The Memory of Fearful Events

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Original article below:

Memory of fearful events: the role of fibroblast growth factor-2 in fear acquisition and extinction.
Graham BM, Richardson R.

Source
Department of Psychiatry, Harvard Medical School and Massachusetts General Hospital, 149 13th St. Charlestown, 02129 Boston, MA, USA. bmgraham@nmr.mgh.harvard.edu

Abstract Research during the past decade has led to a tremendous growth in our understanding of how fear memories are acquired and subsequently inhibited on a neural and molecular level. Such research has contributed to significant developments in the treatment of anxiety disorders, and has considerably advanced our understanding of the neurobiology of learning and memory in general. A number of recent studies have examined the role of growth factors in the formation of long-term memory for fearful events, due to their ability to cause morphological neural changes in response to environmental stimulation. In this review we first describe physiological evidence that fibroblast growth factor-2 (FGF2) receptors are highly expressed in the neural circuitry regulating fear acquisition and extinction, and that FGF2 modulates the molecular signals known to be involved in the formation of fear memories. Then we present emerging behavioral research that demonstrates that exogenous FGF2 can enhance the formation of fear conditioning and extinction memories. Finally, we briefly discuss how

research into the role of FGF2 in learning and memory may be of clinical benefit, particularly in the treatment of anxiety disorders. Copyright 2011 IBRO. Published by Elsevier Ltd. All rights reserved. PMID: 21624434 [PubMed - in process]
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Neuropsychopharmacology. 2009 Jun;34(7):1875-82. Epub 2009 Feb 18.

Acute systemic fibroblast growth factor-2 enhances long-term extinction of fear and reduces reinstatement in rats.
Graham BM, Richardson R.

Source
School of Psychology, University of New South Wales, Sydney, NSW, Australia. bgraham@psy.unsw.edu.au

Abstract

Despite having made substantial advances in the treatment of anxiety disorders over the past few decades it appears that we have now reached a 'therapeutic impasse'. Further clinical progress requires a greater understanding of the neural mechanisms underlying fear inhibition. In this study, we examined, for the first time, the effects of fibroblast growth factor-2 (FGF2), a mitogen involved in the molecular cascade of memory, on extinction and relapse in rats. In all experiments, rats were first trained to fear a white noise-conditioned stimulus, and then had this learned fear extinguished the following day. Extinction is the process underlying

exposure-based therapy in humans. Experiments 1 and 2 demonstrated that FGF2 facilitated the loss of learned fear (ie, extinction) when given either prior to or immediately after extinction but not when given 4 h after extinction. This suggests that FGF2 must be present during the consolidation of the extinction memory to have an effect. Experiment 3 further supported this interpretation by showing that short-term extinction must occur for FGF2 to facilitate long-term extinction, suggesting that FGF2 is facilitating the translation of memory from short-term to long-term storage. In experiment 4 rats given FGF2 immediately after extinction exhibited less shock-induced reinstatement, which is a model preparation of relapse, than did vehicletreated rats. Together, these experiments demonstrate that FGF2 facilitates extinction and attenuates relapse. Thus, FGF2 may be a novel pharmacological adjunct to exposure therapy.