PRIMARY

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German aggressiveness--its reasons and types

Shreier, F.
8300 defect for UNSW Journal of Abnormal and Social Psychology, 1943, Vol.38(2),
pp.211-224 [Peer Reviewed Journal] end of 8300
There are conflicting theories as to the cause of German aggressiveness and the
appropriate cure. Possibly aggressiveness has become an autonomous habit and will not
disappear when the original causes are removed, but the causes should be known before
treating cases. The author describes eleven types of aggressors among the Germans,
showing differences in the source of aggression and in the role of ideational factors. He
considers plans for postwar re-education useless until we know the relative numbers and
location of each type. Until after the war, information can only be obtained from aliens
and prisoners in this country. (PsycINFO Database Record (c) 2013 APA, all rights
reserved)

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Wyatt, F., & Teuber, H. L. (1944). German psychology under the nazi
system: 1933-1940. Psychological Review, 51(4), 229-247.
doi:http://dx.doi.org.proxy.library.vanderbilt.edu/10.1037/h0056107
Ansbacher, H. L. (1941). German military psychology. Psychological Bulletin,
38(6), 370-392.
doi:http://dx.doi.org.proxy.library.vanderbilt.edu/10.1037/h0056263

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Enduring changes in brain and behavior produced by chronic amphetamine
administration: A review and evaluation of animal models of amphetamine
psychosis
Author links open the overlay panel. Numbers correspond to the affiliation
list which can be exposed by using the show more link.
Terry E. Robinson , Jill B. Becker
Department of Psychology and Neuroscience Laboratory Building, The
University of Michigan, Ann Arbor, MI 48104-1687 U.S.A.
Available online 10 March 2003
Brain Research Reviews
Volume 11, Issue 2, June 1986, Pages 157-198
http://www.sciencedirect.com/science/article/pii/0165017386900020

Abstract
Some people who repeatedly use stimulant drugs, such as amphetamine
(AMPH), develop an AMPH-induced psychosis that is similar to paranoid
schizophrenia. There has been, therefore, considerable interest in
characterizing the effects of chronic stimulant drug treatment on brain and
behavior in non-human animals, and in developing an animal model of AMPH
psychosis. A review of this literature shows that in non-human animals
chronic AMPH treatment can produce at least two different syndromes, and
both of these have been proposed as animal models of AMPH psychosis. The
first syndrome is called AMPH neurotoxicity, and is produced by maintaining
elevated brain concentrations of AMPH for prolonged periods of time. AMPH
neurotoxicity is characterized by what has been termed hallucinatory-like
behavior, which occurs in association with brain damage resulting in the
depletion of striatal DA and other brain monoamines. The second syndrome
is called behavioral sensitization, and is produced by the repeated
intermittent administration of lower doses of AMPH. Behavioral sensitization
is characterized by a progressive and enduring enhancement in many AMPHinduced behaviors, and is not accompanied by brain damage or monoamine
depletion. It is argued that the changes in the brain and behavior associated
with the phenomenon of behavioral sensitization provide a better model of
AMPH psychosis than those associated with AMPH neurotoxicity.

Much of the review involves a critical analysis of hypotheses regarding the

biological basis of behavioral sensitization. Research on this question has
focused on mesotelencephalic DA systems, and suggestions that behavioral
sensitization is accompanied by:
1.
(1) an increase in postsynaptic DA receptors
2.
(2) an increase in DA synthesis
3.
(3) an increase in DA utilization and/or release
4.
(4) a decrease in DA autoreceptors, are evaluated. It is concluded that there
is not convincing evidence for an increase in postsynaptic DA receptors or in
DA synthesis in animals sensitized to AMPH. In contrast, there is strong
evidence to support the notion that behavioral sensitization is due to
enhanced mesotelencephalic DA release, especially upon re-exposure to the
drug. The evidence that this enhancement in DA release is due to
autoreceptor subsensitivity was found to be equivocal, and therefore other
hypotheses should be entertained.
Lastly, evidence is discussed in support of the idea that behavioral
sensitization is not unique to the psychopharmacology of stimulant drugs,
but may be produced by many environmental stimuli that directly or
indirectly activate brain catecholamine systems. For example, there are
many studies showing that AMPH and stress are to some extent
interchangeable in producing both behavioral sensitization and long-term
changes in brain DA systems. It is concluded that sensitized animals may be
hyperresponsive to any stimulus that activates brain catecholamine systems,
and that the effects of sensitization are not obvious in the absence of such
stimuli. This may be related to the fact that psychosis only tends to recur in
former AMPH addicts following re-exposure to AMPH or stress, and that
stress is considered a precipitating factor in psychiatric disorders thought to
involve brain catecholamine dysfunction.

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Article
Neuropsychology Review
September 2007, Volume 17, Issue 3, pp 275-297
First online: 13 August 2007
Neurocognitive Effects of Methamphetamine: A Critical Review and Metaanalysis
J. Cobb Scott, Steven Paul Woods , Georg E. Matt,
Rachel A. Meyer, Robert K. Heaton, J. Hampton Atkinson, Igor Grant
Abstract
This review provides a critical analysis of the central nervous system effects
of acute and chronic methamphetamine (MA) use, which is linked to
numerous adverse psychosocial, neuropsychiatric, and medical problems. A
meta-analysis of the neuropsychological effects of MA abuse/dependence
revealed broadly medium effect sizes, showing deficits in episodic memory,
executive functions, information processing speed, motor skills, language,
and visuoconstructional abilities. The neuropsychological deficits associated
with MA abuse/dependence are interpreted with regard to their possible
neural mechanisms, most notably MA-associated frontostriatal neurotoxicity.
In addition, potential explanatory factors are considered, including
demographics (e.g., gender), MA use characteristics (e.g., duration of
abstinence), and the influence of common psychiatric (e.g., other substancerelated disorders) and neuromedical (e.g., HIV infection) comorbidities.
Finally, these findings are discussed with respect to their potential
contribution to the clinical management of persons with MA
abuse/dependence.
Keywords
Central nervous system Methamphetamine Abuse Dependence
Neuropsychological assessment Cognition

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864776/
Neuropharmacology. Author manuscript; available in PMC 2015 Jan 1.
Published in final edited form as:
Neuropharmacology. 2014 Jan; 76(0 0):
10.1016/j.neuropharm.2013.06.016.
Published online 2013 Jun 25. doi: 10.1016/j.neuropharm.2013.06.016
PMCID: PMC3864776
NIHMSID: NIHMS500500
The Impact of Exposure to Addictive Drugs on Future Generations:
Physiological and Behavioral Effects
F.M. Vassoler,1 E.M. Byrnes,1 and R.C. Pierce2
bstract
article-meta
It is clear that both genetic and environmental factors contribute to drug
addiction. Recent evidence indicating trans-generational influences of drug
abuse highlight potential epigenetic factors as well. Specifically, mounting
evidence suggests that parental ingestion of abused drugs influence the
physiology and behavior of future generations even in the absence of
prenatal exposure. The goal of this review is to describe the transgenerational consequences of preconception exposure to drugs of abuse for
five major classes of drugs: alcohol, nicotine, marijuana, opioids, and
cocaine. The potential epigenetic mechanisms underlying the transmission of
these phenotypes across generations also are detailed.
Keywords: Transgenerational, epigenetic, drugs of abuse, alcohol, nicotine,
marijuana, opioids, cocaine
Conclusions
The idea that the environment of one generation can impact the phenotype
of subsequent generations is not new. Jean-Baptiste Lamarck proposed a
theory of evolution that incorporated environmental conditions as well as
reproductive fitness into hereditary changes. His work was largely
discredited and ignored for lack of mechanism and in favor Darwin's elegant
description of survival of the fittest (Burkhardt, 2009). However, it seems

that some of his ideas had merit and can now be explained by the
phenomenon of epigenetics. The way that environmental exposures of one
generation can influence and affect subsequent generations is of critical
importance to the understanding of human behavior and evolution.
This review demonstrated that there are many consequences for the
offspring of parents that were exposed to drugs, even in the absence of
direct fetal exposure (summarized in Table 1). The idea that environmental
toxins ingested prior to conception by either parent can have such a
pronounced impact on the offspring needs further research and should
garner more attention. In fact, one study found that the effects of paternal
and maternal drug use had an additive effect on offspring's adolescent drug
use trajectory rather than an interactive parental effect (Walden et al.,
2007). This suggests the need for policy change and new campaigns to
spread awareness among men and women during adolescence and
throughout child bearing years.
table ft1table-wrap mode=article t1

Table 1
caption a4
caption a8Preconception Effects of Drug Exposure on Subsequent
Generation
The results presented here suggest the intriguing, and potentially alarming,
possibility that exposure to drugs of abuse produce transmissible epigenetic
changes that result in profound alterations to the physiology and behavior of
offspring. However, for an effect to be truly non-genomic epigenetic
inheritance, many of the experiments need to be carried to further
generations to avoid exposure of the germ cells to the drug of abuse. The
few studies that have looked beyond the first generation suggest that many
phenotypes persist. Regardless of the number of future generations

preconception drug use influences, the impact on first generation offspring

alone is sufficient to justify further research defining the extent of epigenetic
heritability of phenotypes associated with parental drug abuse and the
specific mechanisms underlying these effects.