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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
Published on: March 23, 2011
BDNF upregulation rescues synaptic plasticity in middle-aged ovariectomized rats
Enikö A Kramár1, Lulu Y Chen, Julie C Lauterborn
1Department of Psychiatry and Human Behavior, University of California, Irvine, CA 92697-4291, USA. ekramar@uci.edu
Neurobiology of Aging
|August 3, 2010
Summary
Brain-derived neurotrophic factor (BDNF) can reverse cognitive deficits in ovariectomized rats. This neurotrophic factor treatment restored spine plasticity and long-term potentiation, offering hope for memory and cognitive health.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Estrogen deficiency, such as that caused by ovariectomy, is linked to cognitive decline and memory impairment.
- Reduced synaptic plasticity, including actin polymerization in dendritic spines and long-term potentiation (LTP) stabilization, is a hallmark of these deficits.
- Brain-derived neurotrophic factor (BDNF) is implicated in synaptic plasticity and neuronal survival.
Purpose of the Study:
- To investigate the efficacy of BDNF in ameliorating ovariectomy-induced deficits in synaptic plasticity.
- To explore both direct BDNF infusion and strategies for elevating endogenous BDNF levels as potential therapeutic approaches.
Main Methods:
- Utilized hippocampal slices from middle-aged ovariectomized rats to assess synaptic plasticity.
- Measured actin polymerization in dendritic spines following patterned afferent stimulation.
- Evaluated the stabilization of long-term potentiation (LTP).
- Administered direct BDNF infusion (2 nM for 60 minutes) and ampakine treatment to modulate endogenous BDNF.
Main Results:
- Ovariectomy significantly reduced actin polymerization in spines and LTP stabilization.
- A 60-minute infusion of 2 nM BDNF fully restored both actin polymerization and LTP stabilization.
- Elevating endogenous hippocampal BDNF levels via ampakine injections also rescued these plasticity defects.
Conclusions:
- This study provides the first evidence that minimally invasive, mechanism-based treatments can reverse synaptic plasticity deficits caused by reduced estrogen levels.
- BDNF administration, either directly or by enhancing endogenous levels, represents a promising therapeutic strategy for cognitive impairments associated with estrogen deficiency.
