Dopamine plays a critical role in the olfactory adaptive learning pathway in <i>Caenorhabditis elegans</i>

Raj, Vishnu; Thekkuveettil, Anoopkumar

doi:10.1002/jnr.25112

Cited by 5 publications

(16 citation statements)

References 94 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, dopaminergic neurons in C. elegans are responsible for adaptive learning and memory (Raj & Thekkuveettil, 2022). We found that olanzapine caused the degeneration of dopaminergic neurons in C. elegans.…”

Section: Olanzapine Accelerates Aging Via Defective Mitophagymentioning

confidence: 82%

“…As aforementioned, olanzapine caused cognitive decline during aging in C. elegans , therefore, we investigated whether olanzapine leads to the degeneration of dopaminergic neurons, which are critical for adaptive learning and memory (Raj & Thekkuveettil, 2022). The age‐dependent damage of dopaminergic neurons (four CEP neurons) in C. elegans was assessed using the transgenic strain expressing Pdat‐1::GFP (Beilina et al., 2020).…”

Section: Resultsmentioning

confidence: 99%

“…Neurodegeneration is the hallmark of brain aging associated with cognitive decline, and can be investigated using C. elegans models (Cooper et al., 2015; Peng et al., 2011). In addition, dopaminergic neurons in C. elegans are responsible for adaptive learning and memory (Raj & Thekkuveettil, 2022). We found that olanzapine caused the degeneration of dopaminergic neurons in C. elegans .…”

Section: Discussionmentioning

confidence: 99%

Section: Olanzapine Impairs Neuritesmentioning

confidence: 99%

See 3 more Smart Citations

Impaired mitophagosome–lysosome fusion mediates olanzapine‐induced aging

Chen,

Wang,

Zheng

et al. 2023

Aging Cell

View full text Add to dashboard Cite

The lifespan of schizophrenia patients is significantly shorter than the general population. Olanzapine is one of the most commonly used antipsychotic drugs (APDs) for treating patients with psychosis, including schizophrenia and bipolar disorder. Despite their effectiveness in treating positive and negative symptoms, prolonged exposure to APDs may lead to accelerated aging and cognitive decline, among other side effects. Here we report that dysfunctional mitophagy is a fundamental mechanism underlying accelerated aging induced by olanzapine, using in vitro and in vivo (Caenorhabditis elegans) models. We showed that the aberrant mitophagy caused by olanzapine was via blocking mitophagosome–lysosome fusion. Furthermore, olanzapine can induce mitochondrial damage and hyperfragmentation of the mitochondrial network. The mitophagosome–lysosome fusion in olanzapine‐induced aging models can be restored by a mitophagy inducer, urolithin A, which alleviates defective mitophagy, mitochondrial damage, and fragmentation of the mitochondrial network. Moreover, the mitophagy inducer ameliorated behavioral changes induced by olanzapine, including shortened lifespan, and impaired health span, learning, and memory. These data indicate that olanzapine impairs mitophagy, leading to the shortened lifespan, impaired health span, and cognitive deficits. Furthermore, this study suggests the potential application of mitophagy inducers as therapeutic strategies to reverse APD‐induced adverse effects associated with accelerated aging.

show abstract

Section: Olanzapine Accelerates Aging Via Defective Mitophagymentioning

confidence: 82%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Olanzapine Impairs Neuritesmentioning

confidence: 99%

See 2 more Smart Citations

Impaired mitophagosome–lysosome fusion mediates olanzapine‐induced aging

Chen,

Wang,

Zheng

et al. 2023

Aging Cell

View full text Add to dashboard Cite

show abstract

“…The assay was performed by trapping the worms in a sodium alginate scaffold (Raj & Thekkuveettil, 2022).…”

Section: Methodsmentioning

confidence: 99%

Insulin signaling in dopaminergic neurons regulates extended memory formation in Caenorhabditis elegans

Kanakalatha,

Thekkuveettil

2023

J of Neuroscience Research

Self Cite

View full text Add to dashboard Cite

Insulin alters several brain functions, and perturbations in insulin levels could be a precipitating factor for Parkinson's disease, a disease associated with the degeneration of dopaminergic neurons. It is unclear whether insulin alters the dopamine signaling pathway and modulates learning and memory. In Caenorhabditis elegans, daf‐2 insulin receptor mutants have extended memory when trained for olfactory adaptation. In this study, we show that the absence of daf‐2 receptors in dopamine neurons results in this unusual learning behavior. Our results show that insulin function in memory is dopamine‐dependent. In the absence of the daf‐2 receptor, the calcium influx in dopamine neurons shows an altered pattern resulting in memory recall for an extended period. These results indicate that learning and memory involve insulin–dopamine crosstalk. Imbalances in this pathway result in changes in memory recall.

show abstract

Uncovering novel regulators of memory using C. elegans genetic and genomic analysis

Brandel-Ankrapp

Arey

2023

Biochemical Society Transactions

View full text Add to dashboard Cite

How organisms learn and encode memory is an outstanding question in neuroscience research. Specifically, how memories are acquired and consolidated at the level of molecular and gene pathways remains unclear. In addition, memory is disrupted in a wide variety of neurological disorders; therefore, discovering molecular regulators of memory may reveal therapeutic targets for these disorders. C. elegans are an excellent model to uncover molecular and genetic regulators of memory. Indeed, the nematode's invariant neuronal lineage, fully mapped genome, and conserved associative behaviors have allowed the development of a breadth of genetic and genomic tools to examine learning and memory. In this mini-review, we discuss novel and exciting genetic and genomic techniques used to examine molecular and genetic underpinnings of memory from the level of the whole-worm to tissue-specific and cell-type specific approaches with high spatiotemporal resolution.

show abstract

Dopamine plays a critical role in the olfactory adaptive learning pathway in Caenorhabditis elegans

Cited by 5 publications

References 94 publications

Impaired mitophagosome–lysosome fusion mediates olanzapine‐induced aging

Impaired mitophagosome–lysosome fusion mediates olanzapine‐induced aging

Insulin signaling in dopaminergic neurons regulates extended memory formation in Caenorhabditis elegans

Uncovering novel regulators of memory using C. elegans genetic and genomic analysis

Contact Info

Product

Resources

About