The Neurological Research Center (Epilepsy) at Yale is organized as a widely based investigative effort into mechanisms of epileptic seizures and their control, and of biological phenomena associated with seizures, with the aim of discerning factors responsible for the occurrence, frequency and nature of seizure disorders, and how they can be controlled. Both experimental and clinical studies are oriented towards the development of physiological, biochemical-metabolic and pharmacologic methods effective for treatment and control of epileptic seizures. The research includes investigations of physiological, biochemical and structural correlates of cerebral excitability changes and mechanisms related to antiepileptic drug action. The component projects in this research program are: basic cellular neurophysiological mechanisms of antiepileptic drug actions (utilizing invertebrate neurons); patho-physiology of mammalian neocortical epilepsy (role of laminar susceptibility and interaction); role of calcium and calmodulin-stimulated protein phosphorylation in seizure states; calcium, transmitter release and antiepileptic drug action; nuclear magnetic resonance metabolic studies (carbon and phosphorus related) of biochemical changes in """"""""kindled"""""""" brain; epilepsy, taniepileptic drugs and sex hormones (menstrual cycle and epilepsy in female, and testosterone changes in males); evaluation of depth electroencephalagraphy in criteria for surgical treatment of focal epilepsy, comparison with metabolic """"""""imaging"""""""".

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Specialized Center (P50)
Project #
5P50NS006208-24
Application #
3107467
Study Section
Neurological Disorders Program Project Review B Committee (NSPB)
Project Start
1986-09-01
Project End
1991-08-31
Budget Start
1989-09-01
Budget End
1990-08-31
Support Year
24
Fiscal Year
1989
Total Cost
Indirect Cost
Name
Yale University
Department
Type
Schools of Medicine
DUNS #
082359691
City
New Haven
State
CT
Country
United States
Zip Code
06520
Ransom, Christopher B; Wu, Yuanming; Richerson, George B (2010) Postdepolarization potentiation of GABAA receptors: a novel mechanism regulating tonic conductance in hippocampal neurons. J Neurosci 30:7672-84
Radtke, C; Spies, M; Sasaki, M et al. (2007) Demyelinating diseases and potential repair strategies. Int J Dev Neurosci 25:149-53
Wu, Yuanming; Wang, Wengang; Diez-Sampedro, Ana et al. (2007) Nonvesicular inhibitory neurotransmission via reversal of the GABA transporter GAT-1. Neuron 56:851-65
Tokuno, Hajime A; Bradberry, Charles W; Everill, Brian et al. (2004) Local anesthetic effects of cocaethylene and isopropylcocaine on rat peripheral nerves. Brain Res 996:159-67
Everill, B; Cummins, T R; Waxman, S G et al. (2001) Sodium currents of large (Abeta-type) adult cutaneous afferent dorsal root ganglion neurons display rapid recovery from inactivation before and after axotomy. Neuroscience 106:161-9
Everill, B; Kocsis, J D (2000) Nerve growth factor maintains potassium conductance after nerve injury in adult cutaneous afferent dorsal root ganglion neurons. Neuroscience 100:417-22
Yee, J M; Agulian, S; Kocsis, J D (1998) Vigabatrin enhances promoted release of GABA in neonatal rat optic nerve. Epilepsy Res 29:195-200
Honmou, O; Kocsis, J D; Richerson, G B (1995) Gabapentin potentiates the conductance increase induced by nipecotic acid in CA1 pyramidal neurons in vitro. Epilepsy Res 20:193-202
Honmou, O; Oyelese, A A; Kocsis, J D (1995) The anticonvulsant gabapentin enhances promoted release of GABA in hippocampus: a field potential analysis. Brain Res 692:273-7
Utzschneider, D A; Rand, M N; Waxman, S G et al. (1994) Nuclear and cytoplasmic Ca2+ signals in developing rat dorsal root ganglion neurons studied in excised tissue. Brain Res 635:231-7

Showing the most recent 10 out of 16 publications