BDNF is required for the induction of a presynaptic component of the functional conversion of silent synapses

Cabezas, Carolina; Buño, Washington

doi:10.1002/hipo.20754

Cited by 16 publications

(12 citation statements)

References 91 publications

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“…Long-term potentiation (LTP) also develops in the hippocampal-prefrontal pathway after extinction learning occurs (Farinelli et al, 2006), and disrupting this potentiation disrupts fear extinction memory retrieval (Farinelli et al, 2006; Inoue et al, 2013; Judo et al, 2010). Given that BDNF promotes LTP in cortical neurons (Abidin et al, 2007; Cabezas and Buno, 2010; Lu et al, 2010, 2007; Messaoudi et al, 2002), it may simulate fear extinction memory by emulating this neurophysiological plasticity.…”

Section: Bdnf and Extinction Memorymentioning

confidence: 99%

Brain-derived neurotrophic factor and addiction: Pathological versus therapeutic effects on drug seeking

et al. 2015

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Many abused drugs lead to changes in endogenous brain-derived neurotrophic factor (BDNF) expression in neural circuits responsible for addictive behaviors. BDNF is a known molecular mediator of memory consolidation processes, evident at both behavioral and neurophysiological levels. Specific neural circuits are responsible for storing and executing drug-procuring motor programs, whereas other neural circuits are responsible for the active suppression of these “seeking” systems. These seeking-circuits are established as associations are formed between drug-associated cues and the conditioned responses they elicit. Such conditioned responses (e.g. drug seeking) can be diminished either through a passive weakening of seeking-circuits or an active suppression of those circuits through extinction. Extinction learning occurs when the association between cues and drug are violated, for example, by cue exposure without the drug present. Cue exposure therapy has been proposed as a therapeutic avenue for the treatment of addictions. Here we explore the role of BDNF in extinction circuits, compared to seeking-circuits that “incubate” over prolonged withdrawal periods. We begin by discussing the role of BDNF in extinction memory for fear and cocaine-seeking behaviors, where extinction circuits overlap in infralimbic prefrontal cortex (PFC). We highlight the ability of estrogen to promote BDNF-like effects in hippocampal–prefrontal circuits and consider the role of sex differences in extinction and incubation of drug-seeking behaviors. Finally, we examine how opiates and alcohol “break the mold” in terms of BDNF function in extinction circuits.

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Section: Bdnf and Extinction Memorymentioning

confidence: 99%

Brain-derived neurotrophic factor and addiction: Pathological versus therapeutic effects on drug seeking

et al. 2015

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“…The basic question as to whether the mechanisms underlying LTP, both the causes and locus of expression, result from changes in presynaptic or postsynaptic function remains contentious, for more details see Bekkers and Stevens (1990), Kullmann and Nicoll (1992), Isaac et al (1995), Liao et al (1995), Bolshakov et al (1997), Debanne et al (1997), Routtenberg (1999), Zakharenko et al (2001), Emptage et al (2003), Martin and Buno (2003), Nicoll (2003), Huang et al (2005), Bayazitov et al (2007), Lauri et al (2007), Fernandez de Sevilla et al (2008), Kerchner and Nicoll (2008), and Cabezas and Buno (2011). For more details about molecular-cellular mechanisms of LTP, readers are referred to several informative reviews published over the course of three decades (Madison and Schuman, 1991; Bliss and Collingridge, 1993; Malenka, 1994, 2003; Roberson et al, 1996; Nicoll and Malenka, 1999; Sanes and Lichtman, 1999; Sweatt, 1999; Bredt and Nicoll, 2003; Malenka and Bear, 2004; Shi et al, 2005; Miyamoto, 2006; Kerchner and Nicoll, 2008; Minichiello, 2009; Li et al, 2010a; Baudry et al, 2011; Kelly et al, 2011a).…”

Section: Cellular/molecular Mechanisms Involved In Ltpmentioning

confidence: 99%

Long-Term Potentiation at CA3–CA1 Hippocampal Synapses with Special Emphasis on Aging, Disease, and Stress

Kumar¹

2011

Front. Ag. Neurosci.

132

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Synaptic plasticity in the mammalian central nervous system has been the subject of intense investigation for the past four decades. Long-term potentiation (LTP), a major reflection of synaptic plasticity, is an activity-driven long-lasting increase in the efficacy of excitatory synaptic transmission following the delivery of a brief, high-frequency train of electrical stimulation. LTP is regarded as a principal candidate for the cellular mechanisms involved in learning and offers an attractive hypothesis of how memories are constructed. There are a number of exceptional full-length reviews published on LTP; the current review intends to present an overview of the research findings regarding hippocampal LTP with special emphasis on aging, diseases, and psychological insults.

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“…),but also promotes presynaptic neurotransmitter release and neuron maturation(Shen et al . ; Cabezas and Buno ). Although it is reported that BDNF exerts its function on synaptogenesis through multiple signaling pathways, leading to cytoskeletal reorganization or gene expression required for synaptogenesis (Waites et al .…”

mentioning

confidence: 96%

“…Brain-derived neurotrophic factor (BDNF) is a wellknown mediator of synapse formation and plasticity (Huang and Reichardt 2003;Luikart and Parada 2006;Lu et al 2008;Yoshii and Constantine-Paton 2010). BDNF not only increases the number of dendritic synapses of hippocampal neurons (Ji et al 2005;Yoshii and Constantine-Paton 2007;Zhou et al 2008a),but also promotes presynaptic neurotransmitter release and neuron maturation (Shen et al 2006;Cabezas and Buno 2011). Although it is reported that BDNF exerts its function on synaptogenesis through multiple signaling pathways, leading to cytoskeletal reorganization or gene expression required for synaptogenesis (Waites et al 2005;McAllister 2007;Sheng and Hoogenraad 2007), the precise mechanisms that link the BDNF to F-actin remodeling in filopodial motility or synapse/spine formation remain unclear.…”

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confidence: 99%

Geranylgeranyltransferase I mediates BDNF‐induced synaptogenesis

Sun

Zhang

et al. 2013

Journal of Neurochemistry

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Geranylgeranyltransferase I (GGT) is a prenyltransferase that mediates lipid modification of Rho small GTPases, such as Rho, Rac, and Cdc42, which are important for neuronal synaptogenesis. Although GGT is expressed in brain extensively, the function of GGT in central nerves system is largely unknown so far. We have previously demonstrated that GGT promotes the basal and neuronal activity and brain-derived neurotrophic factor (BDNF)-induced dendritic morphogenesis of cultured hippocampal neurons and cerebellar slices. This study is to explore the function and mechanism of GGT in neuronal synaptogenesis. We found that the protein level and activity of GGT gradually increased in rat hippocampus from P7 to P28 and subcellular located at synapse of neurons. The linear density of Synapsin 1 and post-synaptic density protein 95 increased by over-expression of GGT b, while reduced by inhibition or down-regulation of GGT. In addition, GGT and its known substrate Rac was activated by BDNF, which promotes synaptogenesis in cultured hippocampal neurons. Furthermore, BDNF-induced synaptogenesis was eliminated by GGT inhibition or down-regulation, as well as by non-prenylated Rac1 over-expression. Together, our data suggested that GGT mediates BDNF-induced neuronal synaptogenesis through Rac1 activation. Keywords: brain-derived neurotrophic factor, geranylgeranyltransferase I, post-synaptic density protein 95, Rac, Synapsin 1, synaptogenesis. As key regulators of the actin cytoskeleton, members of the Rho-family GTPases, including Rac1, Cdc42, and RhoA, which play essential roles in orchestrating the Abbreviations used: BDNF, brain-derived neurotrophic factor; FT, farnesyltransferase; GEFs, guanine nucleotide exchange factors; GGT, geranylgeranyltransferase I; PBS, phosphate buffered saline; PSD 95, post-synaptic density protein 95; TrkB, tropomyosin-related kinase B.

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BDNF is required for the induction of a presynaptic component of the functional conversion of silent synapses

Cited by 16 publications

References 91 publications

Brain-derived neurotrophic factor and addiction: Pathological versus therapeutic effects on drug seeking

Brain-derived neurotrophic factor and addiction: Pathological versus therapeutic effects on drug seeking

Long-Term Potentiation at CA3–CA1 Hippocampal Synapses with Special Emphasis on Aging, Disease, and Stress

Geranylgeranyltransferase I mediates BDNF‐induced synaptogenesis

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