Fear Conditioning-Induced Alterations of Phospholipase C-β1a Protein Level and Enzyme Activity in Rat Hippocampal Formation and Medial Frontal Cortex

Weeber, Edwin J.; Savage, Daniel D.; Sutherland, Robert J.; Caldwell, Kevin K.

doi:10.1006/nlme.2000.3994

Cited by 41 publications

(45 citation statements)

References 115 publications

(134 reference statements)

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“…Similar to the findings of Weeber et al, (2001) using the rat model, the 10% ethanol mice displayed significant deficits in single trial fear conditioning ( Figure 5). However, with the mouse model, a more robust attenuation of fear conditioned freezing was seen here ( Figure 5) compared to that reported in rat (Weeber et al, 2001).…”

Section: Eifect Of Saccharin Fading Ethanol Exposure Paradigm On Delasupporting

confidence: 81%

“…However, with the mouse model, a more robust attenuation of fear conditioned freezing was seen here ( Figure 5) compared to that reported in rat (Weeber et al, 2001). Impaired contextual conditioning, Identification of a learning/memory deficit in adult offspring demonstrates that the mouse, as well as the previously described rat, FAE model produces learning and memory impairments which persist into adulthood, similar to the clinical course of FASD in humans.…”

Section: Eifect Of Saccharin Fading Ethanol Exposure Paradigm On Delasupporting

confidence: 59%

“…In a recent group of studies, we found that rats that were exposed prenatally to moderate levels of ethanol display deficits in contextual fear conditioning, but not fear of a discrete CS (Weeber et al 2001). …”

Section: Eifect Of Saccharin Fading Ethanol Exposure Paradigm On Delamentioning

confidence: 93%

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99HRT Prenatal Alcohol Exposure Damages Brain Signal Transduction Systems

Caldwell

2003

PsycEXTRA Dataset

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Section: Eifect Of Saccharin Fading Ethanol Exposure Paradigm On Delasupporting

confidence: 81%

Section: Eifect Of Saccharin Fading Ethanol Exposure Paradigm On Delasupporting

confidence: 59%

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99HRT Prenatal Alcohol Exposure Damages Brain Signal Transduction Systems

Caldwell

2003

PsycEXTRA Dataset

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“…Within the hippocampus, phospholipase C (PLC) activation of the Na ϩ -and Ca 2ϩ -conducting transient receptor potential channel channels has been shown to play an important role in synaptic plasticity (Kim et al, 2003). Contextual fear memory formation has been shown to involve PLC within the hippocampus (Weeber et al, 2001). Furthermore, BDNF activates a cationic influx in pontine neurons through the PLC-dependent opening of a TRPC3 channel (Li et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor and Tyrosine Kinase Receptor B Involvement in Amygdala-Dependent Fear Conditioning

Rattiner¹,

Davis²,

French³

et al. 2004

J. Neurosci.

325

273

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Brain-derived neurotrophic factor (BDNF) and its receptor, tyrosine kinase receptor B (TrkB), play a critical role in activity-dependent synaptic plasticity and have been implicated as mediators of hippocampal-dependent learning and memory. The present study is the first to demonstrate a role for BDNF and TrkB in amygdala-dependent learning. Here, the use of Pavlovian fear conditioning as a learning model allows us to examine the concise role of BDNF in the amygdala after a single learning session and within a well understood neural circuit. Using in situ hybridization, mRNA levels of six different trophic factors [BDNF, neurotrophin (NT) 4/5, NGF, NT3, aFGF, and bFGF) were measured at varying time points during the consolidation period after fear conditioning. We found temporally specific changes only in BDNF gene expression in the basolateral amygdala after paired stimuli that supported learning but not after exposure to neutral or aversive stimuli alone. Using Western blotting, we found that the Trk receptor undergoes increased phosphorylation during this consolidation period, suggesting an activation of the receptor subsequent to BDNF release. Furthermore, disruption of neurotrophin signaling with intra-amygdala infusion of the Trk receptor antagonist K252a disrupted acquisition of fear conditioning. To address the specific role of the TrkB receptor, we created a novel lentiviral vector expressing a dominant-negative TrkB isoform (TrkB.T1), which specifically blocked TrkB activation in vitro. In vivo, TrkB.T1 lentivirus blocked fear acquisition without disrupting baseline startle or expression of fear. These data suggest that BDNF signaling through TrkB receptors in the amygdala is required for the acquisition of conditioned fear.

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“…Experimental models of FASD have shown cognitive deficits at all ages, from pre-weaning life through late adulthood (Barr et al, 2005). Deficits have been observed in a wide variety of learning and memory tasks, including spatial reference memory (Gabriel et al, 2005;Kim et al, 1997;Matthews and Simson, 1998;Zimmerberg and Weston, 2002), working memory (Neese et al, 2004), and associative memory (Clausing et al, 1995;Vaglenova, 1992;Vaglenova andPetkov, 1998, 2001;Weeber et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Aniracetam Reversed Learning and Memory Deficits Following Prenatal Ethanol Exposure by Modulating Functions of Synaptic AMPA Receptors

Vaglenova

Pandiella

Wijayawardhane

et al. 2007

Neuropsychopharmacol

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Specific pharmacological treatments are currently not available to address problems resulting from fetal ethanol exposure, described as Fetal Alcohol Syndrome or Fetal Alcohol Spectrum Disorders (FASD). The present study evaluated the therapeutic effects of aniracetam against cognitive deficits in a well-characterized and sensitive FASD Sprague-Dawley rat model. Ethanol, administered orally at a moderate dose (4 g/kg/24 h; 38% v/v) during the entire course of pregnancy, caused severe cognitive deficits in offspring. Furthermore, both progeny genders were affected by a spectrum of behavioral abnormalities, such as a delay in the development of the righting reflex, poor novelty seeking behavior, and high anxiety levels in female rats. Cognitive disabilities, monitored in adult rats by a two-way active avoidance task, correlated well with a significant reduction of AMPA (a-amino-3 hydro-5 methyl-isoxazole propionic acid) receptormediated miniature excitatory postsynaptic responses (mEPSCs) in the hippocampus. Administration of aniracetam for 10 days (postnatal days (PND) 18-27), at a dose of 50 mg/kg reversed cognitive deficits in both rat genders, indicated by a significant increase in the number of avoidances and the number of 'good learners'. After the termination of the nootropic treatment, a significant increase in both amplitude and frequency of AMPA receptor-mediated mEPSCs in hippocampal CA-1 pyramidal cells was observed. Significant anxiolytic effects on PND 40 also preceded acquisition improvements in the avoidance task. This study provides evidence for the therapeutic potential of aniracetam in reversing cognitive deficits associated with FASD through positive post-natal modulation of AMPA receptors.

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Fear Conditioning-Induced Alterations of Phospholipase C-β1a Protein Level and Enzyme Activity in Rat Hippocampal Formation and Medial Frontal Cortex

Cited by 41 publications

References 115 publications

99HRT Prenatal Alcohol Exposure Damages Brain Signal Transduction Systems

99HRT Prenatal Alcohol Exposure Damages Brain Signal Transduction Systems

Brain-Derived Neurotrophic Factor and Tyrosine Kinase Receptor B Involvement in Amygdala-Dependent Fear Conditioning

Aniracetam Reversed Learning and Memory Deficits Following Prenatal Ethanol Exposure by Modulating Functions of Synaptic AMPA Receptors

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