Cortical spreading depression induces an LTP-like effect in rat neocortex in vitro

Role of different voltage-gated Ca2+channels in cortical spreading depression: Specific requirement of P/Q-type Ca2+channels

“…In agreement with our findings, most previous studies investigating the effect of NMDA receptor antagonists on CSD, induced by brief K + pulses in cortical slices, reported complete blockade of CSD recorded at ≥500 mm from the local K + ejection [14][15][16][17] (but see ref. 18 for an exception in hippocampal slices); moreover CSD could not be recorded after perfusing the slices in Ca 2+ -free medium or after blocking the Ca 2+ channels cycle that ignites CSD in normally metabolizing cortical tissue.…”

“…Our findings in cortical slices are consistent with in vivo studies of CSD induced by electrical stimulation of the cortex, showing that, after i.p. injection of NMDA antagonists, even stimulation currents ten times longer and eight times larger than the CSD triggering threshold were unable to induce a CSD, 20 and spontaneous cacna1a mouse mutants, with mutations that produce partial lossof-function of the P/Q-type Ca 2+ channel, required an approximately 10 fold with Cd 2+ , 14,16 or Ni 2+ and Co 2+ . 19 These findings are consistent with the conclusion that activation of NMDA receptors and Ca 2+ influx through Ca v channels are both required for CSD induction and/or propagation (although a possible caveat is the uncertainty regarding how much the K + stimulus exceeded the CSD threshold).…”

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

“…SD may also render the cortex transiently hyperexcitable. For example, SD enhances excitatory postsynaptic field potentials as well as the repetition rate and amplitude of spontaneous rhythmic potentials 20-90 minutes after its induction; it augments long-term potentiation in human neocortical slices (67,68). SD is followed by hyperexcitability in rat neocortex and spinal cord after transient depression of neuronal activity (69,70).…”

Spreading Depression: Imaging and Blockade in the Rat Neocortical Brain Slice

“…SD in normally metabolizing cortical tissue (induced by focal K ϩ , mechanical or tetanic stimulation) is blocked by N-methyl-D-aspartate receptor (NMDAR) antagonists (but not by non-NMDAR antagonists) as reported in vivo (HernandezCaceres et al 1987;Marrannes et al 1988;Lauritzen and Hansen 1992;Nellgard and Wieloch 1992;Koroleva et al 1998) and in hippocampal and neocortical slices (Somjen 2001;Footitt and Newberry 1998). Note that NMDAR participation does not necessarily imply causation (Obrenovitch 2001).…”

“…However, the role of NMDARs in neuroprotection is being increasingly questioned (Jarvis et al 2001;Obrenovitch 2001;Obrenovitch and Urenjak 1997;but see Palmer 2001). Certain 1 R ligands reduce ischemic damage in vivo (George et al 1988;Feeser 1988) andin vitro (Wong et al 1988;Church et al 1991), and there is also evidence for protection independent of NMDARs (Lockhart et al 1995;Klette et al 1997). Here we test 1 R ligands for their ability to prevent SD independent of NMDAR activity and as possible alternatives to NMDAR antagonists, the latter being poorly tolerated clinically.…”