Matrix metalloproteinase activity regulates LTP through L-type voltage-gated calcium channel modulation

• Autorzy: Wiera G. , Mozrzymas J. W.
• Języki publikacji: EN

Abstrakty

EN

Long-term synaptic plasticity at hippocampal CA3-CA1 synapses exhibit NMDAR- and L-type calcium channel (VDCC)- dependent components. To address the role of MMP proteases in mechanism of LTP induction, we used field potentials recordings in acute mice brain slices. LTP was induced by 200 Hz tetanus. We have found that MMP inhibitor (NNGH, inhibits mainly MMP-3) disrupts 200 Hz-LTP (CTR: 164±11%, n=9; NNGH: 117±7%, n=7, P<0.01). Next, we dissected two components of 200 Hz-LTP using nifedipine (L-type blocker) and APV (NMDAR inhibitor). MMP blockade with NNGH prevented only vdccLTP (nmdaLTP in the presence of nifedipine: 140±6%, n=8; nifedipine+NNGH: 141±8%, n=6 P=0.93; vdccLTP in the presence of APV: 168±27%, n=7; APV+NNGH: 110±13%, n=6, P<0.05). Our observations show that MMP activity (presumably MMP3) specifically regulates VDCC-dependent component of hippocampal LTP. Supported by NCN grants: NN401541540 and ETIUDA 2013/08/T/ NZ3/00999.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2014
• Tom: 74
• Numer: 3
• Opis fizyczny: p.335-336

Twórcy

autor

Wiera G.

• Cellular Neuroscience Lab, Wroclaw University, Wrocław, Poland
• Biophysics Department, Wroclaw Medical University, Wrocław, Poland

autor

Mozrzymas J. W.

• Cellular Neuroscience Lab, Wroclaw University, Wrocław, Poland
• Biophysics Department, Wroclaw Medical University, Wrocław, Poland