Donald W. Pfaff

The Rockefeller University, New York, New York, United States

Are you Donald W. Pfaff?

Claim your profile

Publications (744)3379.98 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: This study investigated the role of estrogen receptors alpha (ERα) in the ventromedial nucleus of the hypothalamus (VMN),the preoptic area (POA), the medial amygdala (MePD) and the bed nucleus of stria terminalis (BNST) in sociosexual behavior in female rats. This was done in two sets of experiments, with the VMN and POA investigated in the first set, and the MePD and BNST in the second set. The VMN and POA received intense projections from the MePD and BNST. We used a short hairpin ribonucleic acid (shRNA) encoded within an adeno-associated viral (AAV) vector directed against the ERα gene to reduce the number of ERα in the VMN or POA (First set of experiments), or in BNST or MePD (second set of experiments) in female rats. The rats were housed in groups of four ovariectomized females and three males in a seminatural environment for 8 days. In comparison to traditional test set-ups, the seminatural environment provides an arena in which the rats can express their full behavioral repertoire, which allowed us to investigate multiple aspects of social and sexual behavior in groups of rats. Behavioral observation was performed after estrogen and progesterone injections. A reduction of ERα expression in the VMN or POA diminished the display of paracopulatory behaviors and lordosis responses compared to controls, while the lordosis quotient remained unaffected. This suggests that ERα in the VMN and POA play an important role in intrinsic sexual motivation. The reduction in ERα did not affect the social behavior of the females, but the males sniffed and pursued the females with reduced ERα less than the controls. This suggests that the ERα in the VMN and POA is involved in the regulation of sexual attractiveness of females. The ERα in the MePD and BNST, on the other hand, plays no role in sociosexual behavior. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Neuroendocrinology 08/2015; DOI:10.1111/jne.12321 · 3.14 Impact Factor
  • Eric B Keverne · Donald W Pfaff · Inna Tabansky
    Proceedings of the National Academy of Sciences 06/2015; 112(22). DOI:10.1073/pnas.1501482112 · 9.67 Impact Factor
  • Source
    Xi Chu · Khatuna Gagnidze · Donald Pfaff · Anders Ågmo
    [Show abstract] [Hide abstract]
    ABSTRACT: General arousal has been operationally defined as enhanced motor activity and enhanced intensity of response to sensory stimuli. Even though the effects of gonadal hormones on mating behavior have been much studied, their potential effect on generalized arousal, as defined above, has never been evaluated. In the present study we employed a thoroughly validated assay of general arousal to determine the effects of estradiol (E) and testosterone (T) in gonadectomized female and male mice, respectively. The steroids were administered in three different ways: A fast-acting, water soluble preparation given intraperitoneally, an oil solution given subcutaneously, and an oil solution in a subcutaneous Silastic capsule. Motor activity and responses to sensory stimuli were recorded for 24 h, 91 h, and seven days following hormone administration, respectively. All measures of arousal varied according to the day/night cycle. The water soluble steroid preparation had no reliable effect. When the same doses of estradiol and testosterone were administered subcutaneously in an oil vehicle no effect of either treatment on arousal was observed. The subcutaneously implanted capsule containing estradiol or testosterone had a delayed effect on motor activity in females (four to seven days) but no effect in males. The long time required by the gonadal hormones for affecting arousal would be consistent with, but does not prove, a genomic action. The limited effects of E and T in our arousal assay suggest to us that the strongest actions of these hormones on arousal occur in the context of sequences of responses to sexually relevant stimuli. Copyright © 2015. Published by Elsevier Inc.
    Physiology & Behavior 04/2015; 147. DOI:10.1016/j.physbeh.2015.04.053 · 2.98 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Elevated levels of thyroid hormones (TH) reduce estradiol (E2)-dependent female sexual behavior. E2 stimulates progesterone and oxytocin receptors (Pgr and Oxtr) within the ventromedial hypothalamus and preoptic area, critical hypothalamic nuclei for sexual and maternal behavior, respectively. Here, we investigated the impact of TH on E2-dependent transcriptional mechanisms in female mice. First, we observed that triiodothyronine (T3) inhibited the E2 induction of Pgr and Oxtr. We hypothesized that differences in histone modifications and receptor recruitment could explain the influence of TH on E2-responsive Pgr and Oxtr expression. We observed that histone H3 acetylation (H3Ac) and methylation (H3K4me3) was gene and brain-region specific. We then analyzed the recruitment of estrogen receptor alpha (ERα) and TH receptor alpha (TRα) on the putative regulatory sequences of Pgr and Oxtr. Interestingly, T3 inhibited E2-induced ERααbinding to a specific Pgr enhancer site, whereas TRα binding was not affected, corroborating our theory that the competitive binding of TRα to an ERα binding site can inhibit ERα transactivation and the subsequent E2-responsive gene expression. On the Oxtr promoter, E2 and T3 worked together to modulate ERα and TRααbinding. Finally, the E2-dependent induction of co-factors was reduced by hypothyroidism and T3. Thus, we determined that the Pgr and Oxtr promoter regions are responsive to E2 and that T3 interferes with E2 regulation of Pgr and Otxr expression by altering the recruitment of receptors to DNA and changing the availability of co-factors. Collectively, our findings provide insights into molecular mechanisms of response to E2 and TH interactions controlling sex behavior in the hypothalamus. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 03/2015; 101(4). DOI:10.1159/000381459 · 4.37 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: PurposeUnderstanding the types of sensory nerve termini within the glabrous skin of the human male foreskin could throw light on surgical outcomes and therapeutic possibilities for the future. Various receptor types sense changes in temperature, position, pressure, pain, light touch, itch, burning and pleasurable sexual sensations. Similarities and differences in innervation characteristics and density might become apparent when the glans penis is compared with homologous structures in the female genitalia. The aim of this study is to document the presence and characteristics of cutaneous sensory receptors in the human penile foreskin using a histopathological study of the nerve termini to achieve a more complete understanding of sensory experiences.Methods Foreskin samples were obtained from ten boys (aged 1–9 years) who had undergone circumcision. Informed consent was obtained from the parent/legal guardian. The samples were examined after modified Bielschowsky silver impregnation of neural tissue, and immunocytochemistry against gene protein product (PGP) 9.5 and neuron-specific enolase (NSE).ResultsPGP 9.5 appeared to be the most sensitive neural marker. Free nerve endings were identified in the papillary dermis visualized as thin fibers, mostly varicose, with either branched or single processes, either straight or bent. Two types of sensory corpuscle were identified: capsulated and non-capsulated. Meissner-like corpuscles were located in the papillary dermis. Capsulated corpuscles resembled typical Pacinian corpuscles, comprising a single central axon surrounded by non-neural periaxonic cells and lamellae. The capsulated corpuscles were strongly positive for PGP 9.5 and NSE.Conclusions Free nerve endings, Meissner's corpuscles and Pacinian corpuscles are present in the human male foreskin and exhibit characteristic staining patterns. Clin. Anat., 2014. © 2014 Wiley Periodicals, Inc.
    Clinical Anatomy 02/2015; 28(3). DOI:10.1002/ca.22501 · 1.33 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: IntroductionLittle information is available regarding the sensory nerve endings within the glabrous skin of the external female genitalia. The diversity of possible sensations suggests a variety of receptor types. Comprehensive knowledge of the sensory stimuli, including stimulus position, changes in temperature, pressure and pain, is critical for addressing pain and sexual function disorders clinically. The aim of this neuro-histological study is document the presence and characteristics of cutaneous sensory receptors in female genital tissue.Materials and Methods Labial skin samples were obtained from ten normal girls (aged 1–9 years). The specimens were waste tissue obtained during surgical intervention. They were all obtained by the senior investigator, a pediatric urologist, after the parent or legal guardian had given informed consent. The specimens were stained by Cajal-type silver impregnation and by immunocytochemistry against protein gene product (PGP) 9.5 and neuron-specific enolase (NSE).ResultsPGP 9.5 was the most sensitive neural marker for identifying cutaneous sensory receptors. Free nerve endings (FNEs) in the papillary dermis appeared as thin fibers, varicose, branched or single processed, straight or bent. In the labia minora, FNEs were identified in the strata basale, spinosum and granulosum of the epidermis. Non-capsulated (Meissner-like) corpuscles in the dermal papillae interdigitated with epidermal ridges of the skin. Capsulated corpuscles protruded from the deep dermis into the epidermis. Encapsulated corpuscles and cells located in the inner and outer cores were strongly positive for PGP 9.5.ConclusionsFNEs, Meissner's corpuscles and Pacinian corpuscles are present in the female labia minora and exhibit characteristic staining patterns. Clin. Anat. 00:000–000, 2014. © 2014 Wiley Periodicals, Inc.
    Clinical Anatomy 02/2015; 28(3). DOI:10.1002/ca.22502 · 1.33 Impact Factor
  • Source
    Daniel M Keenan · Amy W Quinkert · Donald W Pfaff
    [Show abstract] [Hide abstract]
    ABSTRACT: In the present paper, we quantify, with a rigorous approach, the nature of motor activity in response to Deep Brain Stimulation (DBS), in the mouse. DBS is currently being used in the treatment of a broad range of diseases, but its underlying principles are still unclear. Because mouse movement involves rapidly repeated starting and stopping, one must statistically verify that the movement at a given stimulation time was not just coincidental, endogenously-driven movement. Moreover, the amount of activity changes significantly over the circadian rhythm, and hence the means, variances and autocorrelations are all time varying. A new methodology is presented. For example, to discern what is and what is not impacted by stimulation, velocity is classified (in a time-evolving manner) as being zero-, one- and two-dimensional movement. The most important conclusions of the paper are: (1) (DBS) stimulation is proven to be truly effective; (2) it is two-dimensional (2-D) movement that strongly differs between light and dark and responds to stimulation; and, (3) stimulation in the light initiates a manner of movement, 2-D movement, that is more commonly seen in the (non-stimulated) dark. Based upon these conclusions, it is conjectured that the above patterns of 2-D movement could be a straightforward, easy to calculate correlate of arousal. The above conclusions will aid in the systematic evaluation and understanding of how DBS in CNS arousal pathways leads to the activation of behavior.
    PLoS Computational Biology 02/2015; 11(2):e1003883. DOI:10.1371/journal.pcbi.1003883 · 4.62 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Patient perceptions of genital esthetics are motivating requests for plastic surgeries that could change sexual sensitivity. There is little information about the sensitivities of labial and introital sites. The aim of this study is to assess the relationship between sexual sensitivity and self-reported sizes of labial and introital sites. Sixty-two healthy, sexually active, adult women (mean age 37.9, range 21-60) with no history of genital or vaginal surgery gave written consent to participate in this study. A modified version of Self-Assessment of Genital Anatomy and Sexual Function (L-SAGASF-F) was used to assess labial and introital size. Site-specific sensation was rated on Likert scales of 1-5. Anatomical locations were compared for ratings. Of 62 responders, 84% (52) described their labia as "average-sized," 11% (7) described their labia minora and 13% (8) their labia majora as "large", and 3% (2) and 5% (3) as "small". Sexual pleasure ratings were "moderate" (median value: 3.0 for external genitalia and vaginal lumen) or "strong" (median value: 4.0 for the interior vagina). Significantly higher rankings related to the vaginal opening (P = 0.007). Orgasm intensity for stimulation of the external genitalia progressively increased toward the vaginal opening, from 1.0 to 3.0 (P = 0.001); vaginal ratings showed a similar progression, from 2.0 at the external luminal margin to 3.0 in the deep interior (P < 0.0001). Orgasm effort scores were intermediate (median: 3.0), uniform throughout the external and internal areas (P = 0.626). Ratings for labial and introital sensitivity, regardless of self-reported size, were very similar to those at other genital sites for sexual pleasure. Surgical excision of labial and introital structures could modify sexual sensation. Clin. Anat., 2014. © 2014 Wiley Periodicals, Inc. © 2014 Wiley Periodicals, Inc.
    Clinical Anatomy 02/2015; 28(3). DOI:10.1002/ca.22503 · 1.33 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Usage of the term 'theory of mind' (ToM) has exploded across fields ranging from developmental psychology to social neuroscience and psychiatry research. However, its meaning is often vague and inconsistent, its biological bases are a subject of debate, and the methods used to study it are highly heterogeneous. Most crucially, its original definition does not permit easy downward translation to more basic processes such as those studied by behavioral neuroscience, leaving the interpretation of neuroimaging results opaque. We argue for a reformulation of ToM through a systematic two-stage approach, beginning with a deconstruction of the construct into a comprehensive set of basic component processes, followed by a complementary reconstruction from which a scientifically tractable concept of ToM can be recovered. Copyright © 2014 Elsevier Ltd. All rights reserved.
    Trends in Cognitive Sciences 12/2014; 19(2). DOI:10.1016/j.tics.2014.11.007 · 21.97 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Stress plays a substantial role in shaping behavior and brain function, often with lasting effects. How these lasting effects occur in the context of a fixed postmitotic neuronal genome has been an enduring question for the field. Synaptic plasticity and neurogenesis have provided some of the answers to this question, and more recently epigenetic mechanisms have come to the fore. The exploration of epigenetic mechanisms recently led us to discover that a single acute stress can regulate the expression of retrotransposons in the rat hippocampus via an epigenetic mechanism. We propose that this response may represent a genomic stress response aimed at maintaining genomic and transcriptional stability in vulnerable brain regions such as the hippocampus. This finding and those of other researchers have made clear that retrotransposons and the genomic plasticity they permit play a significant role in brain function during stress and disease. These observations also raise the possibility that the transposome might have adaptive functions at the level of both evolution and the individual organism.
    Proceedings of the National Academy of Sciences 11/2014; 112(22). DOI:10.1073/pnas.1411260111 · 9.67 Impact Factor
  • Source
    Elysia Poggi Davis · Donald Pfaff
    [Show abstract] [Hide abstract]
    ABSTRACT: During gestation, development proceeds at a pace that is unmatched by any other stage of the life cycle. For these reasons the human fetus is particularly susceptible not only to organizing influences, but also to pathogenic disorganizing influences. Growing evidence suggests that exposure to prenatal adversity leads to neurological changes that underlie lifetime risks for mental illness. Beginning early in gestation, males and females show differential developmental trajectories and responses to stress. It is likely that sex-dependent organization of neural circuits during the fetal period influences differential vulnerability to mental health problems. We consider in this review evidence that sexually dimorphic responses to early life stress are linked to two developmental disorders: affective problems (greater female prevalence) and autism spectrum disorder (greater male prevalence). Recent prospective studies illustrating the neurodevelopmental consequences of fetal exposure to stress and stress hormones for males and females are considered here. Plausible biological mechanisms including the role of the sexually differentiated placenta are discussed.
    Psychoneuroendocrinology 11/2014; 49(1):11–25. DOI:10.1016/j.psyneuen.2014.06.014 · 4.94 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The prenatal brain develops under the influence of an ever-changing hormonal milieu that includes endogenous fetal gonadal and adrenal hormones; placental and maternal hormones; and exogenous substances with hormonal activity that can cross the placental barrier. This review discusses the influences of endogenous fetal and maternal hormones on normal brain development, and potential consequences of pathophysiological hormonal perturbations to the developing brain, with particular reference to autism. We also consider the effects of hormonal pharmaceuticals used for assisted reproduction, the maintenance of pregnancy, the prevention of congenital adrenal hypertrophy, and hormonal contraceptives continued into an unanticipated pregnancy, among others. These treatments, while in some instances life-saving, may have unintended consequences on the developing fetuses. Additional concern is raised by fetal exposures to endocrine-disrupting chemicals (EDCs) encountered universally by pregnant women from food/water containers, contaminated food, household chemicals, and other sources. What are the potential outcomes of prenatal steroid perturbations on neurodevelopmental and behavioral disorders, including autism spectrum disorders? Our purposes here are: (i.) to summarize some consequences of steroid exposures during pregnancy for the development of brain and behavior in the offspring; (ii.) to summarize what is known about the relationships between exposures and behavior, including autism spectrum disorders; (iii.) to discuss the molecular underpinnings of such effects, especially molecular epigenetic mechanisms of prenatal steroid manipulations, a field that may explain effects of direct exposures, and even transgenerational effects; and (iv.) for all of these, to add cautionary notes about their interpretation in the name of scientific rigor.
    Endocrine Reviews 09/2014; 35(6):er20131122. DOI:10.1210/er.2013-1122 · 21.06 Impact Factor
  • Rebecca L Leshan · Donald W Pfaff
    [Show abstract] [Hide abstract]
    ABSTRACT: Reproduction is an energy-expensive process that relies on indicators of energy availability to adjust its proper functioning. The adipokine leptin provides one such metabolic signal, with leptin receptor-expressing neurons at sites widespread within the CNS, including regions associated with the neuroendocrine reproductive axis. One substantial population lies within the hypothalamic ventral premammillary nucleus (PMv), a region itself linked to reproductive control, which may provide a strategic site for the integration of energy availability, sensory and gonadal cues. Here we review our current understanding of leptin and PMv regulation of reproduction, including emerging details about intracellular mechanisms of leptin action at this site.
    Journal of Chemical Neuroanatomy 08/2014; 61-62. DOI:10.1016/j.jchemneu.2014.08.008 · 1.50 Impact Factor
  • Larry J. Young · Donald W. Pfaff
    [Show abstract] [Hide abstract]
    ABSTRACT: •There are many sex differences in physiology, including in the brain.•There are many sex differences in psychiatric and neurological disorders.•This Special Issue highlights etiologies of sex differences in brain disorders.•We hope this SI will lead to more research of sex differences in brain disorders.
    Frontiers in Neuroendocrinology 08/2014; 35(3). DOI:10.1016/j.yfrne.2014.05.005 · 7.04 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: We report that mice with closed-head multiple traumatic brain injury (TBI) show a decrease in the motoric aspects of generalized arousal, as measured by automated, quantitative behavioral assays. Further, we found that temporally-patterned deep brain stimulation (DBS) can increase generalized arousal and spontaneous motor activity in this mouse model of TBI. This arousal increase is input-pattern-dependent, as changing the temporal pattern of DBS can modulate its effect on motor activity. Finally, an extensive examination of mouse behavioral capacities, looking for deficits in this model of TBI, suggest that the strongest effects of TBI in this model are found in the initiation of any kind of movement.
    Behavioural Brain Research 07/2014; 273. DOI:10.1016/j.bbr.2014.07.026 · 3.03 Impact Factor
  • Yan Zhou · Y. Litvin · D. Pfaff · M. Kreek
    Drug and Alcohol Dependence 07/2014; 140:e250. DOI:10.1016/j.drugalcdep.2014.02.692 · 3.42 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: It is not clear how, after a large perturbation, the brain explores the vast space of potential neuronal activity states to recover those compatible with consciousness. Here, we analyze recovery from pharmacologically induced coma to show that neuronal activity en route to consciousness is confined to a low-dimensional subspace. In this subspace, neuronal activity forms discrete metastable states persistent on the scale of minutes. The network of transitions that links these metastable states is structured such that some states form hubs that connect groups of otherwise disconnected states. Although many paths through the network are possible, to ultimately enter the activity state compatible with consciousness, the brain must first pass through these hubs in an orderly fashion. This organization of metastable states, along with dramatic dimensionality reduction, significantly simplifies the task of sampling the parameter space to recover the state consistent with wakefulness on a physiologically relevant timescale.
    Proceedings of the National Academy of Sciences 06/2014; 111(25). DOI:10.1073/pnas.1408296111 · 9.67 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Anabolic-androgenic steroids (AASs) are abused primarily in the context of intense exercise and for the purposes of increasing muscle mass as opposed to drug-induced euphoria. AASs also modulate the HPA axis and may increase the reinforcing value of exercise through changes to stress hormone and endorphin release. To test this hypothesis, 26 adult males drawn from a larger study on AAS use completed a progressive ratio task designed to examine the reinforcing value of exercise relative to financial reinforcer. Method Sixteen experienced and current users (8 on-cycle, 8 off-cycle) and 10 controls matched on quantity x frequency of exercise, age, and education abstained from exercise for 24 hours prior to testing and provided 24-hour cortisol, plasma cortisol, ACTH, β-endorphin samples, and measures of mood, compulsive exercise, and body image. Results Between group differences indicated that on-cycle AAS users had the highest β-endorphin levels, lowest cortisol levels, higher ACTH levels than controls. Conversely, off-cycle AAS users had the highest cortisol and ACTH levels, but the lowest β-endorphin levels. Exercise value was positively correlated with β-endorphin and symptoms of AAS dependence. Conclusion The HPA response to AASs may explain why AASs are reinforcing in humans and exercise may play a key role in the development of AAS dependence.
    Drug and Alcohol Dependence 06/2014; DOI:10.1016/j.drugalcdep.2014.03.008 · 3.42 Impact Factor
  • Yoav Litvin · Giuseppe Cataldo · Donald W. Pfaff · Lee‐Ming Kow
    [Show abstract] [Hide abstract]
    ABSTRACT: Research suggests a causal link between estrogens and mood. Here, we began by examining the effects of estradiol (E2) on rat innate and conditioned defensive behaviors in response to cat odor. Second, we utilized whole-cell patch clamp electrophysiological techniques to assess noradrenergic effects on neurons within the dorsal premammillary nucleus of the hypothalamus (PMd), a nucleus implicated in fear reactivity, and their regulation by E2. Our results show that E2 increased general arousal and modified innate defensive reactivity to cat odor. When ovariectomized females treated with E2 as opposed to oil were exposed to cat odor, they showed elevations in risk assessment and reductions in freezing, indicating a shift from passive to active coping. In addition, animals previously exposed to cat odor showed clear cue + context conditioning 24 h later. However, although E2 persisted in its effects on general arousal in the conditioning task, its effects on fear disappeared. In the patch clamp experiments noradrenergic compounds that typically induce fear clearly excited PMd neurons, producing depolarizations and action potentials. E2 treatment shifted some excitatory effects of noradrenergic agonists to inhibitory, possibly by differentially affecting α- and β-adrenoreceptors. In summary, our results implicate E2 in general arousal and fear reactivity, and suggest these may be governed by changes in noradrenergic responsivity in the PMd. These effects of E2 may have ethological relevance, serving to promote mate seeking even in contexts of ambiguous threat and shed light on the involvement of estrogen in mood and its associated disorders.
    European Journal of Neuroscience 05/2014; 40(2). DOI:10.1111/ejn.12608 · 3.18 Impact Factor
  • Source
    Sara M Schaafsma · Donald W Pfaff
    [Show abstract] [Hide abstract]
    ABSTRACT: The male predominance of autism spectrum disorders (ASD) is one of the best-known, and at the same time, one of the least understood characteristics of these disorders. In this paper we review genetic, epigenetic, hormonal, and environmental mechanisms underlying this male preponderance. Sex-specific effects of Y-linked genes (including SRY expression leading to testicular development), balanced and skewed X-inactivation, genes that escape X-inactivation, parent-of-origin allelic imprinting, and the hypothetical heterochromatin sink are reviewed. These mechanisms likely contribute to etiology, instead of being simply causative to ASD. Environments, both internal and external, also play important roles in ASD's etiology. Early exposure to androgenic hormones and early maternal immune activation comprise environmental factors affecting sex-specific susceptibility to ASD. The gene-environment interactions underlying ASD, suggested here, implicate early prenatal stress as being especially detrimental to boys with a vulnerable genotype.
    Frontiers in Neuroendocrinology 04/2014; 35(3). DOI:10.1016/j.yfrne.2014.03.006 · 7.04 Impact Factor

Publication Stats

35k Citations
3,379.98 Total Impact Points


  • 1968–2015
    • The Rockefeller University
      • • Laboratory of Neurobiology and Behavior
      • • Laboratory of Neuroendocrinology
      New York, New York, United States
  • 2004–2009
    • Mount Sinai School of Medicine
      • Department of Pharmacology and Systems Therapeutics
      Manhattan, NY, United States
  • 1999–2009
    • Universitetet i Tromsø
      • Department of Psychology
      Tromsø, Troms Fylke, Norway
  • 2005–2007
    • Pennsylvania State University
      • • Department of Physics
      • • Department of Biology
      University Park, Maryland, United States
  • 1982–2007
    • CUNY Graduate Center
      New York, New York, United States
  • 2006
    • Kagoshima University
      • Faculty of Law, Economics and the Humanities
      Kagosima, Kagoshima, Japan
  • 2001–2003
    • Weill Cornell Medical College
      • • Department of Neurological Surgery
      • • Department of Psychiatry
      New York City, New York, United States
  • 1998
    • Columbia University
      • Center for Neurobiology and Behavior
      New York, New York, United States
  • 1997
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1995
    • University of Texas MD Anderson Cancer Center
      • Human and Molecular Genetics
      Houston, Texas, United States
  • 1994
    • University of Maryland, Baltimore
      • Department of Medicine
      Baltimore, Maryland, United States
    • Concordia University Montreal
      • Department of Psychology
      Montréal, Quebec, Canada
  • 1992
    • Cornell University
      Итак, New York, United States
  • 1986
    • University of Hamburg
      Hamburg, Hamburg, Germany
  • 1985
    • Purdue University
      • Department of Psychological Sciences
      ウェストラファイエット, Indiana, United States
  • 1984
    • University of Illinois at Chicago
      • Department of Anatomy and Cell Biology (Chicago)
      Chicago, Illinois, United States
  • 1980
    • Boston University
      Boston, Massachusetts, United States
  • 1979
    • Fordham University
      • Department of Psychology
      New York, New York, United States
  • 1977
    • Bucknell University
      • Department of Psychology
      Lewisburg, Pennsylvania, United States
  • 1975
    • University of Pennsylvania
      Philadelphia, Pennsylvania, United States