- Feuerbach, D. et al. (2010) Eur. J. Pharmacol. 637, 46.
- Alomone Labs (±)-CPP inhibits NMDA (NR1+NR2A) channels expressed in Xenopus oocytes.A. Time course of NMDA currents elicited by 10 µM glutamate every 50 sec, while membrane potential was held at -80 mV. 1 and 10 µM (±)-CPP (#C-175), applied for 4 min, reversibly inhibited current amplitude. B. Superimposed current traces taken from experiment described in A.
(±)-CPP is a competitive, highly selective N-methyl-D-aspartate (NMDA) receptor antagonist.
CPP inhibits most NMDA receptor subtypes by reversibly binding to the glutamate binding site. CPP originally synthesized as restricted analog of AP7 and AP5, NMDA antagonists has the ability to cross the blood-brain barrier which makes it useful experimentally and effective even when administered systemically1.
The NMDA receptor is a glutamate-gated, multi-subunit channel complex that is involved in a variety of neural processes, including synaptic transmission, synaptic plasticity, and cell death. CPP has the ability to antagonize the release of acetylcholine from striatal regions evoked by NMDA1,2.
Several studies have shown that systemic administration of CPP in rodent disrupts neurogenesis, learning and memory, blocks stress induced responses, produces antidepressant-like effects, interferes with addiction paradigms, and blocks both long-term potentiation and long-term depression1.
Studies have established CPP as a pharmacological tool to investigate the role of NMDA receptors and the functional consequences of their impairment1.
(±)-CPP (#C-175) is a highly pure, synthetic, and biologically active compound.