DOCSLIB.ORG

Dissociating Hippocampal Versus Basal Ganglia Contributions to Learning and Transfer

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Dissociating Hippocampal Versus Basal Ganglia Contributions to Learning and Transfer Dissociating Hippocampal versus Basal Ganglia Contributions to Learning and Transfer Catherine E. Myers1, Daphna Shohamy1, Mark A. Gluck1, Steven Grossman1, Alan Kluger2, Steven Ferris3, James Golomb3, 4 5 Geoffrey Schnirman , and Ronald Schwartz Downloaded from http://mitprc.silverchair.com/jocn/article-pdf/15/2/185/1757757/089892903321208123.pdf by guest on 18 May 2021 Abstract & Based on prior animal and computational models, we Parkinson’s disease, and healthy controls, using an ‘‘acquired propose a double dissociation between the associative learning equivalence’’ associative learning task. As predicted, Parkin- deficits observed in patients with medial temporal (hippo- son’s patients were slower on the initial learning but then campal) damage versus patients with Parkinson’s disease (basal transferred well, while the hippocampal atrophy group showed ganglia dysfunction). Specifically, we expect that basal ganglia the opposite pattern: good initial learning with impaired dysfunction may result in slowed learning, while individuals transfer. To our knowledge, this is the first time that a single with hippocampal damage may learn at normal speed. task has been used to demonstrate a double dissociation However, when challenged with a transfer task where between the associative learning impairments caused by previously learned information is presented in novel recombi- hippocampal versus basal ganglia damage/dysfunction. This nations, we expect that hippocampal damage will impair finding has implications for understanding the distinct generalization but basal ganglia dysfunction will not. We tested contributions of the medial temporal lobe and basal ganglia this prediction in a group of healthy elderly with mild-to- to learning and memory. & moderate hippocampal atrophy, a group of patients with mild INTRODUCTION responses (Sommer, Grafman, Clark, & Hallett, 1999; The medial temporal (MT) lobe and the basal ganglia Daum, Schugens, Breitenstein, Topka, & Spieker, are thought to play distinct roles in learning and 1996), probabilistic classification (Shohamy et al., memory. Traditionally, the MT lobe has been associ- 2002; Knowlton, Mangels, & Squire, 1996), and cate- ated with declarative memory function in humans, gorization (Maddox & Filoteo, 2001; Reed, Squire, while the basal ganglia are associated with procedural Patalano, Smith, & Jonides, 1999). Together, these or habit learning in animal and humans. Humans with findings suggest that the basal ganglia, but not the damage to the MT lobes, including the hippocampus, hippocampus, play a critical role in stimulus–response- are often spared on a variety of tasks, which seem to based habit learning (e.g., White, 1997; Knowlton & involve incrementally acquired learning of habits or Squire, 1993; Mishkin, Malamut, & Bachevalier, 1984). skills. For instance, individuals with MT damage can However, while the hippocampus may not be critical learn as quickly as healthy controls in paradigms for learning simple stimulus–response-based learning, it ranging from delay eyeblink classical conditioning (Ga- does appear to be critical for some forms of more brieli et al., 1995; Woodruff-Pak, 1993) to category complex learning, such as the ability to transfer when learning (Maddox et al., 1999; Squire & Knowlton, familiar stimuli are presented in novel recombinations 1995). By contrast, humans with damage to the basal (e.g., Myers et al., 2002; Eichenbaum, Mathews, & ganglia often show deficits on these forms of habit Cohen, 1989). For example, in one recent study, non- learning. For example, Parkinson’s disease (PD) devas- demented elderly individuals with hippocampal atrophy tates dopaminergic neurons in the substantia nigra (HA) revealed by neuroimaging were able to learn an compacta, disrupting basal ganglia processing. Parkin- eight-pair concurrent visual discrimination as quickly as son’s patients are slow to acquire conditioned eyeblink nonatrophied controls, but were selectively impaired when challenged by a transfer test in which familiar stimulus features were presented in novel recombina- 1Rutgers University, 2City University of New York, 3New York tions (Myers et al., 2002). This suggests that the hippo- University Medical Center, 4Fordham University, 5Hattiesburg campus and related MT areas may be important for the Clinic ability to generalize learned information. D 2003 Massachusetts Institute of Technology Journal of Cognitive Neuroscience 15:2, pp. 185–193 Downloaded from http://www.mitpressjournals.org/doi/pdf/10.1162/089892903321208123 by guest on 27 September 2021 Table 1. Acquired Equivalence Paradigm in Humans (Collie et al., 2002) Acquisition Acquisition Acquisition Transfer Phase: Stage 1: Shaping Stage 2: Equivalence Training Stage 3: New Consequents Equivalence Testing A1!X1 A1!X1 A1!X1 A2!X1 A2!X2? A2!X1 A1!X2 B1!Y1 Downloaded from http://mitprc.silverchair.com/jocn/article-pdf/15/2/185/1757757/089892903321208123.pdf by guest on 18 May 2021 B1!Y1 B1!Y1 B2!Y1 B2!Y2? B2!Y1 B1!Y2 Note that transfer phase interleaved trials with the previously learned information as well as the novel pairs. If so, then we would expect similar patterns of Thus, patients with basal ganglia dysfunction due to PD spared initial learning but impaired generalization in may be expected to show slower learning of the initial individuals with HA on a range of learning and transfer associations in the acquisition phases—but, once this tests. For example, acquired equivalence is a phenom- information is acquired, there may be normal or near- enon in which prior training to treat two stimuli as normal transfer. equivalent increases generalization between them— If these predictions hold, acquired equivalence may even if those stimuli are superficially very dissimilar be a paradigm that allows double dissociation, within a (e.g., Bonardi, Rey, Richmond, & Hall, 1993; Hall, Ray, single task, between the qualitative pattern of learning & Bonardi, 1993; Grice & Davis, 1960). In one such impairments following damage to the hippocampal study, Bonardi et al. (1993) demonstrated acquired region versus the basal ganglia. equivalence in pigeons. First, the pigeons were trained To test this proposed dissociation, we used a com- to peck at a keylight, where stimulus orderings A1–X1, puter-based acquired equivalence task, shown in Table 1 A2–X1, B1–Y1, and B2–Y1 all predicted food avail- (Collie et al., 2002; Myers, Shohamy, Schwartz, & Gluck, ability. In effect, antecedents A1 and A2 were ‘‘equiv- 2000). In this version, there are three acquisition stages, alent’’ in terms of their pairing with X1, while B1 and antecedent stimuli are represented on the screen as B2 were also ‘‘equivalent’’ in their pairing with Y1. cartoon faces, and consequents are represented as Next, the pigeons were trained to peck to A1 but not different colored cartoon fish. Two antecedent stimuli B1; finally, the pigeons were tested for response to A2 A1 and A2 were associated with the same consequent and B2. The birds tended to respond strongly to A2 stimulus X1, while two antecedent stimuli B1 and B2 but not to B2. Apparently, the birds had learned were associated with consequent Y1. Next, A1 was equivalencies between stimuli with identical conse- associated with a new consequent X2 while B1 was quents: Given that A1 was rewarded and A2 was associated with a new consequent Y2. Finally, a transfer ‘‘equivalent’’ to A1, the birds expected that A2 would phase tested whether patients would show acquired also be rewarded. Similar effects have been shown in equivalence and associate A2 with X2 and B2 with Y2, humans (Spiker, 1956) and rats (Honey & Hall, 1991; even though these particular stimulus pairings had Hall & Honey, 1989). never been trained. This type of acquired equivalence task seems to We administered this acquired equivalence task to a require flexible generalization, of the kind hypothe- group of nondemented elderly individuals with HA sizedtodependonhippocampalregionmediation documented on neuroimaging (n = 12), a group of (Myers & Gluck, 1996; Eichenbaum et al., 1989). Sup- individuals with PD (n = 12), and appropriate matched pose that an individual learned the A1–X1 and A2–X1 controls (n = 24). We expected to find spared acqui- pairings, but this learning was hyperspecific—applying sition, but impaired transfer, in the individuals with HA; only to the trained pairings, without any equivalence conversely, we expected slow acquisition, but spared being formed between A1 and A2. Then, although transfer, in the Parkinson’s patients. initial learning may look the same, subsequent learning about A1 should not transfer at all to A2. This would suggest that hippocampal damage or atrophy might RESULTS spare learning during the acquisition phases but impair the ability to transfer. Behavioral Results: Acquisition Phase Conversely, although basal ganglia damage may im- Figure 1 shows the total errors to criterion in the pair the ability to acquire simple stimulus associations, acquisition phase for each group. Analysis of variance it should not directly affect hippocampal processing. (ANOVA) confirmed a significant effect of group, 186 Journal of Cognitive Neuroscience Volume 15, Number 2 Downloaded from http://www.mitpressjournals.org/doi/pdf/10.1162/089892903321208123 by guest on 27 September 2021 Behavioral Results: Transfer Phase Transfer performance was evaluated only in those par- ticipants who successfully mastered all the initial dis- criminations (i.e., who reached criterion in Acquisition Stage 3). In the transfer
Load more

Recommended publications
  • Behavioral Neuroscience Uab Graduate Handbook
    Behavioral Neuroscience Ph.D. Program Policies, Guidelines, & Procedures Student Handbook 2021-2022 University of Alabama at Birmingham Table of Contents Mission Statement __________________________________________ 3 History of the Program _______________________________________ 3 Policies and Procedures ______________________________________ 4 Overview of Student Career ___________________________________ 5 Typical Courses ____________________________________________ 5 Progress Reports ___________________________________________ 6 2nd Year Research Project __________________________________ 7 Qualifying Examination _______________________________________ 8 Dissertation ________________________________________________ 10 Behavioral Neuroscience Student Checklist _______________________ 13 Master’s Degree ____________________________________________ 15 Policies Regarding Adequate Progress __________________________ 16 Policies on Remunerated Activities _____________________________ 16 Vacation, Leave, Holiday Guidelines ____________________________ 17 Degree Requirements and Associated Procedures ________________ 18 2 BEHAVIORAL NEUROSCIENCE PROGRAM Mission Statement and History of the Program Mission Statement Behavioral neuroscience is represented by scientists with interests in the physiological and neural substrates of behavior. The mission of the Behavioral Neuroscience Ph.D. program is to produce outstanding young scientists capable of pursuing independent research careers in the field of behavioral neuroscience by providing graduate
    [Show full text]
  • Joan Y. Chiao
    JOAN Y. CHIAO Department of Psychology Northwestern University 2029 Sheridan Rd, Evanston, IL 60208 Email: [email protected] Phone: 847.467.0481 ACADEMIC POSITIONS 2006-present Assistant Professor, Department of Psychology, Northwestern University Affiliated Faculty, Neuroscience Institute (NUIN) Affiliated Faculty, Cognitive Science Program Affiliated Faculty, Asian American Studies Program Affiliated Faculty, Cognitive Neurology and Alzheimer’s Disease Center Affiliated Faculty, Multidisciplinary Program in Educational Science Affiliated Faculty, Technology and Social Behavior Program Faculty Associate, Institute for Policy Research EDUCATION Ph.D. Harvard University in Psychology, 2001-2006 B.S. Stanford University in Symbolic Systems with Honors, 1996-2000 RESEARCH INTERESTS • Social affective and cultural neuroscience • Race and its influence on perception, cognition and emotion • Psychological and neural mechanisms underlying social status and dominance • Integration of psychology and neuroscience research to public policy and population health issues HONORS, AWARDS and FELLOWSHIPS 2011 Association for Psychological Science Rising Star Award 2011 NIMH Early Career International Travel Award 2006-07 Japan Society for the Promotion of Science Research Fellow 2003-06 National Science Foundation Graduate Research Fellowship 2005 John Merck Summer Institute: Biology of Developmental Disabilities Allport Travel Funds, Harvard George W. Goethals Teaching Prizes, Harvard Cognitive Neuroscience Society Graduate Student Presenter Award
    [Show full text]
  • Glutamate Binding in Primate Brain
    Journal of Neuroscience Research 27512-521 (1990) Quisqualate- and NMDA-Sensitive [3H]Glutamate Binding in Primate Brain A.B. Young, G.W. Dauth, Z. Hollingsworth, J.B. Penney, K. Kaatz, and S. Gilman Department of Neurology. University of Michigan, Ann Arbor Excitatory amino acids (EAA) such as glutamate and Young and Fagg, 1990). Because EAA are involved in aspartate are probably the neurotransmitters of a general cellular metabolic functions, they were not orig- majority of mammalian neurons. Only a few previous inally considered to be likcl y neurotransmitter candi- studies have been concerned with the distribution of dates. Electrophysiological studies demonstrated con- the subtypes of EAA receptor binding in the primate vincingly the potency of these substances as depolarizing brain. We examined NMDA- and quisqualate-sensi- agents and eventually discerned specific subtypes of tive [3H]glutamate binding using quantitative autora- EAA receptors that responded preferentially to EAA an- diography in monkey brain (Macaca fascicularis). alogs (Dingledine et al., 1988). Coincident with the elec- The two types of binding were differentially distrib- trophysiological studies, biochemical studies indicated uted. NMDA-sensitive binding was most dense in that EAA were released from slice and synaptosome dentate gyrus of hippocampus, stratum pyramidale preparations in a calcium-dependent fashion and were of hippocampus, and outer layers of cerebral cortex. accumulated in synaptosomc preparations by a high-af- Quisqualate-sensitive binding was most dense in den- finity transport system. With these methodologies, EAA tate gyrus of hippocampus, inner and outer layers of release and uptake were found to be selectively de- cerebral cortex, and molecular layer of cerebellum.
    [Show full text]
  • Contributions of the Hippocampus and the Striatum to Simple Association and Frequency-Based Learning
    www.elsevier.com/locate/ynimg NeuroImage 27 (2005) 291 – 298 Contributions of the hippocampus and the striatum to simple association and frequency-based learning Dima Amso,a,b,* Matthew C. Davidson,a Scott P. Johnson,b Gary Glover,c and B.J. Caseya aSackler Institute for Developmental Psychobiology, Weill Medical College of Cornell University, 1300 York Avenue, Box 140, New York, NY 10021, USA bDepartment of Psychology, New York University, NY 10003, USA cDepartment of Radiology, Stanford University, CA 94305, USA Received 8 September 2004; revised 30 January 2005; accepted 8 February 2005 Available online 8 April 2005 Using fMRI and a learning paradigm, this study examined the result from how often an event is encountered or how often it is independent contributions of the hippocampus and striatum to simple presented in a particular context or paired with other events. association and frequency-based learning. We scanned 10 right-handed Understanding the neural bases of these types of learning is the young adult subjects using a spiral in/out sequence on a GE 3.0 T objective of this study. scanner during performance of the learning paradigm. The paradigm A common measure of learning, used in both human infant and consisted of 2 cues that predicted each of 3 targets with varying nonhuman animal research, is response to novelty. The theoretical probabilities. Simultaneously, we varied the frequency with which each target was presented throughout the task, independent of cue framework (Sokolov, 1963) underlying these novelty-preference associations. Subjects had shorter response latencies to frequently paradigms is that attention is oriented more toward novel, relative occurring and highly associated target stimuli and longer response to familiar, stimuli.
    [Show full text]
  • Gene Expression of Prohormone and Proprotein Convertases in the Rat CNS: a Comparative in Situ Hybridization Analysis
    The Journal of Neuroscience, March 1993. 73(3): 1258-1279 Gene Expression of Prohormone and Proprotein Convertases in the Rat CNS: A Comparative in situ Hybridization Analysis Martin K.-H. Schafer,i-a Robert Day,* William E. Cullinan,’ Michel Chri?tien,3 Nabil G. Seidah,* and Stanley J. Watson’ ‘Mental Health Research Institute, University of Michigan, Ann Arbor, Michigan 48109-0720 and J. A. DeSeve Laboratory of *Biochemical and 3Molecular Neuroendocrinology, Clinical Research Institute of Montreal, Montreal, Quebec, Canada H2W lR7 Posttranslational processing of proproteins and prohor- The participation of neuropeptides in the modulation of a va- mones is an essential step in the formation of bioactive riety of CNS functions is well established. Many neuropeptides peptides, which is of particular importance in the nervous are synthesized as inactive precursor proteins, which undergo system. Following a long search for the enzymes responsible an enzymatic cascade of posttranslational processing and mod- for protein precursor cleavage, a family of Kexin/subtilisin- ification events during their intracellular transport before the like convertases known as PCl, PC2, and furin have recently final bioactive products are secreted and act at either pre- or been characterized in mammalian species. Their presence postsynaptic receptors. Initial endoproteolytic cleavage occurs in endocrine and neuroendocrine tissues has been dem- C-terminal to pairs of basic amino acids such as lysine-arginine onstrated. This study examines the mRNA distribution of (Docherty and Steiner, 1982) and is followed by the removal these convertases in the rat CNS and compares their ex- of the basic residues by exopeptidases. Further modifications pression with the previously characterized processing en- can occur in the form of N-terminal acetylation or C-terminal zymes carboxypeptidase E (CPE) and peptidylglycine a-am- amidation, which is essential for the bioactivity of many neu- idating monooxygenase (PAM) using in situ hybridization ropeptides.
    [Show full text]
  • Social Neuroscience and Psychopathology: Identifying the Relationship Between Neural Function, Social Cognition, and Social Beha
    Hooker, C.I. (2014). Social Neuroscience and Psychopathology, Chapter to appear in Social Neuroscience: Mind, Brain, and Society Social Neuroscience and Psychopathology: Identifying the relationship between neural function, social cognition, and social behavior Christine I. Hooker, Ph.D. ***************************** Learning Goals: 1. Identify main categories of social and emotional processing and primary neural regions supporting each process. 2. Identify main methodological challenges of research on the neural basis of social behavior in psychopathology and strategies for addressing these challenges. 3. Identify how research in the three social processes discussed in detail – social learning, self-regulation, and theory of mind – inform our understanding of psychopathology. Summary Points: 1. Several psychiatric disorders, such as schizophrenia and autism, are characterized by social functioning deficits, but there are few interventions that effectively address social problems. 2. Treatment development is hindered by research challenges that limit knowledge about the neural systems that support social behavior, how those neural systems and associated social behaviors are compromised in psychopathology, and how the social environment influences neural function, social behavior, and symptoms of psychopathology. 3. These research challenges can be addressed by tailoring experimental design to optimize sensitivity of both neural and social measures as well as reduce confounds associated with psychopathology. 4. Investigations on the neural mechanisms of social learning, self-regulation, and Theory of Mind provide examples of methodological approaches that can inform our understanding of psychopathology. 5. High-levels of neuroticism, which is a vulnerability for anxiety disorders, is related to hypersensitivity of the amygdala during social fear learning. 6. High-levels of social anhedonia, which is a vulnerability for schizophrenia- spectrum disorders, is related to reduced lateral prefrontal cortex (LPFC) activity 1 Hooker, C.I.
    [Show full text]
  • Rhesus Monkey Brain Atlas Subcortical Gray Structures
    Rhesus Monkey Brain Atlas: Subcortical Gray Structures Manual Tracing for Hippocampus, Amygdala, Caudate, and Putamen Overview of Tracing Guidelines A) Tracing is done in a combination of the three orthogonal planes, as specified in the detailed methods that follow. B) Each region of interest was originally defined in the right hemisphere. The labels were then reflected onto the left hemisphere and all borders checked and adjusted manually when necessary. C) For the initial parcellation, the user used the “paint over function” of IRIS/SNAP on the T1 template of the atlas. I. Hippocampus Major Boundaries Superior boundary is the lateral ventricle/temporal horn in the majority of slices. At its most lateral extent (subiculum) the superior boundary is white matter. The inferior boundary is white matter. The anterior boundary is the lateral ventricle/temporal horn and the amygdala; the posterior boundary is lateral ventricle or white matter. The medial boundary is CSF at the center of the brain in all but the most posterior slices (where the medial boundary is white matter). The lateral boundary is white matter. The hippocampal trace includes dentate gyrus, the CA3 through CA1 regions of the hippocamopus, subiculum, parasubiculum, and presubiculum. Tracing A) Tracing is done primarily in the sagittal plane, working lateral to medial a. Locate the most lateral extent of the subiculum, which is bounded on all sides by white matter, and trace. b. As you page medially, tracing the hippocampus in each slice, the superior, anterior, and posterior boundaries of the hippocampus become the lateral ventricle/temporal horn. c. Even further medially, the anterior boundary becomes amygdala and the posterior boundary white matter.
    [Show full text]
  • Strongly Reduced Volumes of Putamen and Thalamus in Alzheimer's Disease
    doi:10.1093/brain/awn278 Brain (2008), 131,3277^3285 Strongly reduced volumes of putamen and thalamus in Alzheimer’s disease: an MRI study L. W. de Jong,1 K. van der Hiele,2 I. M. Veer,1 J. J. Houwing,3 R. G. J. Westendorp,4 E. L. E. M. Bollen,5 P. W. de Bruin,1 H. A. M. Middelkoop,2 M. A. van Buchem1 and J. van der Grond1 1Department of Radiology, 2Section Neuropsychology of the Department of Neurology, 3Department of Medical Statistics, 4Department of Geriatrics and 5Department of Neurology of the Leiden University Medical Center, Leiden, The Netherlands Correspondence to: L. W. de Jong, MD, Department of Radiology, C3-Q, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands E-mail: [email protected] Atrophy is regarded a sensitive marker of neurodegenerative pathology. In addition to confirming the well- known presence of decreased global grey matter and hippocampal volumes in Alzheimer’s disease, this study investigated whether deep grey matter structure also suffer degeneration in Alzheimer’s disease, and whether such degeneration is associated with cognitive deterioration. In this cross-sectional correlation study, two groups were compared on volumes of seven subcortical regions: 70 memory complainers (MCs) and 69 subjects diagnosed with probable Alzheimer’s disease.Using 3T 3D T1MR images, volumes of nucleus accumbens, amyg- dala, caudate nucleus, hippocampus, pallidum, putamen and thalamus were automatically calculated by the FMRIB’s Integrated Registration and Segmentation Tool (FIRST)çalgorithm FMRIB’s Software Library (FSL). Subsequently, the volumes of the different regions were correlated with cognitive test results.
    [Show full text]
  • Social Cognitive Neuroscience: a Review of Core Systems
    C HAPTER 2 2 SOCIAL COGNITIVE NEUROSCIENCE: A REVIEW OF CORE SYSTEMS Bruce P. Doré, Noam Zerubavel, and Kevin N. Ochsner Descartes famously argued that the mind is both SOCIAL COGNITIVE NEUROSCIENCE everlasting and indivisible (Descartes, 1988). If he APPROACH was right about the first part, he is probably pretty In the past decade, the field of social cognitive neuro- impressed with the advance of human knowledge science (SCN) has attempted to fill this gap, integrat- on the second. Although Descartes’ position on ing the theories and methods of two parent the indivisibility of the mind has been echoed at disciplines: social psychology and cognitive neurosci- times in the history of psychology and neurosci- ence. Stressing the interdependence of brain, mind, ence (Flourens & Meigs, 1846; Lashley, 1929; and social context, SCN seeks to explain psychological Uttal, 2003), the modern field has made steady phenomena at three levels of analysis: the neural level progress in demonstrating that subjective mental of brain systems, the cognitive level of information life can be understood as the product of distinct processing mechanisms, and the social level of the functional systems. Today, largely because of the experiences and actions of social agents (Ochsner & success of cognitive neuroscience models, Lieberman, 2001). In contrast to scientific approaches researchers understand that people’s intellectual that grant near exclusive focus to a single level of anal- faculties emerge from the operation of core ysis (e.g., behaviorism, artificial
    [Show full text]
  • Behavioral Neuroscience and Psychopharmacology
    Behavioral Neuroscience and Psychopharmacology The Behavioral Neuroscience and Psychopharmacology area of concentration is designed to train students broadly in the general theoretical principles and technical approaches used to investigate the neurobehavioral mechanisms of alcohol and drug abuse. Psychopharmacological approaches to understanding basic principles of learning are also emphasized. Students receive a concentrated lab experience using either animal models (quail, mice or rats) or human subjects. Faculty in the program use different levels of analysis including cell culture models, neurochemical assays, developmental toxicology, classical conditioning of drug effects, operant conditioning, human behavioral pharmacology, and cognitive approaches to behavior. Students are expected to receive in depth training in at least one level of analysis although training that integrates more than one level of analysis is strongly encouraged. PROGRAM REQUIREMENTS COURSE REQUIREMENTS (1) Statistics sequence: PSY 610 - Experimental design PSY 611 - Correlational design (2) PSY 780 - Directed BNP studies PSY 780A - first year students only PSY 780B - first year and beyond (3) Any three proseminars selected from the following areas: Learning Cognitive processes Developmental Psychology Sensation & Perception Physiological Psychology (4) Four electives (a minimum of one of these must be outside of the Psychology Department) (see listing of some possible options on page **). (5) Additional course work as recommended by the advisory committee RESEARCH REQUIREMENTS It is expected that all students in the BNP area will be involved in research thorough out their course of study towards the Ph.D. The area has two formalized requirements that are designed to train the student in conducting research: (1) Master's thesis (2) Dissertation ALLIED AREA REQUIREMENT Each student is expected to develop an allied area to gain expertise in some area outside of the student's main research specialty.
    [Show full text]
  • 6950.Full.Pdf
    6950 • The Journal of Neuroscience, July 2, 2008 • 28(27):6950–6959 Behavioral/Systems/Cognitive Functional Interaction between the Hippocampus and Nucleus Accumbens Shell Is Necessary for the Acquisition of Appetitive Spatial Context Conditioning Rutsuko Ito,1,3 Trevor W. Robbins,1 Cyriel M. Pennartz,2 and Barry J. Everitt1 1Department of Experimental Psychology, University of Cambridge, Cambridge CB2 3EB, United Kingdom, 2Graduate School Neurosciences Amsterdam, University of Amsterdam, Faculty of Science, Swammerdam Institute for Life Sciences, 1098 SM Amsterdam, The Netherlands, and 3Department of Experimental Psychology, University of Oxford, Oxford OX1 3UD, United Kingdom The nucleus accumbens (NAc) has been implicated in a variety of associative processes that are dependent on the integrity of the amygdala and hippocampus (HPC). However, the extent to which the two subregions of the NAc, the core and shell, form differentiated circuits within the amygdala- and hippocampal-ventral striatal circuitry remains unclear. The present study investigated the effects of selective excitotoxic lesions of the nucleus accumbens shell or core subregion on appetitive elemental cue and context conditioning, shown previously to be dependent on the basolateral amygdala and hippocampus, respectively. Rats were trained sequentially to acquire discrete conditioned stimulus–sucrose conditioning, followed by spatial context–sucrose conditioning in a place preference apparatus characterized by three topographically identical chambers, the chambers being discriminable only on the basis of path integration. NAc shell lesions selectively impaired the acquisition of conditioned place preference and the use of spatial information to retrieve informa- tion about a discrete cue, whereas, as expected, NAc core lesions attenuated the acquisition of cue conditioning compared with sham rats.
    [Show full text]
  • REVIEW Hormones and the Hippocampus
    205 REVIEW Hormones and the hippocampus R Lathe Centre for Genome Research and Centre for Neuroscience, University of Edinburgh, West Mains Road, Edinburgh EH9 3JQ, UK (Requests for offprints should be addressed to R Lathe, Centre for Genome Research, King’s Buildings, West Mains Road, Edinburgh EH9 3JQ, UK; Email: [email protected]) Abstract Hippocampal lesions produce memory deficits, but the Functionally, hippocampal enteroception may reflect feed- exact function of the hippocampus remains obscure. back control; evidence is reviewed that the hippocampus Evidence is presented that its role in memory may be modulates body physiology, including the activity of the ancillary to physiological regulation. Molecular studies hypothalamus–pituitary–adrenal axis, blood pressure, demonstrate that the hippocampus is a primary target for immunity, and reproductive function. It is suggested that ligands that reflect body physiology, including ion balance the hippocampus operates, in parallel with the amygdala, and blood pressure, immunity, pain, reproductive status, to modulate body physiology in response to cognitive satiety and stress. Hippocampal receptors are functional, stimuli. Hippocampal outputs are predominantly inhibi- probably accessible to their ligands, and mediate physio- tory on downstream neuroendocrine activity; increased logical and cognitive changes. This argues that an early synaptic efficacy in the hippocampus (e.g. long-term role of the hippocampus may have been in sensing soluble potentiation) could facilitate throughput inhibition.
    [Show full text]