DAVID H. FARB, Ph.D.
Professor and Chairman
Department of Pharmacology and Experimental Therapeutics
Director, Program in Biomedical Neuroscience
Boston University School of Medicine
Department of Pharmacology
Office: L-603
Phone: 617-638-4300; Fax: 617-638-4329
Lab Phone: 617-638-5323
Email: dfarb
Ph.D.: Brandeis University
Laboratory Page: Laboratory of Molecular Neurobiology
Recent News Concerning Dr. Farb
Dr. David Farb interviewed by NPR about biomedical funding
Dr. Farb interviewed by the BBC as a part of their “Visions of the Future” series
Abstract Selected by Society for Neuroscience
Dr. Farb is a winner of the 2006 Boston University Ignition Award
Dr. Farb – Content Reviewer for NOVA Science Now “Mirror Neurons”
Dr. David Farb interviewed by ABC News ‘A Perfect Storm’ for Creating Drug Addicts
Professional Background:
David H. Farb was appointed Professor and Chairman of the Department of Pharmacology & Experimental Therapeutics at Boston University School of Medicine in 1990. Dr. Farb chairs the Executive Committee for the Medical Sciences Training Program, is Director of the university-wide NIGMS training program in Biomolecular Pharmacology and Co-Director of the interdepartmental Program in Biomedical Neuroscience, is a member of the Bioinformatics Program, and heads the Laboratory of Molecular Neurobiology. He has also served as neurosciences consultant for WGBH-Boston PBS affiliate on the NOVA episode, “Mirror Neurons” and, as a member of the Drug Development Work Group of Mass Insight, co-authored the Massachusetts Technology Road Map for Drug Discovery.
Prior to joining BU, Dr. Farb was a Fogarty Senior International Fellow (1989 – 1990) with Sydney Brenner, PhD in the Molecular Genetics Unit at the Medical Research Council, Cambridge University, UK. Dr. Farb received his B.A. in Chemistry from Long Island University, where he was President of the American Chemical Society chapter and received honors including the American Institute of Chemists Award. He received the Ph.D. in Biochemistry (enzyme mechanisms/bioorganic chemistry) with William P. Jencks, M.D. at Brandeis University. After completing postdoctoral fellowships at Harvard Medical School in Pharmacology with Gerald D. Fischbach, M.D. and in Physiology with Susan E. Leeman, Ph.D., he became Assistant Professor of Anatomy and Cell Biology at the SUNY Downstate Medical Center. Dr. Farb was promoted to full professor with tenure, Head of the Molecular Pharmacology Research Program, and elected Presiding Officer of the Graduate School at SUNY. While in New York, Dr. Farb was elected Chair of the Section of Biological Sciences at the New York Academy of Sciences, where he subsequently founded the Section of Neuroscience. Dr. Farb has served as a consultant to large and small pharmaceutical companies, intellectual property law and portfolio investment firms. Dr. Farb was a member of the founding Scientific Advisory Boards of CoCensys and DOV Pharmaceuticals. He holds 9 issued U.S. patents and one patent issued in Australia. Dr. Farb pioneered development of technology for high throughput electrophysiology and was the Scientific Founder of Scion Pharmaceuticals (acquired by Wyeth), which commercialized his patents on high throughput electrophysiology and small molecule modulators of amino acid receptors. High throughput electrophysiology is currently in use throughout the pharmaceutical industry for ion channel and receptor directed drug discovery.
As a postdoctoral fellow, Dr. Farb, in collaboration with Dr. Dennis W. Choi and Dr. Gerald D. Fischbach, co-discovered the cellular mechanisms of action of benzodiazepines—the class of anxiolytics, sedative hypnotics, and anticonvulsants that includes trade-name drugs such as Xanax, Valium, and Versed. This research showed that benzodiazepines acted by positive allosteric modulation of the type-A GABA receptor (Nature (1977) 269: 342-344). Dr. Farb’s research program focused on the turnover and regulation of GABA receptor function (Science (1984) 226: 857) as a nexus for the control of nervous system function. Dr. Farb’s current research is directed toward the discovery and development of neuromodulators as therapeutic agents and on the structure, function, and cellular dynamics of ion channels and receptors in the brain and spinal cord. Ongoing studies are directed toward understanding the mechanisms of action of abused substances and steroid modulators (Science Signaling (2000) 60: PE1) and their interactions with excitatory and inhibitory amino acid receptors in the central nervous system. Recently, Dr. Farb’s laboratory demonstrated that pregnanolone hemisuccinate inhibits reinstatement of cocaine seeking behavior, and this compound has been selected by NIDA for preclinical development in its Medications Development Program (PNAS (1997) 94: 10450; PNAS (2004) 101: 8198).
Selected Publications:
Brezhnoy, D., Gibbs T.T., & Farb D.H. (2009). Docking of 1,4-benzodiazepines in the α1/γ2 GABAAR modulator site. Molecular Pharmacology. 2009 May 29. [Epub ahead of print].
Desbiens, S.C., & Farb, D.H. (2009). Current needs for new therapeutic agents and discovery strategies – A systems pharmacology approach. In S. Gad (Ed), Development of Therapeutic Agents. John Wiley and Sons (Hoboken, NJ). In press.
Sadri-Vakili G., Janis, G.C., Pierce, R.C., Gibbs, T.T., Farb, D.H. (2008) Nanomolar Concentration of Pregnenolone Sulfate Enhance Striatal Dopamine Overflow In Vivo. J Pharmacol Exp Ther. 2008 Sep 4 [Epub ahead of print].
Whittaker, M.T., Gibbs, T.T., Farb, D.H. (2008) Pregnenolone sulfate induce NMDA receptor dependent release of dopamine from synaptic terminals in the striatum. J Neurochem 2008 Aug 14 [Epub ahead of print].
Berezhnoy, D., Gravielle, M.C., Downing, S., Kostakis, E., Basile, A.S., Skolnick, P., Gibbs, T.T., Farb, D.H. (2008) Pharmacological Properties of DOV 315,090, an ocinaplon metabolite. BMC Pharmacol. 2008, Jun 13; 8 (1):11. [Epub ahead of print].
Kim, J., Farb, D. H. and Russek, S. J. (2008) Promoter Structure. Encyclopedia of Neuroscience, Springer Publishing, In Press.
Hu, Y., Lund, I. V., Gravielle, M. C., Farb, D. H., Brooks-Kayal, A. R., and Russek, S. J. (2008) Surface expression of GABA(A) receptors is transcriptionally controlled by the interplay of CREB and its binding partner ICER. J. Biol. Chem. Apr 4; 283(14): 9328-40. Jan 7; [Epub ahead of print]
D. Berezhnoy, M.C. Gravielle, and D.H. Farb (2007) Pharmacology of the GABAA Receptor, In: Handbook of Contemporary Neuropharmacology (David Sibley, Michael Kuhar, Israel Hanin, and Phil Skolnick, Eds.) John Wiley & Sons.
D.H. Farb, J.L. Steiger, S.C. Martin, M.C. Gravielle, T.T. Gibbs, and S.J. Russek (2007) Mechanisms of GABAA and GABAB Receptor Gene Expression In: The GABA Receptors (Sam Enna and Hans Mohler, Eds.) Humana Press.
Gibbs TT, Russek SJ, Farb DH. Sulfated steroids as endogenous neuromodulators. Pharmacol Biochem Behav. 2006 Aug;84(4):555-67. Epub 2006 Oct 4. [ Abstract ]
Popik P, Kostakis E, Krawczyk M, Nowak G, Szewczyk B, Krieter P, Chen Z, Russek SJ, Gibbs TT, Farb DH, Skolnick P, Lippa AS, Basile AS. The anxioselective agent 7-(2-chloropyridin-4-yl)pyrazolo-[1,5-a]-pyrimidin-3-yl](pyridin-2-yl)methan one (DOV 51892) is more efficacious than diazepam at enhancing GABA-gated currents at alpha1 subunit-containing GABAA receptors. J Pharmacol Exp Ther. 2006 Dec;319(3):1244-52. Epub 2006 Sep 13. [ Abstract ]
Downing SS, Lee YT, Farb DH, Gibbs TT. Benzodiazepine modulation of partial agonist efficacy and spontaneously active GABA(A) receptors supports an allosteric model of modulation. Br J Pharmacol. 2005 Aug;145(7):894-906. [ Abstract ]
Lippa A, Czobor P, Stark J, Beer B, Kostakis E, Gravielle M, Bandyopadhyay S, Russek SJ, Gibbs TT, Farb DH, Skolnick P. (2005) Selective anxiolysis produced by ocinaplon, a GABA(A) receptor modulator. Proc Natl Acad Sci U S A. 2005 May 17;102(20):7380-5. Epub 2005 May 3. [ Abstract ]
Gravielle MC, Faris R, Russek SJ, Farb DH. (2005) GABA induces activity dependent delayed-onset uncoupling of GABA/benzodiazepine site interactions in neocortical neurons. J Biol Chem. 2005 Jun 3;280(22):20954-60. Epub 2005 Apr 1. [ Abstract ]
Steiger JL, Bandyopadhyay S, Farb DH, Russek SJ. (2004) cAMP response element-binding protein, activating transcription factor-4, and upstream stimulatory factor differentially control hippocampal GABABR1a and GABABR1b subunit gene expression through alternative promoters. J Neurosci. 2004 Jul 7;24(27):6115-26. [ Abstract ]
Jang MK, Mierke DF, Russek SJ, Farb DH. (2004) A steroid modulatory domain on NR2B controls N-methyl-D-aspartate receptor proton sensitivity. Proc Natl Acad Sci U S A. 2004 May 25;101(21):8198-203. Epub 2004 May 18. [ Abstract ]
Martin SC, Steiger JL, Gravielle MC, Lyons HR, Russek SJ, Farb DH. (2004) Differential expression of gamma-aminobutyric acid type B receptor subunit mRNAs in the developing nervous system and receptor coupling to adenylyl cyclase in embryonic neurons. J Comp Neurol. 2004 May 17;473(1):16-29. [ Abstract ]
Steiger JL, Alexander MJ, Galler JR, Farb DH, Russek SJ. (2004) Effects of prenatal malnutrition on GABAA receptor alpha1, alpha3 and beta2 mRNA levels. Neuroreport. 2003 Sep 15;14(13):1731-5. [ Abstract ]
Sadri-Vakili G, Johnson DW, Janis GC, Gibbs TT, Pierce RC, Farb DH. (2003) Inhibition of NMDA-induced striatal dopamine release and behavioral activation by the neuroactive steroid 3alpha-hydroxy-5beta-pregnan-20-one hemisuccinate. J Neurochem. 2003 Jul;86(1):92-101. [ Abstract ]
Steiger JL, Galler JR, Farb DH, Russek SJ. (2002) Prenatal protein malnutrition reduces beta(2), beta(3) and gamma(2L) GABA(A) receptor subunit mRNAs in the adult septum. Eur J Pharmacol. 2002 Jun 20;446(1-3):201-2. [ Abstract ]
Malayev A, Gibbs TT, Farb DH. (2002) Inhibition of the NMDA response by pregnenolone sulphate reveals subtype selective modulation of NMDA receptors by sulphated steroids. Br J Pharmacol. 2002 Feb;135(4):901-9. [ Abstract ]
Martin SC, Russek SJ, Farb DH. (2001) Human GABA(B)R genomic structure: evidence for splice variants in GABA(B)R1 but not GABA(B)R2. Gene. 2001 Oct 31;278(1-2):63-79. [ Abstract ]
Lyons HR, Land MB, Gibbs TT, Farb DH. (2001) Distinct signal transduction pathways for GABA-induced GABA(A) receptor down-regulation and uncoupling in neuronal culture: a role for voltage-gated calcium channels. J Neurochem. 2001 Sep;78(5):1114-26. [ Abstract ]
Gibbs TT, Farb DH. (2000) Dueling enigmas: neurosteroids and sigma receptors in the limelight. Science Signaling 2000 Nov 28;2000(60):PE1. Review. [ Abstract ]
Russek SJ, Bandyopadhyay S, Farb DH. (2000) An initiator element mediates autologous downregulation of the human type A gamma -aminobutyric acid receptor beta 1 subunit gene. Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8600-5. [ Abstract ]
Weaver CE, Land MB, Purdy RH, Richards KG, Gibbs TT, Farb DH. (2000) Geometry and charge determine pharmacological effects of steroids on N-methyl-D-aspartate receptor-induced Ca(2+) accumulation and cell death. J Pharmacol Exp Ther. 2000 Jun;293(3):747-54. [ Abstract ]
McLean PJ, Shpektor D, Bandyopadhyay S, Russek SJ, Farb DH. (2000) A minimal promoter for the GABA(A) receptor alpha6-subunit gene controls tissue specificity. J Neurochem. 2000 May;74(5):1858-69. [ Abstract ]
Lyons HR, Gibbs TT, Farb DH. (2000) Turnover and down-regulation of GABA(A) receptor alpha1, beta2S, and gamma1 subunit mRNAs by neurons in culture. J Neurochem. 2000 Mar;74(3):1041-8. [ Abstract ]
Park-Chung M, Malayev A, Purdy RH, Gibbs TT, Farb DH. (1999) Sulfated and unsulfated steroids modulate gamma-aminobutyric acidA receptor function through distinct sites. Brain Res. 1999 May 29;830(1):72-87. [ Abstract ]
Martin SC, Russek SJ, Farb DH. (1999) Molecular identification of the human GABABR2: cell surface expression and coupling to adenylyl cyclase in the absence of GABABR1. Mol Cell Neurosci. 1999 Mar;13(3):180-91. [ Abstract ]
Weaver CE Jr, Wu FS, Gibbs TT, Farb DH. (1998) Pregnenolone sulfate exacerbates NMDA-induced death of hippocampal neurons. Brain Res. 1998 Aug 24;803(1-2):129-36. [ Abstract ]
Yaghoubi N, Malayev A, Russek SJ, Gibbs TT, Farb DH. (1998) Neurosteroid modulation of recombinant ionotropic glutamate receptors. Brain Res. 1998 Aug 24;803(1-2):153-60. [ Abstract ]
Park-Chung M, Wu FS, Purdy RH, Malayev AA, Gibbs TT, Farb DH. (1997) Distinct sites for inverse modulation of N-methyl-D-aspartate receptors by sulfated steroids. Mol Pharmacol. 1997 Dec;52(6):1113-23. [ Abstract ]
Weaver CE Jr, Marek P, Park-Chung M, Tam SW, Farb DH. (1997) Neuroprotective activity of a new class of steroidal inhibitors of the N-methyl-D-aspartate receptor. Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10450-4. [ Abstract ]
Weaver CE Jr, Park-Chung M, Gibbs TT, Farb DH. (1997) 17beta-Estradiol protects against NMDA-induced excitotoxicity by direct inhibition of NMDA receptors. Brain Res. 1997 Jul 4;761(2):338-41. [ Abstract ]
Patents:
1) May 18, 1993
Patent: 5,212,167
Inventors: Farb, David H.
Title: Modulation of receptor-mediated ion transport
Abstract
The subject application discloses methods for modulating NMDA-mediated ion transport, and inhibiting non-NMDA glutamate-induced ion transport, in neuronal cells. The methods involve contacting a neuronal cell with an effective amount of the neurosteroid pregnenolone sulfate, or pharmacologically effective derivatives thereof.
2) November 22, 1994
Patent: 5,366,968
Inventors: Farb, David H.
Title: Modulation of receptor-mediated ion transport
Abstract
The subject application discloses methods for modulating NMDA-mediated ion transport, and inhibiting non-NMDA glutamate-induced ion transport, in neuronal cells. The methods involve contacting a neuronal cell with an effective amount of the neurosteroid pregnenolone sulfate, or pharmacologically effective derivatives thereof.
3) March 30, 1999
Patent: 5,888,996
Inventors: Farb, David H.
Title: Inhibition of NMDA receptor activity and modulation of glutamate-mediated synaptic activity
Abstract
The present invention relates to a method of inhibiting N-methyl-D-aspartate (NMDA) glutamate receptor-mediated ion channel activity (NMDA receptor activity), comprising contacting a neuronal cell (e.g., hippocampal neuron, spinal cord cell) with an effective amount (e.g., 1 to 500 mu.M) of a derivative of pregnenolone sulfate. Derivatives of pregnenolone sulfate that inhibit NMDA receptor activity include pregnenolone sulfate in which the A ring includes at least one double bond or is fully unsaturated, the double bond at the C5-C6 position is reduced, the moiety at the C3, C10, C11 or C13 position is modified, alone or in combination. It further relates to pregnenolone sulfate derivatives which have modifications at other positions (e.g., C5, C7, C10, C16, C17, C18, C19, C20, C21), alone or in combination, and are inhibitors of NMDA receptor activity. The pregnenolone sulfate derivatives differ from pregnenolone sulfate at least one position. The present invention also relates to a method of modulating or altering (e.g., potentiating; inhibiting) excitatory glutamate-mediated synaptic activity comprising contacting neurons with pregnenolone sulfate and derivatives of pregnenolone sulfate.
4) April 11, 2000
Patent: 6,048,722
Inventors: Farb, David H.; Yaghoubi; Nader; Gibbs; Terrell T.
Title: Cellular physiology workstations for automated data acquisition and perfusion control
Abstract
Cellular physiology workstations for automated data acquisition and perfusion control are described. The cellular physiology workstation may be used for physiological and electrophysiological experiments. Methods for employing such cellular physiology workstations in physiological and electrophysiological experiments are also disclosed. The cellular physiology workstations comprise one or more recording chambers each for holding one or more cells to be measured. One or more cells are place in each recording chamber. Perfusion device, such as an automatic perfusion system is connected to the recording chamber to perfuse the cells with a plurality of solutions containing different concentration of one or more agents to be tested. Biosensors, such as patch clamps, electrodes, or microscopes are positioned to detect a response from the cell. The cellular physiology workstation may optionally comprise injecting device for introducing an injection solution into the cell before and during analysis.
5) May 23, 2000
Patent: 6,066,726
Inventors: Farb, David H. (Cambridge, MA); Russek; Shelley J.
Title: Neuron-specific transcriptional promoter
Abstract
The 5′-flanking region and core regulatory domains that underlie neuronal specific expression of the human .gamma.-aminobutyric acid type A (GABA.sub.A) receptor .beta.1 subunit gene are identified herein. Sequence analysis, mapping of transcriptional initiation sites, and transfection of reporter gene constructs into primary cultures demonstrate that neuronal and region specific activity resides in a TATA-less minimal promoter of 186 bp, comprising an initiator, the major transcriptional start site, a presumptive TFIID binding site, and an enhancer. Enhancer sequence contained within a 26 bp region at the 5′-end of the minimal promoter is essential for activity but not for tissue specificity. Moreover, .beta.1 promoter activity is subject to autologous inhibition, indicating that GABA-induced receptor mRNA downregulation results from an inhibition of gene transcription. Regulation of neurotransmitter receptor gene expression plays an important role in nervous system development and function, and impaired gene regulation may underlie the etiology of certain neurological diseases.
6) July 4, 2000
Patent: 6,083,941
Inventors: Farb, David H.
Title: Inhibition of NMDA receptor activity by pregnenolone sulfate derivatives
Abstract
The present invention relates to a method of inhibiting N-methyl-D-aspartate (NMDA) glutamate receptor-mediated ion channel activity (NMDA receptor activity), comprising contacting a neuronal cell (e.g., hippocampal neuron, spinal cord cell) with an effective amount (e.g., 1 to 500 mu M) of a derivative of pregnenolone sulfate. Derivatives of pregnenolone sulfate that inhibit NMDA receptor activity include pregnenolone sulfate derivatives in which the A ring includes at least one double bond; PS in which the A ring is fully unsaturated; PS derivatives in which the double bond at the C5-C6 position is reduced; and PS in which the moiety at the C3, C5, C6, C7, C11, C17, C20 and/or C21 position is modified. It further relates to PS derivatives which have modifications at other positions (e.g., C10, C10, C13, C18, C19), alone or in combination, and are inhibitors of NMDA receptor activity. The present invention also relates to a method of modulating or altering (e.g., potentiating; inhibiting) excitatory glutamate-mediated synaptic activity comprising contacting neurons with pregnenolone sulfate and derivatives of pregnenolone sulfate. The present invention also relates to a method of treating a disease associated with L-glutamate-induced NMDA receptor activation selected from the group consisting of: neuropathic pain, drug withdrawal/dependency, epilepsy, glaucoma, chronic neurodegenerative diseases, amyotrophic lateral sclerosis, anxiety disorders, brain cell death, ischemia, stroke, trauma in a host comprising administering to the host an effective amount of a derivative of pregnenolone sulfate.
7) July 31, 2001
Patent: 6,268,168
Inventors: Farb, David H.; Yaghoubi; Nader; Gibbs; Terrell T.
Title: Cellular physiology workstations for automated data acquisition and perfusion control
Abstract
Cellular physiology workstations for automated data acquisition and perfusion control are described. The cellular physiology workstation may be used for physiological and electrophysiological experiments. Methods for employing such cellular physiology workstations in physiological and electrophysiological experiments are also disclosed. The cellular physiology workstations comprise one or more recording chambers each for holding one or more cells to be measured. One or more cells are place in each recording chamber. Perfusions means, such as an automatic perfusion system is connected to the recording chamber to perfuse the cells with a plurality of solutions containing different concentration of one or more agents to be tested. Biosensors, such as patch clamps, electrodes, or microscopes are positioned to detect a response from the cell. The cellular physiology workstation may optionally comprise injecting means for introducing an injection solution into the cell before and during analysis.
8) September 23, 2003
Patent: 6,623,933
Inventors: Farb, David H.; Yaghoubi, Nader; Russek, Shelley; Jang, Ming-Kuei; Gibbs, Terrell T.
Title: Methods for identifying a subunit specific modulator of N-methyl-D-asparate receptor
Abstract
Disclosed is a method for identifying a subunit specific modulator of the N-methyl-D-aspartate (NMDA) receptor. The method involves providing a plurality of NMDA receptors which differ in their subunit identity. The receptors are contacted with a neurotransmitter recognition site ligand in the presence and absence of a candidate modulator. Receptor activity is then assayed, with an increase or decrease in activity in at least one, but not all members of the plurality of NMDA receptors, in the presence but not the absence of a candidate modulator, being an indication that the candidate modulator is a subunit specific modulator. The subunit identity of the subset of the NMDA receptors to determine the subunit specificity of the candidate modulator. Various combinations of NMDA receptor subunits are provided.
9) July 13, 2004
Patent: 6,762,036
Inventors: Farb, David H.; Yaghoubi; Nader; Gibbs; Terrell T.
Title: Cellular physiology workstations for automated data acquisition and perfusion control
Abstract
Cellular physiology workstations for automated data acquisition and perfusion control are described. The cellular physiology workstation may be used for physiological and electrophysiological experiments. Methods for employing such cellular physiology workstations in physiological and electrophysiological experiments are also disclosed. The cellular physiology workstations comprise one or more recording chambers each for holding one or more cells to be measured. One or more cells are place in each recording chamber. Perfusions means, such as an automatic perfusion system is connected to the recording chamber to perfuse the cells with a plurality of solutions containing different concentration of one or more agents to be tested. Biosensors, such as patch clamps, electrodes, or microscopes are positioned to detect a response from the cell. The cellular physiology workstation may optionally comprise injecting means for introducing an injection solution into the cell before and during analysis.
United States Patent Applications (published since March 15, 2001)
October 14, 2004
20040204490 Kind Code A1
Inventors: Farb, David H.; Russek, Shelley;; Jang, Ming-Kuei; Gibbs, Terrell T.; Yaghoubi, Nader
Title: Effect of steroids on NMDA receptors depends on subunit composition
Abstract:
Disclosed is a method for identifying a subunit specific modulator of the N-methyl-D-aspartate (NMDA) receptor. The method involves providing a plurality of NMDA receptors which differ in their subunit identity. The receptors are contacted with a neurotransmitter recognition site ligand in the presence and absence of a candidate modulator. Receptor activity is then assayed, with an increase or decrease in activity in at least one, but not all members of the plurality of NMDA receptors, in the presence but not the absence of a candidate modulator, being an indication that the candidate modulator is a subunit specific modulator. The subunit identity of the subset of the NMDA receptors to determine the subunit specificity of the candidate modulator. Various combinations of NMDA receptor subunits are provided.
April 29, 2004
20040082554 Kind Code A1
Inventors: Farb, David H.; (Brookline, MA) ; Sadri-Vakili, Ghazaleh; (Boston, MA) ; Pierce, Robert Christopher; (Boston, MA) ; Johnson, David W; (Kennebunk, ME); Gibbs, Terrell T
Title: Neuroactive steroid derivatives and method of use
Abstract
The invention relates to neuroactive steroid compounds that are useful in modulating CNS effects, diseases or disease symptoms. The invention also relates to use of the compounds in methods of treating or preventing disease or disease symptoms, and methods of modulating or mediating CNS effects or processes
June 20, 2002
20020076689 Kind Code A1
Inventors: Farb, David H.; Yaghoubi, Nader; Gibbs, Terrell T
Title: Cellular physiology workstations for automated data acquisition and perfusion control
Abstract:
Cellular physiology workstations for automated data acquisition and perfusion control are described. The cellular physiology workstation may be used for physiological and electrophysiological experiments. Methods for employing such cellular physiology workstations in physiological and electrophysiological experiments are also disclosed. The cellular physiology workstations comprise one or more recording chambers each for holding one or more cells to be measured. One or more cells are place in each recording chamber. Perfusions means, such as an automatic perfusion system is connected to the recording chamber to perfuse the cells with a plurality of solutions containing different concentration of one or more agents to be tested. Biosensors, such as patch clamps, electrodes, or microscopes are positioned to detect a response from the cell. The cellular physiology workstation may optionally comprise injecting means for introducing an injection solution into the cell before and during analysis.
September 30, 2004
20040191853 Kind Code A1
Inventors: Farb, David H.; Gibbs, Terrell T.; Yaghoubi, Nader
Title: Cellular physiology workstations for automated data acquisition and perfusion control
Abstract:
Cellular physiology workstations for automated data acquisition and perfusion control are described. The cellular physiology workstation may be used for physiological and electrophysiological experiments. Methods for employing such cellular physiology workstations in physiological and electrophysiological experiments are also disclosed. The cellular physiology workstations comprise one or more recording chambers each for holding one or more cells to be measured. One or more cells are place in each recording chamber. Perfusions means, such as an automatic perfusion system is connected to the recording chamber to perfuse the cells with a plurality of solutions containing different concentration of one or more agents to be tested. Biosensors, such as patch clamps, electrodes, or microscopes are positioned to detect a response from the cell. The cellular physiology workstation may optionally comprise injecting means for introducing an injection solution into the cell before and during analysis.
Patents Pending (excluding international phase of above issued patents)
60/229,929
Inventors: Farb, David H.; Martin, Stella C. Title: A Neural Specific Cytosolic Sulfotransferase for Drug Screening (BU 00-29)
BU04-03
Inventors: Russek, Shelley J; Brooks-Kayal, A; Farb, David H.
Title: Seizure -induced upregulation of the GABRA4 promoter identifies a condition-specific vector for the treatment of epilepsy.
