Biology Reference
In-Depth Information
2.2. Spike timing-dependent plasticity
In addition to frequency-dependent Hebbian modifications, another mechanism also has
been proposed to underlie adult functional plasticity (Dan & Poo, 2004; Yao & Dan, 2005).
Changes in synaptic efficacy can be based also on the precise timing of presynaptic and
postsynaptic activity (Levy & Steward, 1983; Markram
et al.
, 1997; Debanne
et al.
, 1998).
This “spike-timing-dependent plasticity” (STDP) has several properties which are believed to
transform changes in environmental inputs into changes in neural representations (Fu
et al.
,
2002; Sur
et al.
, 2002).
The functional consequence of spike-timing plasicity is that synapses
from a presynaptic neuron which contribute to the firing of the postsynaptic neuron will be
strengthened, whereas synapses which are uncorrelated or negatively-paired with postsynaptic
spike times will tend to be weakened (Fig 1B). The amount of LTP falls off roughly
exponentially as a function of the difference between pre- and postsynaptic spike times with a
time constant that is of the same order as a typical membrane time constant. This ensures that
only those presynaptic spikes that arrive within the temporal range over which a neuron
integrates its inputs are potentiated, further enforcing the requirement of causality. STDP
appears to depend on interplay between the dynamics of NMDA receptor channel activation
and the timing of action potentials back-propagating through the dendrites of the postsynaptic
neuron (Magee & Johnston, 1997; Linden, 1999; Sourdet & Debanne, 1999). Repeated
pairing of postsynaptic spiking after presynaptic activation results in larger calcium influx and
LTP (EPSP precedes the back-propagating action potential), whereas postsynaptic spiking
before presynaptic activation (EPSP follows the action potential) leads to a small calcium
transient and LTD (Bell
et al.
, 1997; Markram
et al.
, 1997; Bi & Poo, 1998; Debanne
et al.
,
1998; Zhang
et al.
, 1998; Egger
et al.
, 1999; Feldman, 2000). This temporally-asymmetric
Hebbian synaptic plasticity supports sequence learning because it tends to wire together
neurons that form causal chains (Paulsen & Sejnovski, 2000). Thus, NMDAR-gated
modification of synaptic efficacy is essential for creating and stabilizing activity patterns in
neural networks. STDP can act as a learning mechanism for generating neuronal responses
selective to input timing, order, and sequence. STDP-like rules have been applied to
coincidence detection (Gerstner
et al.
, 1996), sequence learning (Abbott & Blum, 1996;
Roberts, 1999), path learning in navigation (Blum & Abbott, 1996; Mehta
et al.
, 2000), and
direction selectivity in visual responses (Schuett
et al.
, 2001; Yao & Dan, 2001). In general,
STDP greatly expands the capability of frequency-dependent plasticity to address temporally
sensitive computational tasks.
Given that the hippocampus is critical for spatial memory formation, and that its synapses
undergo synaptic plasticity, an important question concerns how the functional activity and
synaptic alterations in this region relate to one another. The first approach in this direction
will be to define the rules under which hippocampal representations are modified with
experience, an issue that we explore in the following section.
