UCLA Neuroscience Program Ph.D. Admissions Neuroscience Faculty UCLA and Beyond  



Carolyn Houser
Morphological Organization and Plasticity of the GABA System; Neurochemical Anatomy of Temporal Lobe Epilepsy

Email Address:  houser@mednet.ucla.edu

Work Address:
CHS
CHS
Phone Numbers:
310-206-1567 Office
310-206-6563 Laboratory

Selected Publications:

Glykys J, Peng Z, Chandra D, Homanics GE, Houser CR, Mody I. A new naturally occurring GABA(A) receptor subunit partnership with high sensitivity to ethanol.. Nat Neurosci 2007; 10(1): 40-8.
Zhang N, Wei W, Mody I, Houser CR. Altered localization of GABA(A) receptor subunits on dentate granule cell dendrites influences tonic and phasic inhibition in a mouse model of epilepsy.. J Neurosci 2007; 27(28): 7520-31.
Houser CR. Interneurons of the dentate gyrus: An overview of cell types, terminal fields and neurochemical identity.. Prog Brain Res 2007; 163: 217-811.
Liang J, Zhang N, Cagetti E, Houser CR, Olsen RW, Spigelman I. Chronic intermittent ethanol-induced switch of ethanol actions from extrasynaptic to synaptic hippocampal GABAA receptors.. J Neurosci 2006; 26(6): 1749-58.
Chandra D, Jia F, Liang J, Peng Z, Suryanarayanan A, Werner DF, Spigelman I, Houser CR, Olsen RW, Harrison NL, Homanics GE. GABAA receptor alpha 4 subunits mediate extrasynaptic inhibition in thalamus and dentate gyrus and the action of gaboxadol.. Proc Natl Acad Sci U S A 2006; 103(41): 15230-5.
Swartz BE, Houser CR, Tomiyasu U, Walsh GO, DeSalles A, Rich JR, Delgado-Escueta A. Hippocampal cell loss in posttraumatic human epilepsy.. Epilepsia 2006; 47(8): 1373-82.
Farrar C, Houser CR, Clarke S. Activation of the PI3K/Akt signal transduction pathway and increased levels of insulin receptor in protein repair-deficient mice.. Aging Cell 2005; 4(1): 1-12.
Farrar CE, Huang CS, Clarke SG, Houser CR. Increased cell proliferation and granule cell number in the dentate gyrus of protein repair-deficient mice.. J Comp Neurol 2005; 493(4): 527-37.
Peng Z, Houser CR. Temporal patterns of fos expression in the dentate gyrus after spontaneous seizures in a mouse model of temporal lobe epilepsy.. J Neurosci 2005; 25(31): 7210-20.
Peng Z, Huang CS, Stell BM, Mody I, Houser CR. Altered expression of the delta subunit of the GABAA receptor in a mouse model of temporal lobe epilepsy.. J Neurosci 2004; 24(39): 8629-39.
Houser CR, Esclapez M. Downregulation of the alpha5 subunit of the GABA(A) receptor in the pilocarpine model of temporal lobe epilepsy.. Hippocampus 2003; 13(5): 633-45.
Wei W, Zhang N, Peng Z, Houser CR, Mody I. Perisynaptic localization of delta subunit-containing GABA(A) receptors and their activation by GABA spillover in the mouse dentate gyrus.. J Neurosci 2003; 23(33): 10650-61.
Peng Z, Hauer B, Mihalek RM, Homanics GE, Sieghart W, Olsen RW, Houser CR. GABA(A) receptor changes in delta subunit-deficient mice: altered expression of alpha4 and gamma2 subunits in the forebrain.. J Comp Neurol 2002; 446(2): 179-97.
Houser CR, Esclapez M, Zhang N. GABA neurons of the hippocampal formation: Localization, vulnerability and plasticity.. GABA in the Nervous System: The View at Fifty Years. 2000; 337-56.
Dupuy-Davies S, Houser CR. Evidence for changing positions of GABA neurons in the developing rat dentate gyrus.. Hippocampus. 1999; 9(2): 186-99.
Houser CR. Neuronal loss and synaptic reorganization in temporal lobe epilepsy.. Adv Neurol 1999; 79: 743-61.
Houser, CR, Dupuy, ST, Zhang N. Prominent expression of glutamate decarboxylase during early hippocampal development. Childhood Epilepsies and Brain Development. 1999; pp.13-24.
Zhang N, Houser CR. Ultrastructural localization of dynorphin in the dentate gyrus in human temporal lobe epilepsy: a study of reorganized mossy fiber synapses.. J Comp Neurol 1999; 405(4): 472-90.
Esclapez M, Houser CR. Up-regulation of GAD65 and GAD67 in remaining hippocampal GABA neurons in a model of temporal lobe epilepsy.. J Comp Neurol 1999; 412(3): 488-505.
Esclapez, M, Chang D, Houser CR. Subpopulations of GABA neurons in the dentate gyrus express high levels of the alpha1 subunit of the GABA-A receptor.. Hippocampus 1996; 6: 225-238.
Esclapez M, Houser CR. Somatostatin neurons are a subpopulation of GABA neurons in the rat dentate gyrus: Evidence from co-localization of pre-prosomatostatin and glutamate decarboxylase mRNAs.. Neuroscience 1995; 64: 339-355.
Houser CR GABA neurons in seizure disorders: A review of immunocytochemical studies. Neurochem Res 1991; 16: 295-308.
Kafman DL, Houser CR, Tocin AJ Two forms of the gamma-aminobutyric acid synthetic enzyme glutamate decarboxylase have distinct intraneuronal distributions and cofactor interactions. J Neurochem 1991; 56: 720-723.
Houser, CR Granule cell dispersion in the dentate gyrus of humans with temporal lobe epilepsy. Brain Res 1990; 535: 195-204.
Dupuy ST, Houser CR. Developmental changes in GABA neurons of the rat dentate gyrus: an in situ hybridization and birthdating study.. J Comp Neurol. 1997; 389(3): 402-18.
Houser CR, Esclapez, M. Vulnerability and plasticity of the GABA system in the pilocarpine model of spontaneous recurrent seizures.. Epilepsy Res. 1996; 26(1): 207-18.
Dupuy ST, Houser CR. Prominent expression of two forms of glutamate decarboxylase in the embryonic and early postnatal rat hippocampal formation.. J Neurosci. 1996; 16(21): 6919-32.
Houser CR, Esclapez M. Localization of mRNAs encoding two forms of glutamic acid decarboxylase in the rat hippocampal formation.. Hippocampus. 1994; 4(5): 530-45.
Esclapez M, Tillakaratne NJ, Kaufman DL, Tobin AJ, Houser CR. Comparative localization of two forms of glutamic acid decarboxylase and their mRNAs in rat brain supports the concept of functional differences between the forms.. J Neurosci. 1994; 14(3 Pt 2): 1834-55.
Obenaus A, Esclapez M, Houser CR. Loss of glutamate decarboxylase mRNA-containing neurons in the rat dentate gyrus following pilocarpine-induced seizures.. J Neurosci. 1993; 13(10): 4470-85.
Esclapez M, Tillakaratne NJ, Tobin AJ, Houser CR. Comparative localization of mRNAs encoding two forms of glutamic acid decarboxylase with nonradioactive in situ hybridization methods.. J Comp Neurol. 1993; 331(3): 339-62.
Houser CR, Miyashiro JE, Swartz BE, Walsh GO, Rich JR, Delgado-Escueta AV. Altered patterns of dynorphin immunoreactivity suggest mossy fiber reorganization in human hippocampal epilepsy.. J Neurosci. 1990; 10(1): 267-82.
Research Interest:

Much of the work in our laboratory is focused on learning more about the basic mechanisms of epilepsy. In epilepsy, neurons in some specific regions of the brain, such as the hippocampus, become hyperexcitable and begin to be activated or "fire" in synchrony, thus producing spontaneous seizures or epilepsy. One of the major causes of epilepsy appears to be damage to the brain through severe, prolonged seizures or head trauma early in life. It then requires some time for spontaneous seizures to develop. Our goal is to identify the anatomical and neurochemical changes that occur between the initial insult and the subsequent development of epilepsy. Our broad hypothesis is that progressive changes in the GABA system, a major neurotransmitter system that normally helps inhibit or control excessive neuronal activity in the brain, are critical for the development of epilepsy. By studying brain tissue from animal models of epilepsy and human tissue from patients with temporal lobe epilepsy, we have identified several interesting changes that could contribute to the development of seizure activity. We are pursuing these findings through immunohistochemical and biochemical studies of the hippocampus. First, some but not all neurons that use GABA as their neurotransmitter are damaged in epilepsy. We are attempting to determine why some GABA neurons are easily damaged while others are spared. Since some GABA neurons remain, we are studying the changes that occur in these neurons to determine if there is reorganization of their axons and synapses with other neurons. Finally, we are studying changes in the receptors through which GABA influences the activity of other neurons. Recently, in a mouse model of temporal lobe epilepsy, we have found that some specific subunits of GABA-A receptors are altered in ways that could contribute to seizure activity. More detailed knowledge of such changes could lead to the development of new pharmacological methods for treating existing epilepsy, and, ultimately, for preventing the development of this disorder.