Glutamate iontophoresis induces long-term potentiation in the absence of evoked presynaptic activity.
Protocols that induce long-term potentiation (LTP) typically involve afferent stimulation. We tested the hypothesis that LTP induction does not require presynaptic activity. The significance of this hypothesis is underscored by results suggesting that LTP expression may involve activity-dependent presynaptic changes. An induction protocol using glutamate iontophoresis was developed that reliably induced LTP in hippocampal slices without afferent stimulation. Iontophoresis LTP was Ca2+ dependent, was blocked by MK-801, and occluded tetanus-induced LTP. Iontophoresis LTP was induced when excitatory postsynaptic potentials were completely blocked by adenosine plus tetrodotoxin. Our results suggest constraints on the involvement of presynaptic mechanisms and putative retrograde messengers in LTP induction and expression; namely, these processes must function without many forms of activity-dependent presynaptic processes.[1]References
- Glutamate iontophoresis induces long-term potentiation in the absence of evoked presynaptic activity. Cormier, R.J., Mauk, M.D., Kelly, P.T. Neuron (1993) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
