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Adenovirus, AAV
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Excellgen

Jennifer L Raymond
Stanford University

Project start date: 1999-09-30

Project end date: 2015-01-31


Sponsored Links Excellgen http://Excellgen.com

Baculovirus Protein Expression
Fast turn around, >95% purity functional protein. No outsourcing to China or India. $5500, $3950
Recombinant Lentivirus & Adenovirus
High Yield and High Titer up to 1010 (lentivirus) and 1013 (adenovirus) for Guaranteed Expression of GOI. $3000, $2500
Transient Protein Expression in CHO and HEK293 Cells
Transient Expression, Truly Functional Protein, 95% purity, 1~20 mg, fast turnaround. $5500, $3950

Vestibular And Visual Control Of Eye Movement

Jennifer L Raymond, Assistant Professor
Stanford University Stanford, Ca 94305

Grant 5R01DC004154-08 from National Institute On Deafness And Other Communication Disorders IRG: SMI

Abstract: The vestibulo-ocular reflex (VOR) reduces motion of visual images on the retina by evoking eye movements in the opposite direction to head movements. A form of motor learning, known as VOR adaptation, calibrates the VOR by gradually correcting the reflex when image motion is persistently associated with head turns. VOR adaptation is essential for ensuring adequate visual acuity during head turns and for restoring proper motor and perceptual orientation in space in response to changes in the organism or its environment, such as occur with growth and development, aging, injury to the peripheral or central nervous system or the donning of a new pair of spectacles. The proposed experiments examine the neural mechanisms of VOR adaptation through a systematic analysis of the correlation between 1) the patterns of neural activity present in the circuit for the VOR during the induction of learning, 2) the altered activity in the circuit during the expression of learning, and 3) the behavioral changes that are induced. The VOR is one of many motor systems that are thought to rely on cerebellum-dependent learning to maintain normal sensorimotor function and for recovery of function following injury. The anatomy and physiology of the cerebellum is very regular across the extent of this structure, therefore, the principles uncovered in studies of VOR adaptation may be useful for the development of rational therapeutic approaches for many forms of sensorimotor dysfunction.

Keywords: eye movement, neural information processing, neuroregulation, vestibuloocular reflex, biological signal transduction, cerebellar Purkinje cell, cerebellar cortex, cerebellum, head movement, neural plasticity, retina, sensorimotor system, smooth pursuit eye movement, visual stimulus, Macaca mulatta, electrode, single cell analysis, statistics /biometry

Project start date: 1999-09-30

Project end date: 2009-05-31

5R01DC004154-08 (2007): $282783


5R01DC004154-07 (2006): $291066

5R01DC004154-05 (2003): $338081

5R01DC004154-04 (2002): $328232

5R01DC004154-03 (2001): $318675

5R01DC004154-02 (2000): $294486


Grants awarded to Jennifer L Raymond

CIRCUIT ANALYSIS BY RAPID SILENCING OF SPECIFIC INTERNEURON POPULATIONS IN VIVO

Jennifer L Raymond, Associate Professor
Stanford University, 340 Panama Street, Stanford, Ca 94305-6203

Grant 3R21NS057488-02S1 from National Institute Of Neurological Disorders And Stroke

Abstract: This project is the initial phase of a systematic research program for the functional dissection of a neural circuit. The experimental approach employs some of the latest transgenic techniques to rapidly and reversibly inactivate distinct classes of interneurons and analyzes the impact of this intervention on both signaling in the neural circuit and behavior. This strategy should yield a deeper and more comprehensive understanding of how a circuit´s architecture shapes neural computations. The proposed experiments focus specifically on analysis of neural circuit function in the cerebellum, a brain structure that plays a central role in motor learning and the coordination of movements. The first Aim of the project is to generate transgenic animals that can be used to rapidly and reversibly inactivate a class of cerebellar interneurons called Golgi cells in a restricted region of the cerebellum, without perturbing any other neurons in the brain. The second Aim of the project is to use the mice generated in the first Aim to analyze the contribution of the Golgi cells to the neural computations supporting the generation of movements with appropriate amplitude and timing. These experiments represent the first step in a systematic analysis of how the different classes of neurons in the cerebellum and other neural circuits support the computational functions supporting perception and action. Many diseases of the nervous system involve the malfunction of neural networks caused by the degeneration of specific classes of neurons. This proposed research develops an experimental approach for analyzing how the function of neural networks is disrupted by the loss of specific populations of neurons. The results will aid in the development of rational therapeutic interventions for pathological states of the nervous system resulting from the degeneration of specific classes of neurons

Keywords: Architecture; Behavior; Behavior Conditioning Therapy; Behavior Modification; Behavior Therapy; Behavior Treatment; Behavior or Life Style Modifications; Behavioral; Behavioral Conditioning Therapy; Behavioral Modification; Behavioral Therapy; Behavioral Treatment; Biological Neural Networks; Brain; Brain region; Cell Communication and Signaling; Cell Signaling; Cells; Cerebellar Cortex; Cerebellar cortex structure; Cerebellum; Classification; Conditioning Therapy; Connector Neuron; DISSEC; Development; Dissection; Electrophysiology; Electrophysiology (science); Encephalon; Encephalons; Engineering / Architecture; Foundations; Future; Gene Targeting; Generations; Golgi; Golgi Apparatus; Golgi Complex; Individual; Influentials; Intercalary Neuron; Intercalated Neurons; Interneurons; Internuncial Cell; Internuncial Neuron; Intervention; Intervention Strategies; Intracellular Communication and Signaling; Learning; Life Style Modification; Mammals, Mice; Methods; Methods and Techniques; Methods, Other; Mice; Modeling; Models, Theoretic; Movement; Murine; Mus; NRVS-SYS; Nerve Cells; Nerve Unit; Nervous; Nervous System; Nervous System Diseases; Nervous System, Brain; Nervous system structure; Neural Cell; Neural Transmission; Neurocyte; Neurologic Body System; Neurologic Disorders; Neurologic Organ System; Neurological Disorders; Neurons; Neurophysiology / Electrophysiology; Perception; Phase; Play; Population; Programs (PT); Programs [Publication Type]; Property; Property, LOINC Axis 2; Reflex, Vestibulo-Ocular; Reflexes, Vestibo-Ocular; Reflexes, Vestibuloocular; Research; Role; Shapes; Signal Transduction; Signal Transduction Systems; Signaling; Specificity; Structure; Synaptic Transmission; Systematics; Targetings, Gene; Techniques; Testing; Theoretical model; Therapeutic Intervention; Time; Transgenic Animals; Transgenic Organisms; Work; base; behavior intervention; behavioral intervention; biological signal transduction; body movement; computerized data processing; data processing; experiment; experimental research; experimental study; in vivo; intervention therapy; interventional strategy; locomotor learning; motor learning; nervous system disorder; neural; neural circuit; neural circuitry; neural network; neurological disease; neuronal; programs; relating to nervous system; research study; signal processing; social role; theories; transgenic; vestibulo-ocular reflex

Project start date: 2007-05-15

Project end date: 2010-03-31

Budget start date: 15-AUG-2009

Budget end date: 31-MAR-2010

PFA/PA: PA-06-181

3R21NS057488-02S1 (2009): $40000


1R21NS057488-01A1 (2007): $246793

DEVELOPMENT OF A MODEL TO STUDY LEARNING IN THE VOR

Jennifer L Raymond, Assistant Professor
University Of California San Francisco 3333 California St., Ste 315 San Francisco, Ca 941430962

Grant 1R03DC003342-01 from National Institute On Deafness And Other Communication Disorders IRG: ZDC1

Abstract: The vetibulo-ocular refle (VOR) reduces motion of images on the retina by evoking eye movements in the opposite direction from head movement. Motor learning calibrates the VOR gradually correcting the reflex whenever image motion is persistently associate with heat turns. In addition, motor learning in the VOR in the VOR depends critically on the function of the cerebellum, and the principles uncovered in studies of the VOR may apply generally to many motor systems that are thought to rely on cerebellum- dependent learning to maintain normal sensory-motor function and for recovery of function following brain damage. The investigator proposes to develop a model system that would take advantage of the genetic tools as well the pharmacological and surgical manipulations available in the mouse to study motor learning in the VOR. Gene knockout mice will be used to more directly link cellular pathways to cerebellar physiology and physiology to motor learning in the VOR. This application aims to perform the necessary preliminary of the basic behavior and physiology of the VOR in normal mice and to begin to use some interesting cerebellar mutants that are available to analyze the neural mechanisms for the induction of learning.

Keywords: learning, model design /development, psychological model, vestibuloocular reflex, head movement, mutant, psychomotor function, smooth pursuit eye movement, behavioral /social science research tag, gene targeting, laboratory mouse, neuropsychological test, transgenic animal

Project start date: 1997-05-01

Project end date: 1999-04-30

1R03DC003342-01 (1997): $49244


5R03DC003342-02 (1998): $50864

Vestibular And Visual Control Of Eye Movement

Jennifer L Raymond, Assistant Professor
Stanford University Stanford, Ca 94305

Grant 2R01DC004154-06A1 from National Institute On Deafness And Other Communication Disorders IRG: SMI

Abstract: The vestibulo-ocular reflex (VOR) reduces motion of visual images on the retina by evoking eye movements in the opposite direction to head movements. A form of motor learning, known as VOR adaptation, calibrates the VOR by gradually correcting the reflex when image motion is persistently associated with head turns. VOR adaptation is essential for ensuring adequate visual acuity during head turns and for restoring proper motor and perceptual orientation in space in response to changes in the organism or its environment, such as occur with growth and development, aging, injury to the peripheral or central nervous system or the donning of a new pair of spectacles. The proposed experiments examine the neural mechanisms of VOR adaptation through a systematic analysis of the correlation between 1) the patterns of neural activity present in the circuit for the VOR during the induction of learning, 2) the altered activity in the circuit during the expression of learning, and 3) the behavioral changes that are induced. The VOR is one of many motor systems that are thought to rely on cerebellum-dependent learning to maintain normal sensorimotor function and for recovery of function following injury. The anatomy and physiology of the cerebellum is very regular across the extent of this structure, therefore, the principles uncovered in studies of VOR adaptation may be useful for the development of rational therapeutic approaches for many forms of sensorimotor dysfunction.

Keywords: eye movement, neural information processing, neuroregulation, vestibuloocular reflex, biological signal transduction, cerebellar Purkinje cell, cerebellar cortex, cerebellum, head movement, neural plasticity, retina, sensorimotor system, smooth pursuit eye movement, visual stimulus, Macaca mulatta, electrode, single cell analysis, statistics /biometry

Project start date: 1999-09-30

Project end date: 2008-05-31

2R01DC004154-06A1 (2005): $297870


3R01DC004154-05S1 (2004): $100000

THE ROLES OF PRESYNAPTIC PLASTICITY IN CIRCUIT FUNCTION AND BEHAVIOR

Jennifer L Raymond
Stanford University, 340 Panama Street, Stanford, Ca 94305-6203

Abstract: Project #4 The Role of Presynaptic Plasticity in Circuit Function and Behavior Long-lasting changes in synaptic efficacy are thought to mediate many of the changes in neural circuit function and behavior that occur during development, learning, and recovery from injury. Such long-term synaptic plasticity can be accomplished through either the modification of presynaptic terminals to alter the the amount of neurotransmitter released by an action potential, or through the modification of the postsynaptic machinery to alter the amplitude of the response to a given amount of transmitter. Some synapses, such as the ones we will focus on in this project, exhibit both presynaptic and postsynaptic forms of plasticity, which suggests that these processes are not simply different means to the same end. Rather, pre- and postsynaptic plasticity mechanisms may play distinct roles in the modification of signal processing in a neural circuit. A vast majority of the work on neural plasticity has focused on postsynaptic plasticity. In this Program Project, we focus on presynaptic plasticity. Projects #1-3 will investigate the molecular, biochemical, and cellular mechanisms of presynaptic plasticity. The results from those projects will yield increasingly precise tools for manipulating presynaptic plasticity in vivo. In Project #4, we will use those tools to analyze how presynaptic plasticity functions in an intact circuit, more specifically, in the well-characterized cerebellar circuit that supports motor learning in the vestibulo-ocular reflex. In Aim #1, we will conduct a detailed behavioral analysis to determine which aspects of motor learning are impaired when presynaptic plasticity is disrupted. In Aim #2, we will record in vivo from individual neurons in the cerebellum, to assess which learning-related changes in neural signaling depend on presynaptic plasticity. In Aim #3, we will perform neural network simulations to integrate the synaptic, circuit level, and behavioral results from the Program Project into a coherent model. Our experiments will help resolve some ongoing controversies about the neural mechanisms of motor learning, and also will serve as a platform for testing more general ideas about the function of presynaptic plasticity in the nervous system. Finally, our results will generate new questions about presynaptic function that can be tested in reduced preparations by our PPG collaborators

Keywords: Action Potentials; Address; Axon Terminals; Behavior; Behavioral; Biochemical; Biological Neural Networks; CNS plasticity; Cell Communication and Signaling; Cell Signaling; Cerebellar Cortex; Cerebellar cortex structure; Cerebellum; Collaborations; Computer Analysis; Connectionist Models; Development; Exhibits; Family; Fiber; Foundations; Frequencies (time pattern); Frequency; Future; Goals; In Vitro; Individual; Injury; Intracellular Communication and Signaling; Investigators; Knockout Mice; Learning; Mammals, Mice; Mediating; Methods; Mice; Mice, Knock-out; Mice, Knockout; Mice, Mutant Strains; Modeling; Modification; Molecular; Murine; Mus; Mutant Strains Mice; NRVS-SYS; Nerve Cells; Nerve Endings, Presynaptic; Nerve Unit; Nervous; Nervous System; Nervous system structure; Neural Cell; Neural Network Models; Neural Network Simulation; Neural Networks (Computer); Neurocyte; Neurologic Body System; Neurologic Organ System; Neuronal Plasticity; Neurons; Neurosciences; Null Mouse; Operation; Operative Procedures; Operative Surgical Procedures; Output; Perceptrons; Phase; Phenotype; Physiology; Play; Preparation; Presynaptic Terminals; Process; Programs (PT); Programs [Publication Type]; Proteins; Publishing; Purkinje Cells; Purkinje`s Corpuscles; Recovery; Reflex, Vestibulo-Ocular; Reflexes, Vestibo-Ocular; Reflexes, Vestibuloocular; Regulation; Research; Research Personnel; Researchers; Role; Signal Transduction; Signal Transduction Systems; Signaling; Site; Slice; Stimulus; Surgical; Surgical Interventions; Surgical Procedure; Synapses; Synaptic; Synaptic Boutons; Synaptic Terminals; Synaptic plasticity; System; System, LOINC Axis 4; Testing; Training; Translations; Work; biological signal transduction; cerebellar Purkinje cell; computational analysis; computerized data processing; data processing; experiment; experimental research; experimental study; gene product; in vivo; locomotor learning; motor learning; mouse mutant; mutant; neural; neural circuit; neural circuitry; neural mechanism; neural network; neural network (computer simulation of nervous system); neural plasticity; neuromechanism; neuronal; neuroplasticity; neurotransmitter release; postsynaptic; presynaptic; programs; relating to nervous system; research study; response; signal processing; social role; surgery; technique development; tool; trafficking; vestibulo-ocular reflex; visual-vestibular

Budget start date: 1-SEP-2010

Budget end date: 31-AUG-2011

5P01NS053862-05_0004 (2010): $206435


5P01NS053862-04_0004 (2009): $219193

INSTRUCTIVE SIGNALS FOR MOTOR LEARNING

Jennifer L Raymond
Stanford University, 340 Panama Street, Stanford, Ca 94305-6203

Grant 1R01NS072406-01 from National Institute Of Neurological Disorders And Stroke

Abstract: Motor learning is the process by which movements become smooth and accurate through practice. Motor learning is important during early childhood development, and continues throughout adulthood, because the neural circuits controlling our movements need to be recalibrated in response to changes in the brain or body due to injury, disease, or the normal aging process. Motor learning depends on a brain region called the cerebellum, and patients with cerebellar dysfunction have clumsy, uncoordinated movements. One of the two main inputs to the cerebellum is the "climbing fiber" input from the inferior olive in the brainstem. An influential theory of cerebellar function suggested that the climbing fibers carry the error signals that control motor learning. However, recent evidence suggests that motor learning can occur in the absence of instructive signals in the climbing fibers. Thus, there seems to be more than one way to implement motor learning in the brain. The goal of this project is to determine which aspects of motor learning are controlled by the activity of the climbing fibers, and which aspects of learning rely on other neural mechanisms. This question will be addressed by studying the eye movement responses to vestibular stimuli (i.e., the sensory signals encoding movements of the head) and their regulation by motor learning. Most, if not all, movements are guided by vestibular signals. The eye movement response to a vestibular stimulus is called the vestibulo-ocular reflex (VOR). This vestibular reflex functions to stabilize visual images on the retina, and is essential for maintaining good vision during movements of the body. Both the amplitude and the timing of the eye movements driven by the VOR can be adaptively modified by cerebellum-dependent learning, and thus the VOR serves as a model system for studying the neural mechanisms controlling movement amplitude and timing more generally. An important characteristic of neural circuits is their plasticity, their ability to change with experience and to compensate when injury or disease damages the nervous system. This project studies the error signals that guide the changes in a neural circuit during learning. An improved understanding of this process will inform the development of more effective interventions for a broad range of neurological and psychiatric disorders

Keywords: 21+ years old; Address; Adult; Aging Process; Aging-Related Process; Algorithms; Back; Behavior; Behavioral; Biological Models; Brain; Brain Stem; Brain region; Brainstem; Cell Communication and Signaling; Cell Signaling; Cerebellar Diseases; Cerebellar Disorders; Cerebellar Dysfunction; Cerebellar Syndromes; Cerebellum; Cerebellum Diseases; Characteristics; Complex; Darkness; Darknesses; Data; Development; Disease; Disorder; Dorsum; Encephalon; Encephalons; Eye Movements; Fiber; Goals; Head Movements; Human, Adult; Image; Inferior; Influentials; Injury; Intracellular Communication and Signaling; Learning; Mammals, Mice; Mental disorders; Mental health disorders; Methods and Techniques; Methods, Other; Mice; Model System; Models, Biologic; Molecular; Molecular Genetic; Molecular Genetics; Monitor; Movement; Murine; Mus; Nerve Cells; Nerve Unit; Nervous; Nervous System Injuries; Nervous System Trauma; Nervous System damage; Nervous System, Brain; Neural Cell; Neurocyte; Neurologic; Neurological; Neurological Damage; Neurological Injury; Neurological trauma; Neurons; Olives; Olives - dietary; Patients; Phase; Play; Process; Programs (PT); Programs [Publication Type]; Property; Property, LOINC Axis 2; Psychiatric Disease; Psychiatric Disorder; Reflex, Vestibulo-Ocular; Reflexes, Vestibo-Ocular; Reflexes, Vestibuloocular; Regulation; Research; Retina; Role; Sensory; Sight; Signal Transduction; Signal Transduction Systems; Signaling; Stimulus; System; System, LOINC Axis 4; Techniques; Time; Training; Trauma, Nervous System; Unspecified Mental Disorder; Vision; Visual; adult human (21+); biological signal transduction; body movement; disease/disorder; early childhood; effective intervention; experience; experiment; experimental research; experimental study; imaging; improved; in vivo; insight; locomotor learning; mental illness; motor learning; neural; neural circuit; neural circuitry; neural mechanism; neuromechanism; neuronal; normal aging; ocular motor; ocularmotor; oculomotor; programs; psychological disorder; public health relevance; relating to nervous system; research study; response; social role; theories; vestibular reflex; vestibulo-ocular reflex; visual stimulus; visual-vestibular

Relevance: An important characteristic of neural circuits is their plasticity, their ability to change with experience and to compensate when injury or disease damages the nervous system. This project studies the error signals that guide the changes in a neural circuit during learning. An improved understanding of this process will inform the development of more effective interventions for a broad range of neurological and psychiatric disorders

Project start date: 2010-09-01

Project end date: 2015-07-31

Budget start date: 1-SEP-2010

Budget end date: 31-JUL-2011

PFA/PA: PA-10-067

1R01NS072406-01 (2010): $443971


VESTIBULAR AND VISUAL CONTROL OF EYE MOVEMENT

Jennifer L Raymond, Associate Professor
Stanford University, 340 Panama Street, Stanford, Ca 94305-6203

Grant 2R01DC004154-09A1 from National Institute On Deafness And Other Communication Disorders

Abstract: Motor learning is the process by which movements become smooth and accurate through practice. Motor learning depends on a brain region called the cerebellum, and patients with cerebellar dysfunction have clumsy, uncoordinated movements. This project examines the error signals that guide motor learning. Which neurons in the cerebellum or related neural circuitry monitor the accuracy of a movement, and determine when the motor program controlling that movement needs to be updated? For decades it was thought that the "climbing fiber" input to the cerebellum from the inferior olive provided the sole instructive signal guiding motor learning. However, we recently showed that motor learning could be induced under training conditions that elicit no response in the climbing fibers. The proposed experiments analyze this climbing fiber-independent component of motor learning. In particular, we will examine the origin of the instructive signals controlling this component of learning, and we will determine which aspects of movement it can and cannot regulate. This project capitalizes on the experimental tractability of eye movements, in particular the vestibulo-ocular reflex (VOR), to analyze the neural mechanisms of motor learning. The VOR is a reflexive eye movement that reduces motion of visual images on the retina by evoking eye movements in the opposite direction to head movements. A form of motor learning, known as VOR adaptation, calibrates the VOR by gradually correcting the reflex when image motion is persistently associated with head turns. VOR adaptation is essential for ensuring adequate visual acuity during head turns and for restoring proper motor and perceptual orientation in space in response to changes in the organism or its environment, such as occur with growth and development, aging, injury to the peripheral or central nervous system or the donning of a new pair of spectacles. This project will improve our understanding of the neural mechanisms controlling the induction of learning. This improved understanding should facilitate the design of effective remediation strategies for disorders of learning and memory and rehabilitation strategies for CNS or peripheral injury

Keywords: Address; Aging; Algorithms; Area; Behavioral; Brain; Brain region; Cell Communication and Signaling; Cell Signaling; Central Nervous System; Cerebellar Diseases; Cerebellar Disorders; Cerebellar Dysfunction; Cerebellar Syndromes; Cerebellum; Cerebellum Diseases; Cognition; DISSEC; Darkness; Darknesses; Dissection; Electric Stimulation; Electrical Stimulation; Electrophysiology; Electrophysiology (science); Encephalon; Encephalons; Ensure; Environment; Event; Eye Movements; Eyeglasses; Fiber; Funding; Growth and Development; Growth and Development function; Head; Head Movements; Heart; Image; Inferior; Injury; Intracellular Communication and Signaling; Laboratories; Learning; Learning Disorders; Macaca mulatta; Mammals, Mice; Memory; Mice; Mining; Minings; Monitor; Motion; Motor; Movement; Murine; Mus; Nerve Cells; Nerve Unit; Nervous; Nervous System, Brain; Nervous System, CNS; Neural Cell; Neuraxis; Neurocyte; Neurons; Neurophysiology / Electrophysiology; Olives; Olives - dietary; Organism; Output; Patients; Peripheral; Phase; Physiologic; Physiological; Play; Process; Programs (PT); Programs [Publication Type]; Purkinje Cells; Purkinje`s Corpuscles; Reflex; Reflex action; Reflex, Vestibulo-Ocular; Reflexes, Vestibo-Ocular; Reflexes, Vestibuloocular; Retina; Rhesus; Rhesus Macaque; Rhesus Monkey; Role; Senescence; Sensory; Signal Transduction; Signal Transduction Systems; Signaling; Spectacles; Stimulus; Structure; Training; Update; Visual Acuity; Visual Motion; biological signal transduction; body movement; cerebellar Purkinje cell; design; designing; experiment; experimental research; experimental study; imaging; improved; in vivo; limb movement; living system; locomotor learning; motor learning; neural; neural circuit; neural circuitry; neural mechanism; neuromechanism; neuronal; new approaches; novel approaches; novel strategies; novel strategy; programs; rehab strategy; rehabilitation strategy; relating to nervous system; remediation; research study; response; senescent; social role; vestibulo-ocular reflex; visual control; visual stimulus

Relevance: This project will improve our understanding of the neural mechanisms controlling the induction of learning. This improved understanding should facilitate the design of effective remediation strategies for disorders of learning and memory and rehabilitation strategies for CNS or peripheral injury

Project start date: 1999-09-30

Project end date: 2015-01-31

Budget start date: 5-FEB-2010

Budget end date: 31-JAN-2011

PFA/PA: PA-07-070

2R01DC004154-09A1 (2010): $350142


Sponsored Links Excellgen http://Excellgen.com

Recombinant Lentivirus & Adenovirus
High Yield and High Titer up to 1010 (lentivirus) and 1013 (adenovirus) for Guaranteed Expression of GOI. $3000, $2500
Baculovirus Protein Expression
Fast turn around, >95% purity functional protein. No outsourcing to China or India. $5500, $3950
Transient Protein Expression in CHO and HEK293 Cells
Transient Expression, Truly Functional Protein, 95% purity, 1~20 mg, fast turnaround. $5500, $3950

Jennifer L Raymond
Stanford University

Project start date: 2010-09-01

Project end date: 2015-07-31


The Roles Of Presynaptic Plasticity In Circuit Function And Behavior

Jennifer L Raymond, Assistant Professor
Stanford University Stanford, Ca 94305

Grant 5P01NS053862-020004 from National Institute Of Neurological Disorders And Stroke IRG: NSD

Keywords: NMDA receptor, behavior, cerebellum, experience, neurotransmitter transport, protein, role


MODULATORY PATHWAYS FOR SIMPLE FORMS OF LEARNING

Jennifer L Raymond, Assistant Professor
University Of Texas Hlth Sci Ctr Houston Box 20036 Houston, Tx 77225

Grant 1F31MH010214-01A1 from National Institute Of Mental Health IRG: CFN

1F31MH010214-01A1 (1992): $11800