Research
Research
Projects
1. Towards a better understanding of maternal mental health: Stress effects on peripartum adaptations (Clara Perani)
(in collaboration with Dr. Stefan Reber) and Prof. Ludwig Aigner (Paracelus University, Salzburg))
Across all mammalian species the peripartum period is characterised by behavioural, neuroendocrine and neuronal adaptations, which prepare a mother for the impending birth and nurturance of the offspring (Brunton and Russell 2008; Slattery and Neumann 2008). While these adaptations are essential to ensure the survival and health of the offspring (Carter et al 2001), we hypothesize that they are also required for maternal mental health (Neumann 2003; Slattery and Neumann 2008). Although anxiolysis, enhanced calmness and attenuated stress-responses of the hypothalamic-pituitary adrenal (HPA) axis are observed in the majority of mothers, a significant percentage display increased vulnerability to mood disorders, such as postpartum anxiety (5-12%; Lonstein 2007), postpartum depression (PPD; 5-25%; Beck 2006) or the much rarer postpartum psychosis (0.1%; Bridges 2008; Jones et al 2008). Despite the high incidence of these disorders, and detrimental outcome for both mother and child, their aetiology remains poorly understood, due in part to the lack of appropriate animal models.
It is feasible that alterations to these normal peripartum adaptations (for more details see Slattery and Neumann, 2008 and Figure 1) caused, for example, by exposure to chronic stress in pregnancy may underlie postpartum mood disorders.
Figure 1: Adapted from Slattery and Neumann, 2008 (J. Physiol)
Figure 2: Data demonstrating the effectiveness of the chronic psycho-social stress paradigm
A) Schematic representation of the chronic stress procedure to be applied to pregnant and virgin rats. B) The effect of chronic stress on body weight gain during pregnancy. C) The relative adrenal weight in virgins, late pregnant (PD 20) or lactation day 8 non-stressed and stressed females.
Therefore, the first aim of the project is to characterise the effects of a novel chronic psychosocial stress paradigm (Figure 2) during pregnancy on established peripartum adaptations. As such, we hypothesize that exposure to chronic stress in pregnancy will, at least partly, prevent behavioural, neurogenesis, neuroendocrine and/or neuronal adaptations and result in alterations specific to the reproductive status of the female and, therefore, include males/virgins as controls. We will then determine whether genetic differences in anxiety-related behaviour (see Figure 1 in project 2) can protect (low-anxiety females) or worsen (high-anxiety females) the observed consequences of this pregnancy stress exposure. Finally, we will attempt to reverse the detrimental effects of stress exposure via chronic application of antidepressants or selected neuropeptides.
Overall, the research objectives aim to demonstrate a causal link between pregnancy stress and postpartum mood disorders and to show that innate anxiety levels and key neuropeptides can protect against such stress exposure.
These studies are supported by the Deutsche Forschungsgemeinschaft (DFG Ne465/16 and DFG SL141/4-1) and the Bayerische Forschungsstiftung (to CP)
2. Assessment of the contribution of the Neuropeptide S (NPS) system in an animal model of high anxiety-related behaviour
(in collaboration with Dr Gregers Wegener: Aarhus University, Prof. Aleksander Mathe; Karolinska Institute, and Prof. Rainer Landgraf; MPI Munich)
Psychiatric disorders are the most common mental illness with anxiety disorders having a lifetime prevalence of 28.8 % {Kessler et al., 2007). While a number of pharmacotherapies are available, the lack of truly novel-acting compounds has lead in recent years to a more endophenotype-based research approach and a focus on the development of non-GABAergic compounds (Cryan and Slattery, 2007; 2010; Hasler et al., 2006). The large number of neuropeptides, characterized by discrete synthesis sites and widespread receptor distribution, represent likely research candidates for novel therapeutic targets {Landgraf and Neumann, 2004; Slattery and Neumann, 2010).
Neuropeptide S (NPS), originally described in mice, is an example of such a neuropeptide {Xu et al., 2004). Central administration of NPS has been shown to elicit potent anxiolytic and arousal effects in rodents (Pape et al., 2010). In addition to these effects on innate anxiety, direct NPS infusion into the endopiriform nucleus (Meis et al., 2008), or the basolateral amygdala (Jungling et al., 2008), has been demonstrated to facilitate extinction from contextual and conditioned fear, respectively. Intriguingly, human studies have revealed that a single nucleotide polymorphism (SNP) in the NPS receptor (Npsr) is associated with increased risk of panic disorder and over-interpretation of fear (Domschke et al., 2010; Donner et al., 2010; Okamura et al, 2007; Raczka et al., 2010). This A to T polymorphism (rs324981) results in an amino acid substitution from Asn to Ile at position 107 and was originally associated with increased susceptibility for asthma (Laitinen et al, 2004). Although animal studies show that acute NPS application is anxiolytic, the human studies suggest that increased NPS potency is detrimental. It has been suggested that this supposed paradox could be due to an increased level of arousal and over-interpretation of stimuli, which is known to increase the possibility of panic disorder (Domschke et al., 2010).
In order to assess such a hypothesis, it has become apparent that it is important to test novel strategies, and examine the underlying neural mechanisms, in appropriate animal models, which attempt to mimic the human situation. These models generally fall into two main categories; chronic stress paradigms and animals bred for extreme behavioral traits (Cryan and Slattery, 2007). The selective breeding of Wistar (NAB) rats for anxiety-related behavior on the elevated-plus maze (EPM) has resulted in breeding lines of high (HAB) and low (LAB) anxiety-related behaviour, confirmed in numerous tests and laboratories (Figure 1; Neumann, 2010). These in-born differences make these HAB and LAB rodents attractive models to assess the underlying aetiology of affective disorders including the involvement of novel neurotransmitter / neuropeptide systems. Indeed, the differences in anxiety behaviour have been related to SNPs in the vasopressin gene (Murgatroyd et al., 2004). However, whether NPS may also contribute to the anxiety phenotypes of these rodents, or differentially alter behaviour acutely is unknown.
Figure 1: Adapted from Neumann et al., in press (Progress in Neuro-Psychopharmacology & Biological Psychiatry)
Therefore, the aim of the project is to determine whether intracerebral administration of NPS results in differential responses in these lines. Further, we intend to determine if receptor or peptide expression differences, or genetic polymorphisms exist between the lines. Taken together, these studies will reveal the contribution of the NPS system in rodents displaying extremes in anxiety-related behaviour and whether NPS can acutely exert its anxiolytic effects in animals with a genetically-determined psychopathology.
3. Behavioural and central consequences of chronic psychosocial stress
(Sebastian Peters)
(in collaboration with Dr. Stefan O. Reber and Prof. Maurizio Popoli; Uni. of Milan)
Despite substantial research efforts in the last decades, the aetiology of stress-based disorders such as major depression and anxiety remains poorly understood. This has led to a resurgence of interest in developing more relevant animal models than the majority currently employed. Therefore, given the evidence purporting chronic social stress to be a risk factor for the development, not only of cardiovascular and inflammatory diseases, but also of depression and anxiety in vulnerable individuals (Cryan & Slattery 2007), recent attempts have focussed on the development of chronic social stress paradigms (Bartolomucci et al 2003; Berton et al 2006; Engler et al 2005; Fuchs & Flugge 2003; Keeney & Hogg 1999; Reber et al 2006; 2007; Schmidt et al 2007; Stefanski et al 2003). Such paradigms are believed to be more relevant to the human situation than non-social stress paradigms (e.g. repeated restraint; (Cryan & Slattery 2007) and, thus, can better reveal the behavioural consequences of stress exposure.
The majority of these social stressor paradigms have been reported to increase both anxiety- and depression-related behaviour. This is perhaps unsurprising, as there is high co-morbidity between the two disorders (Kennedy 2008). In addition, as in humans, these alterations persist for a long-time after the termination of the stressor (Berton et al 2006; Fuchs 2005; Kennedy 2008; Krishnan et al 2007). Thus, such models have enhanced our knowledge of underlying mal-adaptations caused by chronic stress exposure, and continue to do so. However, they also highlight a drawback of the models currently used to assess stress-related disorders. In order to really dissect the mechanisms underlying anxiety or depression, animal models are needed, which specifically induced one phenotype.
We have previously reported the physiological and immunological consequences of exposure to two psychosocial stress paradigms; chronic subordinate colony housing (CSC) and social defeat/ overcrowding (SD/OC) (see Reber publication list [link]). In the former, experimental mice are housed for 19 days in the presence of a larger, resident, con-specific mouse, which assumes dominance and, consequently, places the experimental mice in a subordinate position. In contrast, SD/OC combines repeated social defeats with periods of overcrowding, which adds social instability; a known stressor in mice (Bailey et al 2010). Thus, while CSC reflects a continuous form of chronic stress, SD/OC rather mimics an intermittent stressor. However, only anxiety-related behaviour has been assessed, and only following the CSC paradigm, to date. Here, it has repeatedly been demonstrated that CSC exposure leads to an anxiogenic phenotype immediately following stressor termination (Reber et al 2007; Reber & Neumann 2008; Reber et al 2008; Singewald et al 2009; Veenema et al 2008). However, the effect of CSC on depression-related behaviour remains unknown and no studies have examined the behavioural consequences of SD/OC.
The use of these social stress models has also provided a great deal of evidence as to the molecular and neuroendocrine changes, which may underlie the resultant behavioural phenotype. For example, accumulating evidence supports a key role of neurotrophic factors, such as BDNF and CREB, in the pathology and treatment of stress-related disorders (Krishnan and Nestler, 2008; Fuchs, 2005). In socially-defeated mice, increased BDNF levels in the nucleus accumbens (Krishnan et al, 2007) and decreased levels in the hippocampus (Tsankova et al, 2006) lead to a depressed phenotype. Moreover, intra-hippocampal administration of BDNF has been shown to have antidepressant-like properties under basal conditions and following stress exposure (Shirayama et al., 2002; Gourley et al., 2008). In contrast, increased CREB levels in the nucleus accumbens following long-term social isolation, have been shown to mediate the observed anxiety- but not anhedonic phenotype (Wilkinson et al., 2009; Wallace et al., 2009).
Therefore, in the present study we assessed the impact of these two well-validated, clinically-relevant, psychosocial stress paradigms on short- and long-term anxiety- and depression-related behaviour. Additionally, we aim to reveal whether alterations in neurotrophic factors, BDNF and CREB, could underlie the stress-induced behavioural phenotype.
These studies are supported by the Deutsche Forschungsgemeinschaft (DFG RE-2911/5-1
4. The development of a novel animal model to study social anxiety disorder
(Iulia Toth)
Social anxiety disorder (SAD), often referred to as social phobia, is characterized by persistent fear and avoidance of social situations. Epidemiologically, SAD is the third most common psychiatric disorder, with a 12-month and lifetime prevalence of 6.8% and 12.1%, respectively (Kessler et al., 2005a,b). For diagnostic purposes, SAD has been divided in two subtypes: specific and generalized. Specific SAD refers to the fear and avoidance of a particular situation (e.g. fear of giving a public speech, fear of interaction) and fear of showing anxiety symptoms (Bögels et al., 2010). Generalized SAD patients fear and avoid a wide range of social situations and are, therefore, more impaired than specific SAD patients (den Boer, 1997; Kessler et al., 1998). Avoidance behaviour plays an important role in the maintenance of SAD and prevents the extinction of fear in social situations (American Psychiatric Association, 1994; Stangier et al., 2006). In keeping with this, the treatment for SAD includes psychotherapy (cognitive-behavioral therapy) in combination with medication such as antidepressants, beta-blockers and benzodiazepines. The medication used to relieve anxiety symptoms is rather unspecific and, despite considerable efforts, their efficacy is still unsatisfactory. A high number of SAD patients (one third or more) fail to respond to treatment, or achieve only partial remission of symptoms. Even in patients with good treatment outcome, relapse rates average from 30% to 60% after discontinuing treatment (Cuthbert, 2002; Veale, 2003).
One reason for the limited knowledge about the underlying causes and mechanisms of SAD and the lack of specific medication might be the lack of appropriate animal models available to study the disorder. Although there are numerous tests to assess social behaviour (eg. social interaction test, social recognition/memory, tests for aggression), no convincing models of SAD exist. While social defeat (acute or chronic) or the psychosocial threat paradigm can induce social anxiety, these models tend to be either specific to the dominant male or lead to numerous other behavioural consequences such as anxiety or anhedonia/depression.
Therefore, the aim of this project is to develop an animal model that causes generalized social anxiety without leading to other severe behavioural consequences. Once developed, the paradigm will be used to gain a better understanding of the molecular mechanisms underlying the disorder and also to assess compounds with novel mechanisms of action for its treatment.
These studies are supported by the Bayerische Forschungsstiftung (to IT)
Profile
Profile
2011
Acting Professor of Neurophysiology, Institute of Zoology. University of Regensburg
2010
Commenced Habilitation at the University of Regensburg
2009 - 2011
Akad. Rat. a.Z. University of Regensburg, Institute of Zoology. University of Regensburg
2006 – 2009
Senior Post-doctoral Researcher (ELITE-Network Bavaria funded)
Institute of Zoology, University of Regensburg
2004 – 2006
NIH-Funded Post-doctoral Researcher, Novartis Institutes for Biomedical Research, Basel, Switzerland: “The development of a novel translational animal model of depression”. Supervisor: Dr J.F. Cryan
1999 – 2003
BBSRC Industrial CASE Award PhD Studentship, University of Bristol and Organon Laboratories Ltd, Newhouse, Scotland: “Characterisation of a novel antidepressant: Org34167”. Supervisors: Prof D.J. Nutt, Dr A.L. Hudson, Dr D. Hill
1995 - 1999
Bachelor of Science (Honours) in Pharmacology, University of Glasgow (2,1)
Awards and Achievements:
2011: Co-organiser of Parental Brain 2013 congress (to be held in Regensburg)
since 2011 Editor PLoS ONE
since 2011 Member of ECNP Workshop Committee
since 2011 Editor Acta Neuropsychiatrica
since 2010 Review Editor Frontiers in Psychopharmacology
since 2010 ECNP Ordinary Member
since 2009: Associate Editor BMC Neuroscience
2009: Participant in ECNP Targeted Expert Meeting on Anxiety Disorders and Anxiolytics, Istanbul, Turkey
2007: Post-doctoral Poster Prize winner Parental Brain Conference, Boston, USA
2005: Travel award to ECNP young scientist Workshop, Nice, France
Grants Awarded:
Deutsche Forschungsgemeinschaft: SL141/4-1 "Stress in females", Principle Investigator. Funding period: 36 months beginning 09/2011. Total awarded €295, 350
Research Interests:
1. Neural circuitry underlying behavioural responses relevant to stress, reward, depression and anxiety
2. Molecular and biological mechanisms underlying the actions of antidepressants and anxiolytics
3. The post-partum brain
4. The role of neuropeptides in anxiety and depression disorders
5. The development of animal models to explore social anxiety disorder
Teaching Experience:
since 2010 Lecturer in “Animal Physiology” and “Neurobiology” Undergraduate Lecture Series
since 2006 Bachelor and Master students method practica instructor/demonstrator
since 2006 Lecturer in international ELITE Masters course in Experimental and Clinical Neurosciences
since 2006 Research and Thesis Supervisor for undergraduate, Bachelor, Masters and PhD students
1999 - 2003 Tutor in Pharmacology laboratory practica (University of Bristol)
Professional Skills:
Animal handling, husbandry and welfare: approved for animal research in the U.K., Switzerland and Germany
Biochemical and molecular biology techniques: cryostat sectioning; densitometric image analysis; immunohistochemistry; in situ hybridization; microarray analysis; radioligand binding; receptor autoradiography; RT-PCR; western blotting
Endocrinology: ELISA and radioimmune assays for corticosterone, ACTH, oxytocin and vasopressin; in-vivo blood sampling via indwelling jugular-vein catheter
Behavioural testing (rat and mice unless specified): cued- and contextual-fear conditioning; elevated plus maze; forced swim test; intracranial self-stimulation responding (rats); light-dark box; progressive ratio for sucrose responding; monitoring maternal behaviour; novelty-suppressed feeding; open field test; punished drinking test (Vogel test); rotarod; sucrose preference testing; tail suspension test (mice); social interaction test; stress-induced hypothermia (mice)
Surgical procedures: bilateral olfactory bulbectomy; intra-cardiac perfusion; jugular-vein catheterisation; microdialysis; stereotaxic surgery
Ad-hoc reviewer:
For over 20 journals including Biological Psychiatry, Molecular Psychiatry, Neuropharmacology, Neuropsychopharmacology, Neuroscience and Biobehavioral Reviews and Psychopharmacology
Research Collaborations:
Prof. Girolamo Calo' (Uni. of Ferrara, Italy)
Dr John Cryan (Uni. College Cork, Ireland)
Prof. Aleksander Mathe (Karolinska Institute)
Prof. Maurizio Popoli (Uni. of Milan, Italy)
Dr. Stefan Reber (Uni. Regensburg)
Prof. Andreas Reif (Uni. Würzburg)
Dr Robert Ring (Autism Speaks, Boston, USA)
Prof. Nicolas Singewald (Uni. Innsbruck)
Prof. Per Svenningson (Karolinska Institute)
Dr Gregers Wegener (Aarhus Uni., Denmark)
Language Skills:
English (mother tongue), German (intermediate), Hungarian (basic)
Other:
My current h index is 10 and all published articles older than 2 years are cited higher than the average citation index of the respective journal
Publications
Publications
Wherever appropriate journal impact factor (IF) and number of citations (in brackets) are provided after each article
In Press
Slattery, D.A.#, Jurek, B.#, Maloumby, R., Hillerer, K., Koszinowski, S., Neumann, I.D., van den Burg, E.H. (in press) Differential Contribution of Hypothalamic MAPK Activity to Anxiety-Like Behaviour in Virgin and Lactating Rats. PLoS ONE IF: 4.4 (0)
Toth, I., Neumann, I.D. & Slattery, D.A. (accepted) Central administration of oxytocin receptor ligands affect cued fear extinction in rats and mice in a time-point dependent manner. Psychopharmacology IF: 3.8 (0)
Hillerer, K., Neumann, I.D., & Slattery, D.A. (in press) From stress to postpartum mood disorders: How chronic peripartum stress can impair maternal adaptations. Neuroendocrinology IF: 3.3 (0)
2012
Naoki Okimoto, N., Bosch, O.J., Slattery, D.A., Pflaum, K., Matsushita, H., Wei, F-Y., Ohmori, M., Nishiki, T., Ohmori, I., Hiramatsu, Y., Matsui, H., Neumann, I.D. & Tomizawa, K. (2012) RGS2 mediates the anxiolytic effect of oxytocin. Brain research 1453: 26-33 IF: 2.6 (0)
Slattery, D.A. & Cryan, J.F. (2012) Using the rat forced swim test to assess antidepressant-like activity in rodents. Nature Protocols 7: 1009-14 IF: 8.4 (0)
Toth, I., Neumann, I.D. & Slattery, D.A. (2012) Social fear conditioning: A novel and specific animal model to study Social Anxiety Disorder. Neuropsychopharmacology 37: 1433-43 IF: 6.7 (1)
Toth, I., Dietz, M., Peterlik, D., Huber, S.E., Fendt, M., Neumann, I.D., Flor, P.J., & Slattery, D.A. (2012) Pharmacological interference with metabotropic glutamate receptor subtype 7 but not subtype 5 differentially affects within- and between-session extinction of Pavlovian conditioned fear. Neuropharmacology 62: 1619-26 IF: 4.7 (0)
Slattery, D.A., Uschold, N., Magoni, M., Baer, J., Popoli, M., Neumann, I.D & Reber, S.O. (2012) Behavioural consequences of chronic psychosocial stress: anxiety without depression. Psychoneuroendocrinology 37: 702-14 IF: 5.2 (1)
Hillerer, K., Reber, S.O., Neumann, I.D., Slattery, D.A. (2011) Exposure to chronic pregnancy stress reverses peripartum-associated adaptations: implications for postpartum anxiety and mood disorders. Endocrinology 152: 3930-40 IF: 5.0 (6)
2011
Lukas, M., Toth, I., Reber, S.O., Slattery, D.A., Veenema, A.H., & Neumann, I.D (2011) Brain oxytocin facilitates social preference behavior in male rats and mice. Neuropsychopharmacology 36: 2159-68 IF: 6.7 (9)
Wegener, G., Finger, B.C., Elfving, B., Keller, K., Singewald, N., Slattery, D.A., Neumann, I.D. & Mathé, A.A. (2011) Neuropeptide S alters anxiety, but not depression-like behavior in the Flinders Sensitive Line rats, a genetic animal model of depression. International Journal of Neuropsychopharmacology 9: 1-13 IF: 4.7 (1)
Reber,S.O., Peters, S., Slattery, D.A., Hofmann, C., Schoelmerich, J., Neumann, I.D., & Obermeier, F. (2011) Mucosal immunosuppression and epithelial barrier defects are key events in murine psychosocial stress-induced colitis. Brain, Behavior and Immunity 25: 1153-61 IF: 4.0 (3)
Neumann, I.D., Wegener, G., Homberg, J.R., Cohen, H., Slattery, D.A., Zohar, J., Olivier, J.D.A. & Mathé, A.A. (2011) Animal models of depression and anxiety: what do they tell us about the human condition? Progress in Neuro-Psychopharmacology & Biological Psychiatry 35: 1357-75 IF: 2.9 (8)
Slattery, D.A., Neumann, I.D. & Cryan, J.F. (2011) Transient inactivation of the infralimbic cortex induces antidepressant-like effects in the rat. Journal of Psychopharmacology 25: 1295-303 IF: 3.8 (3)
2010
Cryan, J.F. & Slattery, D.A. (2010) GABAB receptors and depression: Current status. Advances in Pharmacology 58: 427-51 (10)
Slattery, D.A. & Cryan, J.F. (2010) Animal models of depression – where are we going? Depression: From Psychopathology to Pharmacotherapy. Vol 27: 124-138. Editors: Cryan, J.F. & Leonard, B.E. Karger AG, Basel. (0)
Slattery, D.A. & Neumann, I.D. (2010) Oxytocin and Major Depressive Disorder: Experimental and Clinical Evidence for Links to Aetiology and Possible Treatment. Pharmaceuticals 3: 702-724 (7)
Slattery, D.A. & Neumann, I.D. (2010) Chronic icv oxytocin attenuates the pathological high anxiety state of selectively bred Wistar rats. Neuropharmacology 58: 56-61 IF: 4.7 (24)
2009
Cryan, J.F. & Slattery, D.A. (2009) GABA receptors and depression: Focus on GABAB. Recent developments on depression research; Research Signpost. Editors Shirayama, Y. & Chaki, S.
2008
Slattery, D.A. & Neumann, I.D. (2008) No stress please! Mechanisms of stress hyporesponsiveness of the maternal brain. Journal of Physiology 586: 377-385 IF: 5.1 (62)
2007
Bosch, O.J., Müsch, W., Bredewold, R., Slattery, D.A. & Neumann, I.D. (2007). Prenatal stress increases HPA axis activity and impairs maternal care in lactating female offspring: implications for postpartum mood disorder. Psychoneuroendocrinology 32: 267-78 IF: 5.2 (50)
Slattery, D.A., Markou, A. & Cryan, J.F. (2007) Evaluation of reward processes in an animal model of depression Psychopharmacology 190: 555-568 IF: 3.8 (30)
Cryan, J.F. and Slattery, D.A. (2007) Animal models of mood disorders: recent developments. Current Opinion in Psychiatry 20: 1-7 IF: 3.0 (93)
2006
Slattery, D.A. & Cryan, J.F. (2006) The role of GABAB receptors in depression and the antidepressant response. Drug Development Research 67: 477-494 IF: 1.1 (7)
2005
Slattery, D.A., Markou, A., Froestl, W. & Cryan, J.F. (2005) The GABAB receptor-positive modulator GS39783 and the GABAB receptor agonist baclofen attenuate the reward-facilitating effects of cocaine: Intracranial self-stimulation studies in the rat. Neuropsychopharmacology 30: 2065-72 IF: 6.7 (50)
Slattery, D.A., Morrow, J.A., Hudson, A.L., Hill, D.R., Nutt, D.J. & Henry, B. (2005) Comparison of Alterations in c-fos and Egr-1 (zif268) expression throughout the rat brain following acute administration of different classes of antidepressant compounds. Neuropsychopharmacology 30: 1278-87 IF: 6.7 (21)
Slattery, D.A., Desrayaud, S. & Cryan, J.F. (2005) GABAB receptor antagonist-mediated antidepressant-like behavior is serotonin-dependent. Journal of Pharmacology and Experimental Therapeutics 312: 290-296 IF: 4.0 (60)
2004
Slattery, D.A., Hudson, A.L. & Nutt, D.J. (2004) The evolution of antidepressant mechanisms Fundamental and Clinical Pharmacology 18: 1-22 IF: 2.2 (56)
Sumner, B.E., Cruise, L., Slattery, D.A., Hill, D.R., Shahid, M. & Henry, B. (2004) Testing the validity of c-fos expression profiling to aid the therapeutic classification of psychoactive drugs Psychopharmacology 172: 306-321 IF: 3.8 (38)
