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The AIN-centered DCN of delayed-type eyeblink conditioned mice: 7-d paired and 7-d unpaired training groups

ABSTRACT: Anterior interpositus nucleus (AIN) is a proposed site of memory formation of eyeblink conditioning. A large part of the underlying molecular events, however, remains unknown. To elucidate molecular mechanisms, we examined transcriptional changes in the AIN of mice trained with delayed-type eyeblink conditioning Keywords: 7-d paired training, 7-d unpaired training, delayed-type eyeblink conditioning of mice, anterior interpositus nucleus-centered deep cerebellar nuclei

ORGANISM(S): Mus musculus

PROVIDER: GSE3652 | GEO | 2006/04/04

SECONDARY ACCESSION(S): PRJNA94285

REPOSITORIES: GEO

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The AIN-centered DCN of delayed-type eyeblink conditioned mice: 3-d paired training and sham negative control groups

2006-04-04 | GSE3651 | GEO

Transcription profiling of mouse AIN-centered DCN of delayed-type eyeblink conditioned mice (GEO Super Series)

Project description:This SuperSeries comprises the following subset Series:; GSE3651: The AIN-centered DCN of delayed-type eyeblink conditioned mice: 3-d paired training and sham negative control groups; GSE3652: The AIN-centered DCN of delayed-type eyeblink conditioned mice: 7-d paired and 7-d unpaired training groups; Anterior interpositus nucleus (AIN) is a proposed site of memory formation of eyeblink conditioning. A large part of the underlying molecular events, however, remains unknown. To elucidate molecular mechanisms, we examined transcriptional changes in the AIN of mice trained with delayed-type eyeblink conditioning; The data are not directly comparable between GSE3651 and GSE3652, given the different experimental time periods and amounts of cRNA used for hybridizations. Experiment Overall Design: Refer to individual Series

2008-06-12 | E-GEOD-3713 | biostudies-arrayexpress

The AIN-centered DCN of delayed-type eyeblink conditioned mice

2006-04-04 | GSE3713 | GEO

Transcription profiling of mouse anterior interpostus nucleus (AIN) in delayed type eyeblink conditioned mice after training to investigate memory formation of eyeblink conditioning

Project description:Anterior interpositus nucleus (AIN) is a proposed site of memory formation of eyeblink conditioning. A large part of the underlying molecular events, however, remains unknown. To elucidate molecular mechanisms, we examined transcriptional changes in the AIN of mice trained with delayed-type eyeblink conditioning Experiment Overall Design: 7-d paired training group: Mice received a surgery for implanting four Teflon-coated stainless-steel wires in their left eyelid and a headstage on their head. After 3daysâ?? recovery, they were trained with paired paradigm of conditioned stimulus (CS) and unconditioned stimulus (US) for 7 days: A 352-ms tone CS (1kHz, 83~85dB) was delivered first and a 100ms periorbital shock US (100kHz square pluses) were delivered with 252ms after the onset of CS, and they co-terminated. In case of 7-d unpaired training group, A CS and a US were delivered in an explicitly unpaired, pseudorandomized manner for 7 days. After the last trial was given, anterior interpositus was immediately sampled in 10 to 30 min from the sacrifice.

2008-06-12 | E-GEOD-3652 | biostudies-arrayexpress

Transcription profiling of mouse Anterior interpositus nucleus centred DCN from mice with of delayed-type eyeblink conditioned mice: 3-d paired training and sham negative control groups

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2008-06-12 | E-GEOD-3651 | biostudies-arrayexpress

The AIN-centered DCN of delayed-type eyeblink conditioned mice

Project description:The AIN-centered DCN of delayed-type eyeblink conditioned mice

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AIN-2::GFP IP of mRNAs associated with miRISC in stage sychronized C. elegans populations

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Astrocyte-derived thrombospondins 1 and 2 are required for cortical synapse development controlling goal-directed action performance.

Project description:During development, controlled synaptogenesis is required to form functioning neural circuits that underlie cognition and behavior. Astrocytes, a major glial-cell type in the central nervous system (CNS), promote synapse formation by secreting synaptogenic proteins. Thrombospondins 1 and 2 (TSP1/2), which act through their neuronal receptor α2δ-1, are required for proper intracortical excitatory synaptogenesis. In the adult brain, the loss of α2δ-1 impairs training-induced excitatory synaptogenesis in the anterior cingulate cortex (ACC), and this impairment leads to increased effort-exertion during high-effort tasks. Here, we tested whether TSP1 and TSP2 are required for controlling effort during operant conditioning by using a lever press for food reward training in mice. Surprisingly, we found that constitutive loss of TSP1/2 significantly reduced lever pressing performance when the effort required for a food reward was increased, a phenotype opposite of α2δ-1 loss. Loss of TSP1/2 reduced excitatory synapse number significantly in adult brains. However, in the ACC of TSP1/2 knockout mice, there was still training-induced excitatory synaptogenesis, likely through the upregulation of TSP4, a TSP isoform that is also synaptogenic. Unexpectedly, we also found a significant increase in inhibitory synapse number and function in the ACC of TSP1/2 knockout mice, which were eliminated after training. Finally, we found that astrocyte-specific ablation of TSP1/2 in developing but not adult astrocytes is sufficient to reduce performance during high-effort tasks. Taken together, our study highlights the importance of developmental astrocyte-derived synaptogenic cues TSP1 and 2 in establishing excitatory and inhibitory circuits that control effort during operant conditioning in adults.

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