The Journal of Neuroscience, October 31, 2007 • 27(44):11803–11806 • 11803

Symposium

Neurobiology of Escalated Aggression and Violence

Klaus A. Miczek,1,2 Rosa M. M. de Almeida,3 Edward A. Kravitz,4 Emilie F. Rissman,5 Sietse F. de Boer,6 and
Adrian Raine7
1Department of Psychology, Tufts University, Medford, Massachusetts 02155, 2Departments of Psychiatry, Pharmacology and Experimental Therapeutics,
and Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02110, 3Laboratory of Neuroscience, Universidade do Vale do Rio dos Sinos,
São Leopoldo, Rio Grande do Sul, Brazil, 4Department of Neurobiology, Harvard University Medical School, Boston, Massachusetts 02115, 5Department of
Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, Virginia 22908, 6Department of Behavioral Physiology,
University of Groningen, 9700 AB Groningen, The Netherlands, and 7Department of Criminology, Psychiatry, and Psychology, University of Pennsylvania,
Philadelphia, Pennsylvania 19104

Psychopathological violence in criminals and intense aggression in fruit flies and rodents are studied with novel behavioral, neurobio-
logical, and genetic approaches that characterize the escalation from adaptive aggression to violence. One goal is to delineate the type of
aggressive behavior and its escalation with greater precision; second, the prefrontal cortex (PFC) and brainstem structures emerge as
pivotal nodes in the limbic circuitry mediating escalated aggressive behavior. The neurochemical and molecular work focuses on the
genes that enable invertebrate aggression in males and females and genes that are expressed or suppressed as a result of aggressive
experiences in mammals. The fruitless gene, immediate early genes in discrete serotonin neurons, or sex chromosome genes identify
sexually differentiated mechanisms for escalated aggression. Male, but not female, fruit flies establish hierarchical relationships in fights
and learn from previous fighting experiences. By manipulating either the fruitless or transformer genes in the brains of male or female
flies, patterns of aggression can be switched with males using female patterns and vice versa. Work with Sts or Sry genes suggests so far
that other genes on the X chromosomes may have a more critical role in female mouse aggression. New data from feral rats point to the
regulatory influences on mesocortical serotonin circuits in highly aggressive animals via feedback to autoreceptors and via GABAergic
and glutamatergic inputs. Imaging data lead to the hypothesis that antisocial, violent, and psychopathic behavior may in part be attrib-
utable to impairments in some of the brain structures (dorsal and ventral PFC, amygdala, and angular gyrus) subserving moral cognition
and emotion.
Key words: aggression; alcohol; genetics; learning; prefrontal cortex; serotonergic 1A receptor; serotonin; sex difference

Research on aggression and violence is pursued by social and behaviors altogether (Krug et al., 2002). Here we point to several
biological scientists with profoundly divergent approaches. At emerging successes in behavioral and molecular biology of ag-
present, the schism between these approaches promises to be gression research that may have important implications not only
overcome by advancing our knowledge of the molecular events for diagnosis, prevention, and treatment but also for guidance of
through which social experiences sculpt future aggressive acts. public and judicial policies.
Insights into the gene– environment interactions are critical for
the way in which the criminal justice and the public health sys-
Aggression as an adaptive behavior in males and females:
tems deal with aggression and violence. Neurobiological research
quantitative ethological analysis
of aggressive behavior is emerging from several shameful epi-
Classic ethological studies have focused on aggression because
sodes during the past century ranging from the eugenics move-
this behavior is typical for both invertebrate and vertebrate spe-
ment to lobotomies to stigmatizing individuals with phrenolog-
cies during particular situations of conflict. The study of the phy-
ically defined biomarkers (Valenstein, 1987). As a matter of fact,
the World Report on Violence and Health (2002) by the World logeny, ontogeny, and functional significance of these complex
Health Organization ignores the neuroscience approach to these behavioral adaptations in different kinds of aggressive confron-
tations provides the foundation for neurobiological analyses. The
salient acts, postures, and communicative signals of aggressive
Received Aug. 1, 2007; revised Aug. 24, 2007; accepted Sept. 3, 2007.
behavior follow an intricate temporal and sequential organiza-
This work was supported by National Institutes of Health Grants AA013983 and DA02632 (K.A.M.), NS055218
(E.F.R.), and HD42259 (A.R.), National Institute of General Medical Sciences Grants 067645 and 072411 (E.A.K.), tion, some are common to males and females, and others are
National Science Foundation Grant IBN 0090730 (E.A.K.), Universidade do Vale do Rio dos Sinos, and Conselho sexually dimorphic (Nilsen et al., 2004; Miczek et al., 2007). In a
Nacional de Desenvolvimento Cientifico e Tecnológico and Coordenação de Aperfeiçoamento de Pessoal de Nı́vel newly studied invertebrate model, male fruit flies (Drosophila
Superior (R.M.M.A.). melanogaster) establish hierarchical relationships in fights,
Correspondence should be addressed to Klaus A. Miczek, Tufts University, 530 Boston Avenue (Bacon Hall),
Medford, MA 02155. E-mail: [email protected].
whereas female flies do not. Like mammals, flies learn from pre-
DOI:10.1523/JNEUROSCI.3500-07.2007 vious fighting experiences and use this information for establish-
Copyright © 2007 Society for Neuroscience 0270-6474/07/2711803-04$15.00/0 ing and maintaining hierarchical relationships (Yurkovic et al.,
11804 • J. Neurosci., October 31, 2007 • 27(44):11803–11806 Miczek et al • Escalated Aggression and Violence

2006). In adult male and female mice, exposure to androgenic males (Y. B. Chan and E. A. Kravitz, unpublished observations)
steroids during critical prenatal and postnatal periods are among (Kimura et al., 2005). Furthermore, Certel, Kravitz, and cowork-
the distal determinants of subsequent aggressive behavior, and ers have demonstrated that the amine octopamine, the inverte-
these influences during early development are readily seen in brate homolog to norepinephrine, is involved in the behavioral
adult male and female aggression in mice (Vom Saal and Bron- choice between courtship and aggression in male flies (Certel et
son, 1978; Mann and Svare, 1983). An important task is to extend al., 2007) (S. J. Certel, unpublished observations). Of the ⬃80
the insights from species-normative aggression to clinical con- octopamine neurons normally found in the fly CNS, three within
cerns with pathological aggression. the subesophageal ganglion show colocalization of the amine
with Fru M. Eliminating Fru M expression in these three neurons
The need for valid experimental models of by either feminizing the neurons in otherwise male brains or
escalated aggression eliminating Fru M by RNA interference yields the same behavioral
Examples from clinical research on aggressive behavior illustrate phenotype as eliminating octopamine; male flies have difficulty
the focus on behavioral phenotypes that exceed the species- determining whether to court or fight other males.
normative patterns and represent behavioral pathologies (Raine
and Yang, 2006). New experimental models of escalated aggres- Sex chromosome genes and female aggression
sive behavior in mice, hamsters, and rats attempt to translate In complement to the early hypothesis that the Sry (sex determin-
more adequately to clinically problematic violent outbursts ing region Y) gene, located on the Y chromosome, acted as a
(Miczek et al., 2004, 2007; Haller and Kruk, 2006; Nelson and candidate gene for differentiating aggression between sexes and
Trainor, 2007). Many experimental models rely on noxious en- among strains of mice (Maxson, 1996), Rissman and colleagues
vironmental stimuli, neural lesions, or pharmacological or ge- investigate Sry and another sex chromosome candidate gene, Sts
netic manipulations to engender aggressive behavior in otherwise (steroid sulfatase) (E. F. Rissman, unpublished data). This latter
placid laboratory animals (de Boer and Koolhaas, 2005). For ex- gene encodes the steroid sulfatase enzyme; it is located on the
ample, the preferential use of mice of the 129 Sv strain for tar- pseudoautosomal region of the Y chromosome and is expressed
geted gene manipulations triggers aggressive behavior in a strain in both sexes. It is pivotal in the regulation of neurosteroid bio-
that, uncharacteristic for this pugnacious species, usually does synthesis and altered brain activity of Sts, attributable to either
not fight (Miczek et al., 2001). In extension of the original ac- genetic (Le Roy et al., 1999) or pharmacological (Nicolas et al.,
count in mice (Ginsburg and Allee, 1942), a new model uses 2001) manipulations, and is correlated with levels of aggression
feral-derived resident rats that escalate their aggressive behavior among male mice.
as a result of repeated victories in aggressive confrontations with Although resting brain levels of Sts are similar in both sexes, it
intruders (i.e., short latency, high frequency and intensity, per- increases dramatically in females after parturition and during
sistent attacks that are indiscriminate of opponent, impervious to lactation, corresponding to the onset of maternal aggression in
signals of submission, and potentially injurious) (de Boer and many species. Rissman and coworkers hypothesized that Sts may
Koolhaas, 2005). This methodological approach highlights the exert a critical role in aggression expressed by females, but data
rewarding nature of aggressive behavior that has begun to be from females with sex chromosome aneuploidy appear negative
characterized in terms of its neurobiology in mice (Fish et al., so far. Ongoing work using females that have a Y chromosome
2002, 2005, 2007). with spontaneous deletion of the Sry testes determining gene
(referred to as Y ⫺) shows that the Sry gene is not needed for
Ethical dilemma of aggression research enhanced aggression when a resident female confronts an in-
To be clinically relevant, experimental model systems for aggres- truder female. Moreover, females with XY ⫺ chromosome com-
sive behavior need to be valid, and this development crystallizes a plements initiate offensive attacks on intruders faster than XX
central ethical dilemma of aggression research, namely harm and females (Gatewood et al., 2006). So far, this work shows that,
injury. Two countervailing principles govern this research: face although sex chromosome complement is involved in aggression,
validity is achieved when the behavior is potentially harmful and an X or Y gene other than Sts or Sry may have more critical roles
injurious, yet, at the same time, every ethical research guideline in female aggression.
emphasizes the reduction and avoidance of the risk to be harmed
or injured. Each research question and protocol needs to probe Serotonin—revisited
how much harm and injury is necessary or acceptable to generate Brain serotonin (5-HT) has been implicated in the neurobiolog-
scientifically valid information that can be translated into con- ical mechanisms of aggression and violence more than any other
cerns of the public health system. Although this discussion fo- molecule in the brain (Miczek et al., 2002, 2007; Kravitz and
cuses primarily on mammals, it is pertinent to all species. Huber, 2003). The early proposal of a tropotrophic action of this
evolutionary ancient indolamine was extended to a calming effect
The genetics of learning to be aggressive on impulsively aggressive behavior, and this characterization was
New studies show how the fruitless gene in D. melanogaster, which supported by correlational data from low CSF metabolite levels
has been shown previously to be necessary and sufficient in de- and blunted responses to serotonergic drug challenges in violent
termining whether a fly courts males or females, is also a critical individuals (Linnoila et al., 1983; Coccaro, 1989). Recent data
determinant for how flies fight. By manipulating either the fruit- confirm lower levels of release of 5-HT in the nucleus accumbens
less or transformer genes in the brains of male or female flies, and in prefrontal cortex (PFC) in rats with extensive experiences
patterns of aggression can be switched with males using female of aggressive behavior (Van Erp and Miczek, 2000; de Boer et al.,
patterns of aggression or females using male patterns (Vrontou et 2003; Ferrari et al., 2003). Tonic brain levels of 5-HT decrease as
al., 2006). Male protein products of fruitless (Fru M) normally are a consequence of acquiring repeated victorious experiences. In
found in 20 clusters of neurons in male CNS. Mechanistically, the contrast, the level of adaptive aggressive behavior is positively
expression of Fru M must occur in a particular one of these 20 related to basal CSF concentrations of 5-HT in wild-type rats
clusters of neurons in female flies to make the females fight like (Van der Vegt et al., 2003a,b). These data point to opposite roles
Miczek et al • Escalated Aggression and Violence J. Neurosci., October 31, 2007 • 27(44):11803–11806 • 11805

of mesocortical serotonin activity in adaptive and escalated forms fenders are not fully responsible for the source of the brain dys-
of aggressive behavior. function that impairs their moral decision making, this raises
The regulation of 5-HT release from serotonergic neurons via significant neuroethical issues regarding the appropriate level of
5-HT1A and 5-HT1B autoreceptors and via GABAergic and gluta- punishment for those who show morally inappropriate acts.
matergic input to these neurons have emerged as candidate
mechanisms for the transition between adaptive and escalated Discussion
types of aggressive behavior. Evidence points to potent and selec- A research agenda should consider the following points emanat-
tive anti-aggressive effects of 5-HT1A and 5-HT1B receptor ago- ing from the recent findings in various model systems.
nists on both somatodendritic autoreceptors and on postsynaptic (1) Advances in understanding of experience-dependent and
receptors in male and female rodents (de Almeida and Lucion, sexually dimorphic gene expression need to be translated into the
1997; de Boer and Koolhaas, 2005; Olivier and Van Oorschot, clinical practice of diagnosing and treating pathologically violent
2005; Bannai et al., 2007). Highly aggressive rats are characterized individuals. The more accessible invertebrate and rodent model
by upregulated somatodendritic 5-HT1A and terminal 5-HT1B systems demonstrating gene– environment interactions should
autoreceptor (Caramaschi et al., 2007), and this activity can be enlighten the search for the primate counterparts of these
further enhanced by victorious aggressive experiences. Based on mechanisms.
their recent findings, de Boer and colleagues hypothesize that the (2) Interdisciplinary rivalries are rendered irrelevant as the
enhanced inhibitory autoreceptor function is a normal compen- molecular mechanisms of salient social experiences and learning
satory adaptation to the more reactive state of the brain 5-HT during aggressive confrontations are deciphered. The next step
system in highly aggressive animals. They further speculate that for the study of aggressive behavior should be to elucidate how
an excessive activation (i.e., overshoot) of an autoreceptor brake the molecular mechanisms underlying these salient experiences
may be a causative link in the cascade of events leading to the interact with genetic and environmental factors that predispose
hypofunction of 5-HT neurons that characterizes violent and some individuals to engage in escalated aggressive behavior.
pathological forms of aggressive behavior. (3) Mesocortical serotonin circuits are intricately regulated
via feedback from autoreceptors and via GABAergic and gluta-
5-HT receptor gene expression in PFC matergic inputs. Future work must take into account the regional
In rodents, 5-HT1 and 5-HT2 receptor genes are expressed at and temporal specificity of the molecular changes taking place
lower levels in the PFC of individuals who engage in escalated during the transition from adaptive to escalated aggressive
aggression after consumption of alcohol relative to those who behavior.
fight at a species-typical level (Chiavegatto et al., 2007). Intact (4) Neuroethical concerns require discussion in open dis-
alcohol-heightened and other escalated forms of aggression are course among representatives of the criminal justice system, psy-
potently inhibited by activation of 5-HT1B receptors in subre- chiatry, neuroscience, and the social sciences.
gions of the prefrontal cortex, possibly involving terminal auto-
receptors or postsynaptic heteroreceptors (Faccidomo et al., References
Bannai M., Fish EW, Faccidomo S, Miczek KA (2007) Anti-aggressive ef-
2005; de Almeida et al., 2006). If this is attributable to actions on
fects of agonists at 5-HT1B receptors in the dorsal raphe nucleus of mice.
postsynaptic receptors, compromised glutamatergic feedback Psychopharmacology 193:295–304.
from the prefrontal cortex to the raphe nuclei may serve as a Caramaschi D, de Boer SF, Koolhaas JM (2007) Differential role of the
necessary link for the expression of escalated aggression to be 5-HT1A receptor in aggressive and non-aggressive mice: an across-strain
expressed. A focus on receptor pools in the prefrontal cortex is comparison. Physiol Behav 90:590 – 601.
consistent with imaging data obtained from violent psychopaths, Certel SJ, Savella MG, Schlegel DCF, Kravitz EA (2007) Modulation of Dro-
although in the latter case the anatomical resolution is more sophila male behavioral choice. Proc Natl Acad Sci USA 104:4706 – 4711.
Chiavegatto S, Quadros IMH, Trindade A, Ambar G, Miczek KA (2007)
limited. Selective reduction of prefrontal cortex serotonin receptors gene expres-
sion in alcohol-heightened aggressive mice. Soc Neurosci Abstr
Brain systems common to violence and moral 33:531.24.
decision making Coccaro EF (1989) Central serotonin and impulsive aggression. Br J Psychi-
An increasing body of brain imaging research is documenting atry 155:52– 62.
functional and structural brain impairments in antisocial and de Almeida RM, Rosa MM, Santos DM, Saft DM, Benini Q, Miczek KA
(2006) 5-HT1B receptors, ventral orbitofrontal cortex, and aggressive be-
violent populations (Raine and Yang, 2006). Recent imaging re-
havior in mice. Psychopharmacology 185:441– 450.
search also is beginning to elucidate the neural correlates of moral de Almeida RMM, Lucion AB (1997) 8-OH-DPAT in the median raphe,
decision making in normal individuals (Greene et al., 2001; Moll dorsal periaqueductal gray and corticomedial amygdala nucleus de-
et al., 2005). Key areas found to be functionally or structurally creases, but the medial septal area it can increase maternal aggressive
impaired in antisocial populations include dorsal and ventral re- behavior in rats. Psychopharmacology 134:392– 400.
gions of the PFC, amygdala, hippocampus, angular gyrus, ante- de Boer SF, Koolhaas JM (2005) 5-HT1A and 5-HT1B receptor agonists and
aggression: a pharmacological challenge of the serotonin deficiency hy-
rior cingulate, and temporal cortex (Raine and Yang, 2006). Re-
pothesis. Eur J Pharmacol 526:125–139.
gions most commonly activated in moral judgment tasks consist de Boer SF, Van Der Vegt BJ, Koolhaas JM (2003) Individual variation in
of the polar/medial and ventral PFC, amygdala, angular gyrus, aggression of feral rodent strains: a standard for the genetics of aggression
and posterior cingulate (Raine and Yang, 2006). Although the and violence? Behav Genet 33:485–501.
overlap is by no means complete, some common ground exists Faccidomo S, Bannai M, van Trigt RL, DeBold JF, Miczek KA (2005)
between the neural circuitry underlying antisocial, violent behav- Alcohol-heightened aggression and corticolimbic 5-HT: reverse microdi-
ior and moral decision making. Raine hypothesizes that the rule- alysis and microinjection of 5-HT1B agonists in male mice. Soc Neurosci
Abstr 31:76.18.
breaking behavior common to antisocial, violent, and psycho- Ferrari PF, Van Erp AMM, Tornatzky W, Miczek KA (2003) Accumbal do-
pathic individuals may in part be attributable to impairments in pamine and serotonin in anticipation of the next aggressive episode in
some of the structures (dorsal and ventral PFC, amygdala, and rats. Eur J Neurosci 17:371–378.
angular gyrus) subserving moral cognition and emotion. If of- Fish EW, DeBold JF, Miczek KA (2002) Aggressive behavior as a reinforcer
11806 • J. Neurosci., October 31, 2007 • 27(44):11803–11806 Miczek et al • Escalated Aggression and Violence

in mice: activation by allopregnanolone. Psychopharmacology (2004) Escalated aggressive behavior: new pharmacotherapeutic ap-
163:459 – 466. proaches and opportunities. Ann NY Acad Sci 1036:336 –355.
Fish EW, De Bold JF, Miczek KA (2005) Escalated aggression as a reward: Miczek KA, Faccidomo SP, Fish EW, DeBold JF (2007) Neurochemistry and
corticosterone and GABAA receptor positive modulators in mice. Psycho- molecular neurobiology of aggressive behavior. In: Behavioral neuro-
pharmacology 182:116 –127. chemistry, neuroendocrinology and molecular neurobiology (Blaustein J,
Fish EW, McKenzie-Quirk SD, Bannai M, Miczek KA (2007) 5-HT1B recep- ed), pp 285–336. New York: Springer.
tor inhibition of alcohol-heightened aggression in mice: comparison to Moll J, Oliveira-Souza R, Moll FT, Ignacio FA, Bramati IE, Caparelli-Daquer
drinking and running. Psychopharmacology, in press. EM, Eslinger PJ (2005) The moral affiliations of disgust—a functional
Gatewood JD, Wills A, Shetty S, Xu J, Arnold AP, Burgoyne PS, Rissman EF MRI study. Cogn Behav Neurol 18:68 –78.
(2006) Sex chromosome complement and gonadal sex influence aggres- Nelson RJ, Trainor BC (2007) Neural mechanisms of aggression. Nat Neu-
sive and parental behaviors in mice. J Neurosci 26:2335–2342. rosci Rev 8:536 –546.
Ginsburg B, Allee WC (1942) Some effects of conditioning on social domi- Nicolas LB, Pinoteau W, Papot S, Routier S, Guillaumet G, Mortaud S (2001)
nance and subordination in inbred strains of mice. Physiol Zool Aggressive behavior induced by the steroid sulfatase inhibitor COU-
15:485–506. MATE and by DHEAS in CBA/H mice. Brain Res 922:216 –222.
Greene JD, Sommerville RB, Nystrom LE, Darley JM, Cohen JD (2001) An Nilsen SP, Chan YB, Huber R, Kravitz EA (2004) Gender-selective patterns
fMRI investigation of emotional engagement in moral judgment. Science of aggressive behavior in Drosophila melanogaster. Proc Natl Acad Sci USA
293:2105–2108. 101:12342–12347.
Haller J, Kruk MR (2006) Normal and abnormal aggression: human disor- Olivier B, Van Oorschot R (2005) 5-HT1B receptors and aggression: a re-
ders and novel laboratory models. Neurosci Biobehav Rev 30:292–303.
view. Eur J Pharmacol 526:207–217.
Kimura K, Ote M, Tazawa T, Yamamoto D (2005) Fruitless specifies sexu-
Raine A, Yang Y (2006) The anatomical bases of psychopathy: a review of
ally dimorphic neural circuitry in the Drosophila brain. Nature
brain imaging findings. In: Handbook of psychopathy (Patrick CJ, ed), pp
438:229 –233.
278 –295. New York: Guilford.
Kravitz EA, Huber R (2003) Aggression in invertebrates. Curr Opin Neuro-
Valenstein ES (1987) Great and desperate cures: the rise and decline of psy-
biol 13:736 –743.
chosurgery and other radical treatments for mental illness. New York:
Krug EG, Dahlberg LL, Mercy JA, Zwi AB, Lozito R (eds.) (2002) World
Harper Collins.
report on violence and health. Geneva: World Health Organization.
Le Roy I, Mortaud S, Tordjman S, Donsez-Darcel E, Carlier M, Degrelle H, Van der Vegt BJ, Lieuwes N, van de Wall EH, Kato K, Moya-Albiol L,
Roubertoux PL (1999) Genetic correlation between steroid sulfatase Martinez-Sanchis S, de Boer SF, Koolhaas JM (2003a) Activation of se-
concentration and initiation of attack behavior in mice. Behav Genet rotonergic neurotransmission during the performance of aggressive be-
29:131–136. havior in rats. Behav Neurosci 117:667– 674.
Linnoila M, Virkkunen M, Scheinin M, Nuutila A, Rimon R, Goodwin FK Van der Vegt BJ, Lieuwes N, Cremers TIFH, de Boer SF, Koolhaas JM
(1983) Low cerebrospinal fluid 5-hydroxyindoleacetic acid concentra- (2003b) Cerebrospinal fluid monoamine and metabolite concentrations
tion differentiates impulsive from nonimpulsive violent behavior. Life Sci and aggression in rats. Horm Behav 44:199 –208.
33:2609 –2614. Van Erp AMM, Miczek KA (2000) Aggressive behavior, increased accumbal
Mann MA, Svare B (1983) Prenatal testosterone exposure elevates maternal dopamine, and decreased cortical serotonin in rats. J Neurosci
aggression in mice. Physiol Behav 30:503–507. 20:9320 –9325.
Maxson SC (1996) Searching for candidate genes with effects on an agonis- Vom Saal FS, Bronson FH (1978) Inutero proximity of female mouse fe-
tic behavior, offense, in mice. Behav Genet 26:471– 475. tuses to males: effect on reproductive-performance during later life. Biol
Miczek KA, Maxson SC, Fish EW, Faccidomo S (2001) Aggressive behav- Reprod 19:842– 853.
ioral phenotypes in mice. Behav Brain Res 125:167–181. Vrontou E, Nilsen SP, Demir E, Kravitz EA, Dickson BJ (2006) fruitless reg-
Miczek KA, Fish EW, DeBold JF, de Almeida RMM (2002) Social and neural ulates aggression and dominance in Drosophila. Nat Neurosci
determinants of aggressive behavior: pharmacotherapeutic targets at se- 9:1469 –1471.
rotonin, dopamine and ␥-aminobutyric acid systems. Psychopharmacol- Yurkovic A, Wang O, Basu AC, Kravitz EA (2006) Learning and memory
ogy 163:434 – 458. associated with aggression in Drosophila melanogaster. Proc Natl Acad Sci
Miczek KA, Faccidomo S, de Almeida RMM, Bannai M, Fish EW, DeBold JF USA 103:17519 –17524.