ArticleCellular and molecular neurobiology1996
Modulation and selection of neurotransmitter responses during synapse formation between identified leech neurons.
Article in Cellular and molecular neurobiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Development of Ca2+ hotspots between Lymnaea neurons during synaptogenesis.The Journal of physiology · 2002Article
- Serotonin depletion does not prevent intrinsic sensitization in the leech.Learning & memory (Cold Spring Harbor, N.Y.)Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Serotonin (5-HT) modulates two different responses in the pressure sensitive neurons (P) of the leech: an inhibitory, Cl- dependent synaptic response and a depolarizing extrasynaptic response. 2. Serotonergic Retzius cells (R) in vivo and in culture elicit inhibitory Cl- dependent responses in P neurons. Moreover, at discrete sites of contact between R and P cells, the excitatory response to 5-HT is gradually lost prior to synapse formation. This phenomenon is specifically mediated by R cells. 3. The extrasynaptic response is mediated by cation channels sensitive to protein kinase C (PKC). Cation channels are present at the sites of contact but they become insensitive to PKC. Moreover, cation channels from single P cells are no longer modulated by PKC if they are inserted (by cramming the patch pipette) into the cytoplasm of a P cell in contact with an R cell. 4. Blockers of tyrosine kinases prevent the uncoupling of cation channel modulation and inhibit synapse formation between the R and the P neurons. 5. We suggest that cell contact induces an intracellular, tyrosine kinase-dependent signal as part of the mechanism of neuronal recognition leading to synapse formation.
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