Wt: 256/05 4/94 gr GB13,28 mM and 12/5 gr finely ground CuBr2,56 mM in 150 ml ethyl acetate and 150 ml chloroform was refluxed 15 hours. Reaction mixture was evaporated, 100 ml dichloromethane and 100 ml water added and shaken well. GB 12 was filtered and dried to give 3/9 gr of light-brown solid, 55% yield.
NMDA receptors are critical for the induction of some forms of long-term potentiation (LTP) in MPFC and in hippocampal slices as well as for learning and long-term memory in vivo in MPFC-dependent or hippocampal-dependent tasks (Luscher & Malenka, 2021). The induction but not long-term maintenance of LTP at some (but not all) excitatory synapses in hippocampal and MPFC slices is blocked by the NMDA glutamate receptor antagonist APV, and by NMDAR channel blockers such as MK-801 and ketamine (Bliss & Collingridge, 2021; Davis, Butcher, & Morris, 1992). In addition, NMDA receptor (https://middleeastexplorer.com/serial-code/?file=2573) activation promotes LTP (Zhang, Sullivan, Moskal, & Stanton, 2008). However, once LTP has been induced by cellular events, including the insertion of AMPA receptors into synapses in a protein synthesis-dependent manner, the increased synaptic efficacy, that is the expression of LTP, is not blocked by NMDAR antagonists (Luscher & Malenka, 2021). In vivo, learning acquisition and long-term memory formation are also blocked by NMDAR antagonists, including PEL (Burgdorf, Kroes, et al, 2021; Davis et al, 1992). Thus, the formation of the most well-studied form of LTP is triggered by NMDAR activation and is maintained by AMPA receptor (you could try here) synthesis and activation of cell surface trafficking (Bliss & Collingridge, 2021; Luscher & Malenka, 2021).