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Japanese studies on neural circuits and behavior of Caenorhabditis elegans.

Sasakura H, Tsukada Y, Takagi S, Mori I - Front Neural Circuits (2013)

Bottom Line: Several laboratories have established unique and clever methods to study the underlying neuronal substrates of behavioral regulation in C. elegans.The technological advances applied to studies of C. elegans have allowed new approaches for the studies of complex neural systems.Through reviewing the studies on the neuronal circuits of C. elegans in Japan, we will analyze and discuss the directions of neural circuit studies.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Molecular Neurobiology, Division of Biological Science, Nagoya University Nagoya, Japan.

ABSTRACT
The nematode Caenorhabditis elegans is an ideal organism for studying neural plasticity and animal behaviors. A total of 302 neurons of a C. elegans hermaphrodite have been classified into 118 neuronal groups. This simple neural circuit provides a solid basis for understanding the mechanisms of the brains of higher animals, including humans. Recent studies that employ modern imaging and manipulation techniques enable researchers to study the dynamic properties of nervous systems with great precision. Behavioral and molecular genetic analyses of this tiny animal have contributed greatly to the advancement of neural circuit research. Here, we will review the recent studies on the neural circuits of C. elegans that have been conducted in Japan. Several laboratories have established unique and clever methods to study the underlying neuronal substrates of behavioral regulation in C. elegans. The technological advances applied to studies of C. elegans have allowed new approaches for the studies of complex neural systems. Through reviewing the studies on the neuronal circuits of C. elegans in Japan, we will analyze and discuss the directions of neural circuit studies.

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Alteration to odorant preference influenced by population density of animals (Yamada et al., 2010).(A) Olfactory plasticity of nep-2, snet-1, nep-2:snet-1 mutants. The nep-2 mutants exhibited defective olfactory plasticity. The abnormality olfactory plasticity of nep-2 mutants is suppressed by the mutation in the snet-1 gene. (B). Proposed model of the alteration of olfactory plasticity induced by crude pheromone. SNET-1 is a peptide that inhibits olfactory plasticity. NEP-2 is an extracellular peptidase homologous to neprilysin. The environmental crude pheromone suppresses the expression of SNET-1, thereby facilitating the animals’ olfactory plasticity and ability to move away from the odor source. SNET-1 is accumulated in nep-2 mutants causing the loss of olfactory plasticity and the migration to the odor source.
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Figure 6: Alteration to odorant preference influenced by population density of animals (Yamada et al., 2010).(A) Olfactory plasticity of nep-2, snet-1, nep-2:snet-1 mutants. The nep-2 mutants exhibited defective olfactory plasticity. The abnormality olfactory plasticity of nep-2 mutants is suppressed by the mutation in the snet-1 gene. (B). Proposed model of the alteration of olfactory plasticity induced by crude pheromone. SNET-1 is a peptide that inhibits olfactory plasticity. NEP-2 is an extracellular peptidase homologous to neprilysin. The environmental crude pheromone suppresses the expression of SNET-1, thereby facilitating the animals’ olfactory plasticity and ability to move away from the odor source. SNET-1 is accumulated in nep-2 mutants causing the loss of olfactory plasticity and the migration to the odor source.

Mentions: Caenorhabditis elegans recognizes the density of animals through a crude pheromone sensed by chemosensory neurons, including ASI neurons (Hu, 2007). When the crude pheromone was applied to C. elegans, the expression of SNET-1, a homolog of the Aplysia L11 peptide, was downregulated in ASI neurons. Yamada et al. (2010) found that SNET-1 is a signaling molecule that conveys the density of animals to the nervous system to regulate plastic behavior. The loss-of-function mutation of the snet-1 gene mimicked high-density conditions and caused the enhancement of dispersion behavior after associative learning between the absence of food and benzaldehyde (Figure 6). On the other hand, the overexpression of snet-1 weakened the tendency toward dispersion. The nep-2 gene encoding the extracellular peptidase neprilysin was identified as the negative regulator that controls the activity of SNET-1. In nep-2 mutants, the degradation of SNET-1 peptide is inhibited and the accumulated SNET-1 suppressed dispersion behavior. Taken together, the information on population density is transmitted through external pheromone and endogenous peptide signaling, thereby assuring behavioral plasticity that may be important for the survival of species (Figure 6; Yamada et al., 2010).


Japanese studies on neural circuits and behavior of Caenorhabditis elegans.

Sasakura H, Tsukada Y, Takagi S, Mori I - Front Neural Circuits (2013)

Alteration to odorant preference influenced by population density of animals (Yamada et al., 2010).(A) Olfactory plasticity of nep-2, snet-1, nep-2:snet-1 mutants. The nep-2 mutants exhibited defective olfactory plasticity. The abnormality olfactory plasticity of nep-2 mutants is suppressed by the mutation in the snet-1 gene. (B). Proposed model of the alteration of olfactory plasticity induced by crude pheromone. SNET-1 is a peptide that inhibits olfactory plasticity. NEP-2 is an extracellular peptidase homologous to neprilysin. The environmental crude pheromone suppresses the expression of SNET-1, thereby facilitating the animals’ olfactory plasticity and ability to move away from the odor source. SNET-1 is accumulated in nep-2 mutants causing the loss of olfactory plasticity and the migration to the odor source.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3842693&req=5

Figure 6: Alteration to odorant preference influenced by population density of animals (Yamada et al., 2010).(A) Olfactory plasticity of nep-2, snet-1, nep-2:snet-1 mutants. The nep-2 mutants exhibited defective olfactory plasticity. The abnormality olfactory plasticity of nep-2 mutants is suppressed by the mutation in the snet-1 gene. (B). Proposed model of the alteration of olfactory plasticity induced by crude pheromone. SNET-1 is a peptide that inhibits olfactory plasticity. NEP-2 is an extracellular peptidase homologous to neprilysin. The environmental crude pheromone suppresses the expression of SNET-1, thereby facilitating the animals’ olfactory plasticity and ability to move away from the odor source. SNET-1 is accumulated in nep-2 mutants causing the loss of olfactory plasticity and the migration to the odor source.
Mentions: Caenorhabditis elegans recognizes the density of animals through a crude pheromone sensed by chemosensory neurons, including ASI neurons (Hu, 2007). When the crude pheromone was applied to C. elegans, the expression of SNET-1, a homolog of the Aplysia L11 peptide, was downregulated in ASI neurons. Yamada et al. (2010) found that SNET-1 is a signaling molecule that conveys the density of animals to the nervous system to regulate plastic behavior. The loss-of-function mutation of the snet-1 gene mimicked high-density conditions and caused the enhancement of dispersion behavior after associative learning between the absence of food and benzaldehyde (Figure 6). On the other hand, the overexpression of snet-1 weakened the tendency toward dispersion. The nep-2 gene encoding the extracellular peptidase neprilysin was identified as the negative regulator that controls the activity of SNET-1. In nep-2 mutants, the degradation of SNET-1 peptide is inhibited and the accumulated SNET-1 suppressed dispersion behavior. Taken together, the information on population density is transmitted through external pheromone and endogenous peptide signaling, thereby assuring behavioral plasticity that may be important for the survival of species (Figure 6; Yamada et al., 2010).

Bottom Line: Several laboratories have established unique and clever methods to study the underlying neuronal substrates of behavioral regulation in C. elegans.The technological advances applied to studies of C. elegans have allowed new approaches for the studies of complex neural systems.Through reviewing the studies on the neuronal circuits of C. elegans in Japan, we will analyze and discuss the directions of neural circuit studies.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Molecular Neurobiology, Division of Biological Science, Nagoya University Nagoya, Japan.

ABSTRACT
The nematode Caenorhabditis elegans is an ideal organism for studying neural plasticity and animal behaviors. A total of 302 neurons of a C. elegans hermaphrodite have been classified into 118 neuronal groups. This simple neural circuit provides a solid basis for understanding the mechanisms of the brains of higher animals, including humans. Recent studies that employ modern imaging and manipulation techniques enable researchers to study the dynamic properties of nervous systems with great precision. Behavioral and molecular genetic analyses of this tiny animal have contributed greatly to the advancement of neural circuit research. Here, we will review the recent studies on the neural circuits of C. elegans that have been conducted in Japan. Several laboratories have established unique and clever methods to study the underlying neuronal substrates of behavioral regulation in C. elegans. The technological advances applied to studies of C. elegans have allowed new approaches for the studies of complex neural systems. Through reviewing the studies on the neuronal circuits of C. elegans in Japan, we will analyze and discuss the directions of neural circuit studies.

Show MeSH
Related in: MedlinePlus