Limits...
Mechanisms of plasticity in a Caenorhabditis elegans mechanosensory circuit.

Bozorgmehr T, Ardiel EL, McEwan AH, Rankin CH - Front Physiol (2013)

Bottom Line: As worms develop through young adult and adult stages there is a shift toward deeper habituation of response probability that is likely the result of changes in sensitivity to stimulus intensity.Overall, the mechanosensory system of C. elegans shows a great deal of experience dependent plasticity both during development and as an adult.The simplest form of learning, habituation, is not so simple and is mediated and/or modulated by a number of different processes, some of which we are beginning to understand.

View Article: PubMed Central - PubMed

Affiliation: Brain Research Centre, University of British Columbia Vancouver, BC, Canada.

ABSTRACT
Despite having a small nervous system (302 neurons) and relatively short lifespan (14-21 days), the nematode Caenorhabditis elegans has a substantial ability to change its behavior in response to experience. The behavior discussed here is the tap withdrawal response, whereby the worm crawls backwards a brief distance in response to a non-localized mechanosensory stimulus from a tap to the side of the Petri plate within which it lives. The neural circuit that underlies this behavior is primarily made up of five sensory neurons and four pairs of interneurons. In this review we describe two classes of mechanosensory plasticity: adult learning and memory and experience dependent changes during development. As worms develop through young adult and adult stages there is a shift toward deeper habituation of response probability that is likely the result of changes in sensitivity to stimulus intensity. Adult worms show short- intermediate- and long-term habituation as well as context dependent habituation. Short-term habituation requires glutamate signaling and auto-phosphorylation of voltage-dependent potassium channels and is modulated by dopamine signaling in the mechanosensory neurons. Long-term memory (LTM) for habituation is mediated by down-regulation of expression of an AMPA-type glutamate receptor subunit. Intermediate memory involves an increase in release of an inhibitory neuropeptide. Depriving larval worms of mechanosensory stimulation early in development leads to fewer synaptic vesicles in the mechanosensory neurons and lower levels of an AMPA-type glutamate receptor subunit in the interneurons. Overall, the mechanosensory system of C. elegans shows a great deal of experience dependent plasticity both during development and as an adult. The simplest form of learning, habituation, is not so simple and is mediated and/or modulated by a number of different processes, some of which we are beginning to understand.

No MeSH data available.


Related in: MedlinePlus

An example of the candidate gene approach: eat-4 encodes a glutamate vesicle transporter and is expressed on the touch cells. Worms with a mutation in eat-4 show rapid and complete habituation and slower recovery compared to wild-type worms (Rankin and Wicks, 2000).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3750945&req=5

Figure 2: An example of the candidate gene approach: eat-4 encodes a glutamate vesicle transporter and is expressed on the touch cells. Worms with a mutation in eat-4 show rapid and complete habituation and slower recovery compared to wild-type worms (Rankin and Wicks, 2000).

Mentions: The C. elegans homologue of the mammalian glutamate vesicular transporter (VGLUT1), encoded by eat-4 expressed in the touch cells ALM, AVM, and PLM (Lee et al., 1999) was the first candidate gene to be tested by Rankin and Wicks (2000). Rankin and Wicks hypothesized that if chemical synapses between the touch cells and the interneurons are glutamatergic then mutations in eat-4 should cause some deficits in habituation to tap. They found that eat-4 mutants responded normally to the initial tap, however, they habituated significantly more rapidly and to a deeper asymptotic level than wild-type worms (Figure 2). In addition, eat-4 mutants did not show dishabituation after receiving a shock following habituation. Reintroducing the eat-4 gene in the nervous system of the eat-4 mutant (rescuing eat-4) ameliorated the habituation and dishabituation deficits of the mutant. Their findings supported the hypothesis that neurotransmitter release plays a role in habituation and also may play a role in dishabituation (Rankin and Wicks, 2000).


Mechanisms of plasticity in a Caenorhabditis elegans mechanosensory circuit.

Bozorgmehr T, Ardiel EL, McEwan AH, Rankin CH - Front Physiol (2013)

An example of the candidate gene approach: eat-4 encodes a glutamate vesicle transporter and is expressed on the touch cells. Worms with a mutation in eat-4 show rapid and complete habituation and slower recovery compared to wild-type worms (Rankin and Wicks, 2000).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750945&req=5

Figure 2: An example of the candidate gene approach: eat-4 encodes a glutamate vesicle transporter and is expressed on the touch cells. Worms with a mutation in eat-4 show rapid and complete habituation and slower recovery compared to wild-type worms (Rankin and Wicks, 2000).
Mentions: The C. elegans homologue of the mammalian glutamate vesicular transporter (VGLUT1), encoded by eat-4 expressed in the touch cells ALM, AVM, and PLM (Lee et al., 1999) was the first candidate gene to be tested by Rankin and Wicks (2000). Rankin and Wicks hypothesized that if chemical synapses between the touch cells and the interneurons are glutamatergic then mutations in eat-4 should cause some deficits in habituation to tap. They found that eat-4 mutants responded normally to the initial tap, however, they habituated significantly more rapidly and to a deeper asymptotic level than wild-type worms (Figure 2). In addition, eat-4 mutants did not show dishabituation after receiving a shock following habituation. Reintroducing the eat-4 gene in the nervous system of the eat-4 mutant (rescuing eat-4) ameliorated the habituation and dishabituation deficits of the mutant. Their findings supported the hypothesis that neurotransmitter release plays a role in habituation and also may play a role in dishabituation (Rankin and Wicks, 2000).

Bottom Line: As worms develop through young adult and adult stages there is a shift toward deeper habituation of response probability that is likely the result of changes in sensitivity to stimulus intensity.Overall, the mechanosensory system of C. elegans shows a great deal of experience dependent plasticity both during development and as an adult.The simplest form of learning, habituation, is not so simple and is mediated and/or modulated by a number of different processes, some of which we are beginning to understand.

View Article: PubMed Central - PubMed

Affiliation: Brain Research Centre, University of British Columbia Vancouver, BC, Canada.

ABSTRACT
Despite having a small nervous system (302 neurons) and relatively short lifespan (14-21 days), the nematode Caenorhabditis elegans has a substantial ability to change its behavior in response to experience. The behavior discussed here is the tap withdrawal response, whereby the worm crawls backwards a brief distance in response to a non-localized mechanosensory stimulus from a tap to the side of the Petri plate within which it lives. The neural circuit that underlies this behavior is primarily made up of five sensory neurons and four pairs of interneurons. In this review we describe two classes of mechanosensory plasticity: adult learning and memory and experience dependent changes during development. As worms develop through young adult and adult stages there is a shift toward deeper habituation of response probability that is likely the result of changes in sensitivity to stimulus intensity. Adult worms show short- intermediate- and long-term habituation as well as context dependent habituation. Short-term habituation requires glutamate signaling and auto-phosphorylation of voltage-dependent potassium channels and is modulated by dopamine signaling in the mechanosensory neurons. Long-term memory (LTM) for habituation is mediated by down-regulation of expression of an AMPA-type glutamate receptor subunit. Intermediate memory involves an increase in release of an inhibitory neuropeptide. Depriving larval worms of mechanosensory stimulation early in development leads to fewer synaptic vesicles in the mechanosensory neurons and lower levels of an AMPA-type glutamate receptor subunit in the interneurons. Overall, the mechanosensory system of C. elegans shows a great deal of experience dependent plasticity both during development and as an adult. The simplest form of learning, habituation, is not so simple and is mediated and/or modulated by a number of different processes, some of which we are beginning to understand.

No MeSH data available.


Related in: MedlinePlus