumed non-genomic GC effect on memory retrieval.
Follow-up animal studies on this phenomenon revealed
that NA arousal and an intact basolateral amygdala (BLA)
are pre-requisites for its occurrence [17]. Similar findings
could be demonstrated in humans: GC administration or
exposure to a psychosocial laboratory stressor resulted in
impaired memory retrieval [18,19]. It is to be noted that
only free recall, but not recognition or cued recall, was
impaired in these initial studies, a fact which will be
picked up again later in this review. Additional studies
further revealed that the impairing effect of cortisol on
memory retrieval depends on testing-induced arousal [20]
and can be blocked by the administration of a beta
Stress and memory retrieval Wolf 41
Box 1 Summary of key points
The effects of stress on memory retrieval last longer than initially
expected. They reflect non-genomic and genomic GC effects.
The effects of stress on memory retrieval are not restricted to
hippocampus-based episodic memory retrieval. Striatum-based SR
memory retrieval as well as PFC-based (fear) extinction memory
retrieval are two examples for this.
The impairing effect of stress on retrieval can have long-lasting
consequences through the modification of re-encoding and re-
consolidation. This feature could make cortisol a useful add-on to
therapeutic interventions (e.g., exposure psychotherapy).
Patients with mental disorders (e.g., MDD and PTSD) show different
responsivities to GC, which are in line with an altered central GC
sensitivity in these disorders.
Figure 1
Noradrenalin
Cortisol
1 20 60 90 180 (time, in minutes)
S
NA GC non-
genomic GC -genomic
E
salient
E
impaired
I retriev ;
encoding
novel material
Current Opinion in Behavioral Sciences
Neuroendocrine stress responses to a brief stressor (e.g., the Trier Social Stress Test) and their transcriptional and cognitive consequences.
Stress influences the brain via a rapid increase in noradrenalin (NA). With a slight delay, glucocorticoids (GCs) are released. These hormones can
exert rapid non-genomic and delayed genomic effects. Both effects are likely to co-occur around one hour after stress exposure. Genomic and
non-genomic GC effects typically cause impaired memory retrieval. In contrast, initial encoding as well as consolidation of material perceived
around the time of the stressor is enhanced. Note: The depicted temporal development is based on a broad estimate derived from the literature.
For further explanations, see the associated text.
www.sciencedirect.com Current Opinion in Behavioral Sciences 2017, 14:40–46
blocker preventing this arousal [21]. Regarding the neural
correlates of GC-induced memory retrieval impairments,
pharmacological neuroimaging studies were able to show
GC-mediated reduced activity in the hippocampus and
adjacent cortical structures during memory retrieval
[22,23].
Stimulated by the mounting evidence for rapid non-
genomic GC effects, studies have started to compare
rapid and delayed effects of stress or GC treatment in
several cognitive domains, including memory [1
,24].
While substantial progress has been made, time-depen-
dent variations in the effect of stress on memory retrieval
have received relatively little attention. One relevant
pharmacological study was recently able to show that a
cortisol injection affected memory retrieval within eight
minutes, which is strongly suggestive of a non-genomic
effect [25]. Another recent study in humans reported that
memory retrieval was impaired 25 min (at the time of
peak cortisol) but also 90 min stress exposure, illustrating
that the impairing effect of stress on memory might last
longer than initially expected [26
]. Interestingly, cortisol
concentrations were already back to baseline levels in the
group tested 90 min after stress exposure, demonstrating
that impairing effects of stress on memory retrieval can
occur even when GC levels are no longer elevated.
Together with the initial findings observed in rodents
[16
], this study suggests that the impairing effects of
stress on memory retrieval occur rapidly once cortisol
concentrations are sufficiently elevated, but that these
effects also persist for at least 90 min. This implies that
both initial non-genomic effects and later genomic effects
lead to impaired memory retrieval (for an in-depth re-
view, see [11
]). This interpretation is also in line with
recent studies in rodents [27]. Roozendaal postulates that
membrane-bound GRs in the BLA interact with central
NA signaling in rapidly boosting memory consolidation
and impairing memory retrieval [8]. In contrast, work by
Dorey and colleagues has provided evidence that hippo-
campal membrane-bound MRs, but not GRs, play a role
in mediating the rapid stress effects on memory retrieval
[28]. With respect to genomic effects, Rimmele and
colleagues could demonstrate that blocking the MR im-
paired memory retrieval, while blocking the GR en-
hanced retrieval [29]. In this study, the drugs were
administered several hours before memory retrieval
was tested, which suggests that it was indeed the con-
sequences of genomic GC actions that were being mea-
sured. In summary, it seems that both non-genomic and
genomic GC effects induce memory retrieval deficits (see
Figure 1).
While an inverted-U-shaped dose–response curve be-
tween GCs and memory consolidation is well-established
[14], the investigation of dose–response relationships has
received little attention with respect to memory retrieval.
Stress studies in humans illustrate that even a moderate
increase in cortisol in the late afternoon (when endoge-
nous cortisol concentrations are low) can impair memory
retrieval [30]. In contrast, a recent pharmacological study
using cortisol injections provided initial evidence for
an inverted-U-shaped function instead [25]. The dose–
response curve might differ depending on the presence
(stress) or absence (pharmacological cortisol administra-
tion) of strong prior noradrenergic activation [1
]. More-
over, there may be differences in dose–response
relationships between non-genomic and genomic effects.
If an inverted-U-shaped dose–response curve indeed
exists, its peak may lie in the range of basal (stress-free)
physiological cortisol concentrations.
Conceptually, it has been proposed that the retrieval
impairment is restricted to the ‘memory formation mode’
but is no longer present during the ‘memory storage
mode’ (during consolidation) [31]. However, the findings
discussed above indicate that the effects occur later and
last longer, thus primarily occurring during the consolida-
tion phase.
Stress and memory retrieval outside the
domain of hippocampus-based memories
Initially, it appeared that the effects of stress on memory
retrieval are restricted to hippocampus-based episodic/
spatial memory tasks [16
,19]. This was in line with the
notion that the hippocampus is especially sensitive to
stress due to its high number of MRs and GRs [32].
Indeed, recognition and cued recall were not influenced
by stress in initial studies in humans, further supporting
the notion of a specific effect on hippocampus-based
episodic recollection [18,19]. More recently, however,
several studies have demonstrated stress-induced recog-
nition impairments, evidencing that not only free recall is
affected by stress [33]. Accumulating evidence reviewed
below has quite convincingly shown that the effects of
stress on memory retrieval are far broader than initially
conceived.
Stimulus-response (SR) memory describes the learned
association between a specific cue and a specific response.
It has been linked to the basal ganglia [34] and can be
tested in humans and rodents by using maze tasks with a
single, clearly visible cue [35]. In the first human study on
this topic, participants exposed to stress prior to SR
retrieval showed impaired retrieval performance [36].
Similar findings were obtained recently in rodents
[37
]. In this study, the authors could additionally dem-
onstrate that the SR retrieval deficit is indeed mediated
by GCs. These findings thus highlight that stress and the
associated release of GCs can also impair the retrieval of
striatal-based SR memories.
Another area of research in which the impairing effects of
stress on memory retrieval have received considerable
attention is the field of (fear) extinction. When a neutral
42 Stress and behavior
Current Opinion in Behavioral Sciences 2017, 14:40–46 www.sciencedirect.com
stimulus (e.g., a tone; the conditioned stimulus or CS) is
coupled with an aversive event (e.g., a shock; the uncon-
ditioned stimulus, or UCS), the organism quickly learns to
respond to the CS alone (e.g., by showing freezing be-
havior; the conditioned response, or CR). During extinc-
tion, the CS is no longer coupled with the UCS, and the
CR disappears. The majority of current learning models
postulate that this decreased responding is not caused by
an erasure of the original acquisition memory trace, but
rather reflects new inhibitory learning [38,39
]. This is
demonstrated by the occurrence of several recovery phe-
nomena such as contextual renewal, reinstatement or
spontaneous recovery [40]. When it comes to the impact
of stress, the fascinating question arises whether stress
prior to extinction retrieval will impair the original acqui-
sition memory trace or the inhibitory extinction memory
trace formed later on. Evidence is accumulating that
stress exposure prior to retrieval typically impairs extinc-
tion retrieval, leading to a return of fear in human parti-
cipants [41] as well as in patients with anxiety disorders
[42]. We have demonstrated similar findings using a
predictive learning task. Stress induction in the laboratory
caused impaired extinction retrieval, manifested as en-
hanced conditioned responding in the acquisition context
(i.e., an enhanced renewal effect) [43]. In a pharmacolog-
ical fMRI study with the same predictive learning task,
cortisol administration prior to extinction retrieval led to
impaired extinction retrieval, as evidenced by an en-
hanced renewal effect. This was associated with reduced
neural activity in the ventromedial prefrontal cortex
(vmPFC) [44], a key region in the extinction network
(e.g., [45]). The available data supports the notion that
GCs impair the extinction memory trace. The reason for
this selective impairment might be the younger age of
this memory trace, its context dependency, or its reliance
on the vmPFC for retrieval. By impairing the extinction
memory trace, GCs thus cause a return of the initially
acquired response (see Figure 2). However, enhanced
retrieval of the original memory trace could still be co-
occurring — an explanation in need of empirical assess-
ment. A mechanistic understanding of the impact of stress
on extinction retrieval will pave the way toward better,
targeted relapse prevention.
Long-term consequences of retrieval
impairment
Another important issue concerns the long-term conse-
quences of the stress-induced retrieval failure. Is this a
temporal blockage which completely disappears once
stress has ceased, or does the impaired retrieval have
consequences beyond the stressful episode, for example,
due to an effect on (re)consolidation? A pharmacological
study using cortisol administration before memory re-
trieval observed that the cortisol group showed a memory
Stress and memory retrieval Wolf 43
Figure 2
CS CR Successful fear
extinction
stress induced
return of fear
Stress
CR
CS
+
+
–
–
Current Opinion in Behavioral Sciences
Impact of stress on extinction memory retrieval. Top row: After successful extinction, the conditioned stimulus (CS; e.g., a tone) no longer leads to
a conditioned response (CR; an increase in heart rate). This is due to the inhibitory action of the extinction memory trace (green arrow). The
original acquisition memory trace (red arrow), however, is not erased but still intact. Bottom row: Stress appears to weaken this inhibitory memory
trace, causing a return of the initial response.
www.sciencedirect.com Current Opinion in Behavioral Sciences 2017, 14:40–46
impairment as long as one week after the retrieval under
the influence of cortisol had taken place [46]. In addition,
another recent study found impaired memory retrieval at
very low cortisol levels, induced by the cortisol-synthesis-
inhibitor metyrapone [47
]. Again, this impairment was
still detectable a week later. Conceptually, the poor
retrieval at times of high (or very low) GC concentrations
could lead to impaired re-encoding and/or impaired re-
consolidation [48]. Taken together, these findings illus-
trate that impaired retrieval under stress can have long-
lasting consequences for the specific memory.
Beneficial effects of the long-term consequences of cor-
tisol administration on human memory have been ob-
served in the context of extinction-based (i.e., exposure)
psychotherapy. Cortisol administered before exposure
treatment enhanced the long-term success of therapy
in patients with fear of heights and in patients with spider
phobia [49
,50]. The combination of impaired retrieval
of the initial fear memory with enhanced consolidation of
the newly acquired extinction (safety) memory could be
the underlying mechanism of this therapeutic effect of
the stress hormone [51].
Alterations in patients with mental disorders
There is increasing evidence that the effects of stress on
memory retrieval are altered in patients with mental
disorders. Dysfunctions in the hypothalamic–pituitary–
adrenal (HPA) axis have been reported for several mental
disorders. While major depressive disorder (MDD) seems
to be characterized by enhanced cortisol release in con-
cert with a reduced feedback sensitivity of the HPA axis
[52], the opposite pattern has been reported in post-
traumatic stress disorder (PTSD) [53]. In a series of
studies, we investigated the effects of cortisol on memory
retrieval in MDD and PTSD. While cortisol administra-
tion failed to affect memory retrieval in MDD patients,
patients with PTSD showed enhanced, rather than im-
paired, memory retrieval after cortisol [54]. These results
indicate an altered sensitivity to cortisol in these disor-
ders, which not only influences the HPA axis and its
negative feedback, but extends to an altered sensitivity of
brain functions involved in episodic memory retrieval
(presumably the hippocampus [55]). Future studies are
required in order to determine whether these alterations
are reversed after successful treatment, thereby elucidat-
ing whether they reflect pre-morbid risk factors or revers-
ible disease consequences.
Conclusion
Taken together, empirical evidence obtained in recent
years has changed the way we look at the impact of stress
on memory retrieval. The impairing effects of stress last
longer, concern a broader range of memory systems, have
lasting consequences and are altered in several mental
disorders. These novel findings raise new questions for
future research. Some of the most central are summarized
in the Box 2.
Conflict of interest statement
The author declares no conflict of interest.
Acknowledgements
The author’s work was supported by grants from the German Research
Foundation (DFG). I thank Shira Meir Drexler for most helpful comments
on an earlier version of this manuscript. In addition I thank Eve Hessas for
language editing and Melinda Baranyai for support regarding the creation of
Figure 1.
References and recommended reading
Papers of particular interest, published within the period of review,
have been highlighted as:
of special interest
of outstanding interest
1.
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memory: a matter of timing.Trends Cogn Sci 2011, 15:280-288.
Important review describing the time-dependent interaction of the SNS
and the HPA in influencing emotional memories.
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Hermans EJ, Henckens MJ, Joels M, Fernandez G: Dynamic
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Benchmark summary on the membrane version of the MR.
44 Stress and behavior
Box 2 Open questions
How does activation of membrane-bound MRs and GRs influence
memory retrieval?
How do non-genomic and genomic GC effects interact in influencing
memory retrieval?
What is the dose–response relationship between GCs and memory
retrieval?
Are there memory systems which are resistant to the impairing effect
of stress on retrieval?
Are the effects of stress modulated by genetic and epigenetic
factors?
Do the GC alterations observed in several mental disorders (e.g.,
MDD, PTSD) reflect predispositions or consequences of the
disorders?
Can the beneficial effects of GCs observed in clinical intervention
studies be translated into the clinical praxis?
Current Opinion in Behavioral Sciences 2017, 14:40–46 www.sciencedirect.com
8. Roozendaal B, Hernandez A, Cabrera SM, Hagewoud R,
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46 Stress and behavior
Current Opinion in Behavioral Sciences 2017, 14:40–46 www.sciencedirect.com
Running head: JOURNAL ARTICLE SUMMARY 1
Journal Article Summary
Name
Institution
JOURNAL ARTICLE SUMMARY 2
Journal Article Summary
1. APA reference of article being reviewed
Wolf, O. T. (2017). Stress and memory retrieval: mechanisms and consequences. Current
Opinion in Behavioral Sciences, 14, 40-46.
2. What is the research problem that is being investigated? What is the purpose of the
research being conducted?
This article seeks to establish that stress damages memory recovery. Specifically, the study
addresses the transitory growth and causal systems of recovery damage, its incidence beyond the
realm of hippocampus-centered recollections, lasting outcomes of this recovery deficiency, and
its applicability for psychological ailments (Wolf, 2017).
3. What is the research question?
Essentially, some of the key research questions are: How does the initiation of membrane-
constrained mineralocorticoid and glucocorticoid receptors impact memory recovery? How do
non-genetic and genetic glucocorticoid influences relate in shaping memory recovery? What is
the prescription-reaction correlation amid glucocorticoids and memory recovery? Do memory
structures that are unaffected by the damaging impact of pressure on recovery exist?
4. What are 2 or more theories that are discussed in the Introduction? How are they
used to motivate (or set up) the research question? Do the authors agree or disagree
with these theories?
The discussed theories are that animals react with intricate and well-schemed neuroendocrine
tension reactions in the cases of actual or expected dangers, and that the mineralocorticoid and
glucocorticoid receptors occur entirely in the cell and exert sluggish, although possibly long-term
actions through openly impelling the genetic outcomes.
While the authors concur with the first theory, they refute the second one claiming that three
cooperating and partly intersecting tension reaction indicators ought to be initially deliberated.
They include the primary stimulation reaction facilitated by (nor) adrenalin, abbreviated NA and
corticotrophin-releasing hormone, shortened CRH, the marginally slow non-genetic indicator
with largely excitatory attributes, which ensues in collaboration with the first NA sign, and the
extra deferred genetic indicator that decreases neuronal edginess and stimulates a stabilized
structure, after being commonly facilitated by the intracellular glucocorticoid receptors (Wolf,
2017).
5. How is the research question operationalized? First, identify the abstract constructs
being studied. Next, identify the concrete way these are being observed or measured.
This should include your IV and DV.
Since the paper is related to stress and memory recovery, the dependent variable (DV) is the
extent to which the impacts of pressure last with regard to retrieval. On the other hand, the
independent variable (IV) is the different responses that the organisms, either humans or rodents,
have to different levels of stress. At large, these constructs are measured throughout the paper by
use of diverse studies that have different findings, as depicted (Wolf, 2017).
JOURNAL ARTICLE SUMMARY 3
6. What is the research design (i.e. between or within subjects, what type of statistical
tests were used, what were the levels of each variable)?
The research design of this article is qualitative in nature as it primarily includes the use of
surveys and experiments on both animals and human beings.
7. Describe the results (but not their broader implications). Were the results
significant? Which ones? Do these support or not support the hypothesis?
According to Wolf (2017), a certain pertinent therapeutic probe was currently able to illustrate
that a cortisol inoculation influenced memory recovery in about 8 minutes, which potently
proposes a non-genetic consequence. Further, a different contemporary research on human
beings also displayed that memory recovery was decreased at about 25 min, during the highest
cortisol, although at a 90 minutes contact with stress, demonstrating that the damaging influence
of pressure on remembrance could persist for an extensive period than originally anticipated. In
view of that, these findings fully support the theories since they infer that both primary non-
genetic and advanced genetic impacts normally cause a weakened memory recovery.
8. What limitations are mentioned? Why are these limitations theoretically
interesting?
The main limitation of this article is that it requires imminent studies to establish if modifications
to cortisol in both major depressive and post-traumatic stress maladies can be inverted following
effective medications. Ideally, this is academically thought-provoking since it clarifies if the
disorders either mirror pre-pathological threat aspects or changeable ailment effects (Wolf,
2017).
JOURNAL ARTICLE SUMMARY 4
References
Wolf, O. T. (2017). Stress and memory retrieval: mechanisms and consequences. Current
Opinion in Behavioral Sciences, 14, 40-46.
OUTLINE
Topic: Journal Article Summary
Thesis Statement: This paper summarizes a journal article titled ‘Stress and memory
retrieval: mechanisms and consequences’ by Wolf (2017).
1. APA reference of article being reviewed
2. Research problem that is being investigated and purpose of the study
3. Research questions
4. Theories that are discussed in the Introduction and how they are used to motivate (or
set up) the research questions and the author’s views
5. How the research question is operationalized
6. Research design
7. Significance of the results and if they support the hypothesis
8. Mentioned limitations and why they are theoretically interesting
9. References
