By Steven E Ed Hyman
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Additional resources for Annual Review of Neuroscience 2008
The highly irregular ﬁring of cortical cells is inconsistent with temporal integration of random EPSPs. J. Neurosci. 13:334–50 Spruston N, Schiller Y, Stuart G, Sakmann B. 1995. Activity-dependent action potential invasion and calcium inﬂux into hippocampal CA1 dendrites. Science 268:297–300 Stanton PK, Sejnowski TJ. 1989. Associative long-term depression in the hippocampus induced by Hebbian covariance. Nature 339:215–18 Stefan K, Kunesch E, Benecke R, Cohen LG, Classen J. 2002.
In the Schaffer collateral pathway to hippocampal CA1, pairing a weak and a strong input (which evokes postsynaptic spiking) at positive intervals can induce NMDA receptor–dependent tLTP within a narrow window of 3–10 ms. Bath application of isoproterenol, a β-adrenergic receptor agonist, broadens the window to 15 ms without changing the magnitude of tLTP (Lin et al. 2003), an effect that depends on PKA and mitogen-activated protein kinase (MAPK) signaling. In the amygdala, dopamine can gate the induction of tLTP by suppressing feedforward inhibitory inputs to the postsynaptic cell (Bissiere et al.
In the neocortex, a similar boosting of the BAP by the preceding EPSP is achieved by voltage-gated Na2+ channel activation in the distal dendrites (Stuart & Hausser 2001). Such nonlinear interactions between the EPSP and BAP at short positive intervals could explain the supralinear summation of Ca2+ inﬂux to the active synapse in both hippocampal (Magee & Johnston 1997) and neocortical (Koester & Sakmann 1998) (Nevian & Sakmann 2004) neurons. tLTD Window Models based on the Ca2+ hypothesis have also been used to explain the tLTD window (post → pre, negative intervals) (Karmarkar & Buonomano 2002, Shouval et al.