Retina- and ventral forebrain-specific Cre recombinase activity in transgenic mice

Furuta, Yasuhide; Lagutin, Oleg V.; Hogan, Brigid L.M.; Oliver, Guillermo

doi:10.1002/(sici)1526-968x(200002)26:2<130::aid-gene9>3.0.co;2-i

Cited by 188 publications

(240 citation statements)

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“…Deficits in synaptic plasticity in the hippocampus have been linked to spatial memory impairments in the MWM (5). To avoid the muscular dysfunction deficit in VAChT KD HOM mice (20) we produced a forebrain-specific knockout mouse line using our recently generated floxed VAChT mouse line [VAChT flox/flox (22)] and a Six3-Cre mouse line, which expresses the Cre recombinase enzyme (Cre) under the control of the Six3 promoter, broadly active in the ventral forebrain (26). We crossed the Six3-Cre line (B) WT (white, n = 9) and VAChT KD HOM (black, n = 11) mice were subject to the Barnes maze.…”

supporting

confidence: 73%

Elimination of the vesicular acetylcholine transporter in the forebrain causes hyperactivity and deficits in spatial memory and long-term potentiation

Martyn¹,

Jaeger

Magalhães³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Basal forebrain cholinergic neurons, which innervate the hippocampus and cortex, have been implicated in many forms of cognitive function. Immunolesion-based methods in animal models have been widely used to study the role of acetylcholine (ACh) neurotransmission in these processes, with variable results. Cholinergic neurons have been shown to release both glutamate and ACh, making it difficult to deduce the specific contribution of each neurotransmitter on cognition when neurons are eliminated. Understanding the precise roles of ACh in learning and memory is critical because drugs that preserve ACh are used as treatment for cognitive deficits. It is therefore important to define which cholinergic-dependent behaviors could be improved pharmacologically. Here we investigate the contributions of forebrain ACh on hippocampal synaptic plasticity and cognitive behavior by selective elimination of the vesicular ACh transporter, which interferes with synaptic storage and release of ACh. We show that elimination of vesicular ACh transporter in the hippocampus results in deficits in long-term potentiation and causes selective deficits in spatial memory. Moreover, decreased cholinergic tone in the forebrain is linked to hyperactivity, without changes in anxiety or depression-related behavior. These data uncover the specific contribution of forebrain cholinergic tone for synaptic plasticity and behavior. Moreover, these experiments define specific cognitive functions that could be targeted by cholinergic replacement therapy.Alzheimer's disease | Morris water maze | synaptic vesicle | Barnes maze T he mechanisms that underlie the formation of hippocampaldependent spatial memory have been broadly explored (1). However, the neurochemical basis underlying changes in the strength of synaptic connections necessary for memories to persist is still not precisely understood. In the case of the hippocampus, mechanisms for memory processing include mRNA-dependent (2) and mammalian target of rapamycin (mTOR)-mediated protein synthesis (3) as well as a sequence of biochemical events shared with or closely similar to that of long-term potentiation (LTP) (2). Indeed, the consolidation of two different aversive tasks (4) and of spatial recognition memory (5) is accompanied by LTP of the CA3-CA1 synapse and can be occluded by a preceding LTP.The basal forebrain cholinergic system, which innervates the hippocampus and cortex, has been suggested to modulate LTP in the hippocampus (6-9) and has been implicated in many forms of behavior (10). In addition, spatial memory has also been suggested to depend on cholinergic activity (10), although there are numerous controversies surrounding which behaviors acetylcholine (ACh) regulates (11, 12). Moreover, in few studies cholinergic denervation did not affect expression of LTP (13). Understanding the precise roles of ACh in learning and memory is of importance because in different types of dementia cholinergic function is decreased (14), and manipulations that boost ACh levels at synapses are used a...

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supporting

confidence: 73%

Elimination of the vesicular acetylcholine transporter in the forebrain causes hyperactivity and deficits in spatial memory and long-term potentiation

Martyn¹,

Jaeger

Magalhães³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…2, B and C). To remove Sox11 in the retina, we used Six3-cre mice, which express Cre recombinase in the eye field and ventral forebrain starting at E9 to E9.5 (24,29). Homozygous Sox11 loxP/loxP mice were bred with Six3-cre mice to yield retina-specific Sox11 CKO (Sox11 loxP/loxP ; Six3-cre) mice.…”

Section: Resultsmentioning

confidence: 99%

“…loxP/loxP mice were described previously (24,25). To generate Sox11 loxP allele, genomic sequences from mouse 129S6 BAC library was isolated using Sox11-coding sequences as a probe.…”

Section: Animals-six3-cre and Sox4mentioning

confidence: 99%

Transcription Factors SOX4 and SOX11 Function Redundantly to Regulate the Development of Mouse Retinal Ganglion Cells

Jiang

Ding

Xie

et al. 2013

Journal of Biological Chemistry

123

106

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“…Another strain of mice having a deletion of trkB gene in the retina (TrkB f/f , Six3-Cre/ϩ) were generated using Cre-mediated recombination. Mice heterozygous for TrkB f/ϩ were crossed with Six3-Cre transgenic mice (Furuta et al, 2000) Transgenic mice were identified by PCR using genomic DNA isolated from clipped tails. TrkB hypomorphic mice and Six3-Cre mice were genotyped according to Furuta et al (2000) and Xu et al (2000).…”

Section: Methodsmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor and TrkB Modulate Visual Experience-Dependent Refinement of Neuronal Pathways in Retina

et al. 2007

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Sensory experience refines neuronal structure and functionality. The visual system has proved to be a productive model system to study this plasticity. In the neonatal retina, the dendritic arbors of a large proportion of ganglion cells are diffuse in the inner plexiform layer. With maturation, many of these arbors become monolaminated. Visual deprivation suppresses this remodeling. Little is known of the molecular mechanisms controlling maturational and experience-dependent refinement. Here, we tested the hypothesis that brainderived neurotrophic factor (BDNF), which is known to regulate dendritic branching and synaptic function in the brain, modulates the developmental and visual experience-dependent refinement of retinal ganglion cells. We used a transgenic mouse line, in which a small number of ganglion cells were labeled with yellow fluorescence protein, to delineate their dendritic structure in vivo. We found that transgenic overexpression of BDNF accelerated the laminar refinement of ganglion cell dendrites, whereas decreased TrkB expression or retina-specific deletion of TrkB, the cognate receptor for BDNF, retarded it. BDNF-TrkB signaling regulated the maturational formation of new branches in ON but not the bilaminated ON-OFF ganglion cells. Furthermore, BDNF overexpression overrides the requirement for visual inputs to stimulate laminar refinement and dendritic branching of ganglion cells. These experiments reveal a previously unrecognized action of BDNF and TrkB in controlling cell-specific, experience-dependent remodeling of neuronal structures in the visual system.

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Retina- and ventral forebrain-specific Cre recombinase activity in transgenic mice

Cited by 188 publications

References 5 publications

Elimination of the vesicular acetylcholine transporter in the forebrain causes hyperactivity and deficits in spatial memory and long-term potentiation

Elimination of the vesicular acetylcholine transporter in the forebrain causes hyperactivity and deficits in spatial memory and long-term potentiation

Transcription Factors SOX4 and SOX11 Function Redundantly to Regulate the Development of Mouse Retinal Ganglion Cells

Brain-Derived Neurotrophic Factor and TrkB Modulate Visual Experience-Dependent Refinement of Neuronal Pathways in Retina

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