Neuroscience 2002 Abstract
| Presentation Number: | 435.4 |
|---|---|
| Abstract Title: | Progesterone Increases Cell Surface GABA<sub>B</sub> Receptors in Cultured Cortical Neurons. |
| Authors: |
Wong, C. G. T.*1
; Wang, Y. T.2
; Mielke, J. G.1
; Snead, O. C.1
1Brain & Behaviour, Hosp Sick Children, Toronto, Canada 2Medicine, University of British Columbia, Vancouver, Canada |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - G-Protein Linked Receptors -- GABAb receptors |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Epilepsy<br />-- Basic mechanisms |
| Session: |
435. G-protein linked receptors: GABAB receptors Poster |
| Presentation Time: | Tuesday, November 5, 2002 11:00 AM-12:00 PM |
| Location: | Hall A2-B3 C-77 |
| Keywords: | Absence Seizures, Intracellular Trafficking |
Progesterone Increases Cell Surface GABAB Receptors in Cultured Cortical Neurons
C. Guin Ting Wong1, Yu Tian Wang2, John G. Mielke1, O. Carter Snead III1
1. Brain and Behaviour Program, Hospital for Sick Children, Toronto, Canada.
2. Brain Research Center, Vancouver Hospital and University of British Columbia.
Absence seizures are characterized by a loss of consciousness of abrupt onset and offset, that is accompanied by an EEG pattern known as spike and wave discharge (SWD). The GABAB Receptor (GABABR) is believed to mediate the events that lead to this SWD and consequently, absence seizures. The severity of absence seizures vary as a function of the estrus cycle in rat [Persad V.et. al, (2001) SFN Abstract]. GABABR binding also varies as a function of the estrus cycle [Al-Dahan M et. al, Brain Res. 640:33-9]. We hypothesize that fluctuations in GABABR's during the estrus cycle are caused by hormone-induced changes in its intracellular trafficking, and that it is this perturbation that ultimately mediates the severity of absence seizures. Trafficking studies have revealed that progesterone treatment of neuronal cultures results in a 27% increase in the number of cell-surface GABABR’s. This increase is unaffected by the co-administration of the progesterone receptor antagonist, mifepristone, nor is it due to the conversion of progesterone to its metabolite alloprenanolone. These data raise the possibility that a novel cellular mechanism underlies the hormonal cycling of GABABR and the pro-absence effects of progesterone.
C. Guin Ting Wong1, Yu Tian Wang2, John G. Mielke1, O. Carter Snead III1
1. Brain and Behaviour Program, Hospital for Sick Children, Toronto, Canada.
2. Brain Research Center, Vancouver Hospital and University of British Columbia.
Absence seizures are characterized by a loss of consciousness of abrupt onset and offset, that is accompanied by an EEG pattern known as spike and wave discharge (SWD). The GABAB Receptor (GABABR) is believed to mediate the events that lead to this SWD and consequently, absence seizures. The severity of absence seizures vary as a function of the estrus cycle in rat [Persad V.et. al, (2001) SFN Abstract]. GABABR binding also varies as a function of the estrus cycle [Al-Dahan M et. al, Brain Res. 640:33-9]. We hypothesize that fluctuations in GABABR's during the estrus cycle are caused by hormone-induced changes in its intracellular trafficking, and that it is this perturbation that ultimately mediates the severity of absence seizures. Trafficking studies have revealed that progesterone treatment of neuronal cultures results in a 27% increase in the number of cell-surface GABABR’s. This increase is unaffected by the co-administration of the progesterone receptor antagonist, mifepristone, nor is it due to the conversion of progesterone to its metabolite alloprenanolone. These data raise the possibility that a novel cellular mechanism underlies the hormonal cycling of GABABR and the pro-absence effects of progesterone.
Supported by Canadian Institute for Health Research (CIHR) and the Bloorview Children’s Foundation
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
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