Biology Reference
In-Depth Information
information is represented in the hippocampal formation and how this information is
encoded.
In order
to gain a better understanding of hippocampal experience-dependent
synaptic plasticity we also will create parallels between the synaptic alterations in the
declarative memory system and the equivalent synaptic changes throughout the
functionally well-known perceptual and procedural memory systems.
We review the
development of hippocampus-dependent memory models and stress the importance of
functional patterns that characterize the remodeling of the neural connectivity.
1.
E
XPERIENCE
-D
EPENDENT
C
HANGES OF
S
YNAPTIC
S
TRENGTH
A cardinal feature of neurons in the cerebral cortex comprises stimulus selectivity, and
experience-dependent shifts in selectivity are a common correlate of memory formation.
Many synapses in the hippocampus and neocortex are bidirectionally modifiable and depend
on the recent history of cortical activity. For memory to occur, these modifications must
persist long enough to contribute to long-term memory storage. This definitely appears to be
the case for the forms of synaptic plasticity known as long-term potentiation (LTP) and long-
term depression (LTD). Extensive research has been conducted to establish the contribution
of LTP to spatial learning (Castro
et al.
, 1989; Barnes, 1995; Moser, 1995; Morris & Frey,
1997) and validate it as a mechanism encoding spatial learning.
Hippocampal synapses are known to respond with long-term potentiation, to a brief
tetanus both in in vivo (Bliss & Lomo, 1973) and in vitro
(Deadwyler
et al.
, 1975) .
Electrophysiologically expressed, LTP was originally described by (Bliss & Lomo, 1973) as
having two components: (1) synaptic, expressed by an increase
in the synaptic efficacy, i.e.,
enhanced field excitatory postsynaptic potential (EPSP) with the same number of stimulated
fibersand (2) non-synaptic, concerned with an increase in the probability that an EPSP will
elicit an action potential. In some cases tetanic stimulation results in increased ability of an
EPSP to fire an action potential, even when the EPSP amplitude is unchanged. This
phenomenon is referred to as the non-synaptic component of LTP (Douglas & Goddard,
1975; Wilson, 1981; Taube & Schwartzkroin, 1988) and also as EPSP-spike or E-S
potentiation (Andersen
et al.
, 1980; Wigstrom & Swann, 1980). The intracellular correlate of
E-S potentiation is an increased probability of firing for a given EPSP amplitude (Chavez-
Noriega
et al.
, 1990). The mechanisms underlying E-S potentiation are believed to be
decrease in the ratio of inhibitory to excitatory drive (Wilson, 1981; Abraham
et al.
, 1987;
Chavez-Noriega
et al.
, 1990) and/or an increase in the intrinsic excitability of the
postsynaptic neuron through modulation of postsynaptic voltage-gated conductances (Hess &
Gustafsson, 1990; Bernard & Wheal, 1996; Noguchi
et al.
, 1998)
Frick et al., 2004 -Nature
Neurosci, 7:126-135. Although non-synaptic mechanisms comprise important part of
information processing in brain networks, we will focus further on the synaptic component of
neuronal plasticity, as it is proposed to underline long-term memory processes.
LTD is a lasting activity-dependent decrease in synaptic efficacy (Lynch
et al.
, 1977).
Both hetero- and homosynaptic forms of LTD can be induced in various pathways of the
hippocampal formation in vitro (Dunwiddie & Lynch, 1978; Dudek & Bear, 1992) and in
vivo (Levy & Steward, 1979; Thiels
et al.
, 1994; Doyere
et al.
, 1996; Heynen
et al.
, 1996;
Thiels
et al.
, 1996). It has become apparent that LTD may be equally important for spatial
