Neural compartmental extracell (s) having beta Amyloid as Extracellular element
||"...beta-Amyloid(1-40) is related to an increase of non-L-type Ca channels ..." (Rovira C, et al. 2002).
||"The effect of intracerebroventricular (icv) injections of beta-amyloid peptide fragments Abeta[15-25], Abeta[25-35], and Abeta[35-25] were examined on synaptic transmission and long-term potentiation (LTP) in the hippocampal CA1 region in vivo. ... LTP was, however, markedly reduced by Abeta[25-35; 10 nmol] (129 +/- 9%, n = 6, P < 0.001) and blocked by Abeta[25-35; 100 nmol] (99 +/- 6%, n = 6, P < 0.001). ... The Abeta-peptides tested were also shown to have no significant effect on paired pulse facilitation (interstimulus interval of 50 ms), suggesting that neither presynaptic transmitter release or activity of interneurons in vivo are affected. The effects of Abeta on LTP are therefore likely to be mediated via a postsynaptic mechanism. This in vivo model of LTP is extremely sensitive to Abeta-peptides that can impair LTP in a time- ([25-35]) and concentration-dependent manner ([25-35] and [35-25]). These effects of Abeta-peptides may then contribute to the cognitive deficits associated with Alzheimer's disease."
(Freir DB et al. 2001)
||"The toxicity of beta-Amyloid(25-35) implicates a potentiation of L-type Ca currents ..." (Rovira C, et al. 2002).
||A model shows that block of I_A is sufficient to cause membrane depolarization, calcium influx, and increased excitability (Good TA, Murphy RM 1996).
||Application of beta-amyloid to outside-out patches reduces the A-current; leading to increased dendritic calcium influx and loss of calcium homeostasis, potentially causing synaptic failure and initiating neuronal degenerative proceses(Chen C 2005).
||Impairment of LTP by beta-Amyloid is independent of NMDA receptors or voltage dependent Ca currents (Nomura I et al. 2005)