Biology Reference
In-Depth Information
S
YNAPTIC
P
LASTICITY
It is now clear that the mammalian brain is able to take advantage of the neuronal
capacity to express long-lasting, activity-dependent synaptic modifications as mechanisms by
which experience modifies neural circuits and behavior.
Plasticity is the ability of a structure to change its shape and/or function in response to
change in environmental conditions. From the neurobiological point of view, plasticity is the
capacity of neural activity to modify neural circuitry and function in response to
environmental stimuli, manifesting as changes in thoughts, feelings and behavior. The term
synaptic plasticity refers to the ability of the nervous system to modify the strength and the
efficacy of synaptic transmission at preexisting synapses in an activity-dependent manner.
One of the first people to introduce the concept of behavior modificability was Freud in
his topic
Project for a Scientific Psychology
(1895), in which he explained his ideas about the
neural basis of learning. Freud hypothesized a relationship between traumatic events, synaptic
plasticity, memory processes and psychopathology in light of contemporary ideas about the
neuronal bases of psychic symptoms and the synaptic substrate of learning and memory
(Freud, 1895). Freud's interest in the neural basis of memory was based on the discoveries of
Ramon y Cajal regarding the organization of the nervous system. Some years later, Ramon y
Cajal in his topic
Texture of the Nervous System
(1904), proposed that the ability of mammals
to adapt their behavior to external conditions must be due to changes in brain anatomy,
extending the notion of plasticity to the neural substrate.
The concept of synaptic plasticity
was articulated for the first time by Donald Hebb (1949) who proposed that associative
memories can result from subtle alterations in synapses widely distributed throughout the
brain. He proposed that memory is the result of the internal brain representation of an object,
and is comprised of all of the cortical cells that are activated by the external stimuli. If
activation of the representational group of cells persisted long enough, memory consolidation
would take place. This process makes the reciprocal interconnection between involved
neurons more effective in firing together. Hebb also proposed that in a synaptic cleft, the
contact between the presynaptic axon and the postsynaptic neuron is strengthened when the
presynaptic axon is active at the same time the postsynaptic neuron is strongly activated by
other inputs. This results in a reorganization of pre-existing neural circuits, which he called
synaptic plasticity (Hebb, 1949). Hebb proposed that synaptic plasticity forms a memory trace
after the detection of two coincident events. This concept provides a model for the cellular
and even the molecular basis underlying not only declarative memory, but also for behavioral
processes such as Pavlovian and Instrumental learning. These last memory processes are
associative and constitute the basis of emotions and behavior.
Later, physiological studies of the hippocampus provided experimental evidence for
long-lasting changes in synaptic strength (Bliss and Lomo, 1973; Collingridge and Bliss,
1995; Cooke and Bliss 2005, 2006). Brief, high-frequency electrical stimulation of an
excitatory pathway to the hippocampus was found to produce a long-lasting enhancement of
the strength of the stimulated synapses (Bliss and Lomo, 1973; Bliss and Gardner-Medwin,
1973).
Since the hippocampus is involved in processes such as declarative memory (Scoville
and Milner, 2000; Teyler and Discenna, 1984), different authors have hypothesized that long-
lasting activity-dependent synaptic changes can represent the neural basis of learning and
memory (Bliss and Lomo, 1973; Morris et al., 1986). The synaptic activity that leads to
