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Section: Research
Postdoctoral
Position
Available

Mark Alkema, Ph.D.

Academic Role: Assistant Professor

Faculty Appointment(s) In:
   Neurobiology

Other Affiliation(s):
   Program in Neuroscience

C. elegans Behavioral Genetics


Mark Alkema, Ph.D. Our focus is to understand the molecular and cellular basis of behavioral plasticity. We are studying how the environment modulates behavior of the nematode Caenorhabditis elegans. The C. elegans nervous system is very simple and extraordinarily well described. The detailed knowledge  of the C. elegans nervous system combined with its amenability to genetic analysis and laser microsurgery allows us to define neural circuits that control behavior and study behavior at the molecular and cellular level.

C. elegans drastically changes it’s behavior in response to food: in ample food, pharyngeal pumping (feeding) and egg laying are stimulated, whereas locomotion is inhibited. In the absence of food, pharyngeal pumping and egg laying are inhibited and locomotion is stimulated. We are examining the role of the biogenic amines, serotonin and octopamine, in the modulation of these food dependent behaviors. Through the analysis of octopamine deficient mutants we found that octopamine stimulates locomotion and inhibits pharyngeal pumping and egg laying in the absence of food and directly antagonizes the role of serotonin in these behaviors. We are characterizing C. elegans octopamine and serotonin receptors to define how octopaminergic and serotonergic neural circuits interface and control food dependent behaviors.

We also found that tyramine, the biosynthetic precursor of octopamine, has a role independent of octopamine in C. elegans behavior. The analysis of tyramine-deficient animals showed that tyramine is required for the inhibition of head movements in response to gentle touch with an eye lash  (Fig. 1) Forward locomotion of wild-type animals is accompanied by oscillatory head movements. Anterior touch of wild-type animals with an eyelash induces backing during which head oscillations are suppressed. Tyramine deficient mutants fail to suppress head oscillations during backing. Using laser microsurgery we defined a neural circuit that regulates the suppression of head oscillations in response to the stimulation of mechanosensory neurons (Fig. 2) We identified several mutants that, like the tyramine deficient mutants, fail to suppress head oscillations in response to anterior touch. The characterization of these mutants should allow us to identify new tyraminergic signaling components.

The repeated action of biogenic amines can cause long-term changes in synaptic function. Studies in Aplysia, Drosophila and mice have found an important role for the cyclic AMP-response binding protein, CREB in long-term memory formation. To explore the role of C. elegans CREB crh-1 we isolated crh-1 mutant animals. We found that crh-1 mutants have behavioral and developmental defects consistent with the hypothesis that crh-1 functions downstream of serotonin to mediate behavioral and developmental changes that depend on long-term assessment of food availability.

Ultimately, we hope that our studies will teach us more about the basic principles that underlie behavioral plasticity of more complex neural systems.


Office: 717
Phone: 508-856-6158
E-mail: Mark.Alkema@umassmed.edu
Keywords: Neurobiology, Organisms - C. elegans, Learning and Memory, Neuromodulation , Genetics

More on Mark Alkema's Research
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Postdoctoral Position Available

A postdoctoral position is available to study in this laboratory. Contact Dr. Mark Alkema for additional details.

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