Biology Reference
In-Depth Information
number of synapses in the nervous system change under the influence of a variety of normal
physiological factors, including hormonal status (Kretz et al., 2004), activity (Devaud and
Ferrus, 2003; Harris et al., 2003), or age (Gan et al., 2003; Rosenzweig and Barnes, 2003;
Coggan et al., 2004). Also, cognitive deficits associated with aging or certain pathologies
result from widespread synapse loss in brain neurons (Spires and Hyman, 2004). Synaptic
loss is currently established as the best neurobiological correlate of the cognitive and motor
deficits in neurodegenerative diseases (Honer, 2003; Scheff and Price, 2003), schizophrenia
and mood disorders (Kolomeets et al., 2005). The changes that have been observed include
alterations of the postsynaptic structure (Forno and Norville, 1979; Machado-Salas et al.,
1989; Roberts and DiFiglia 1990; Ingham et al., 1991; Pickel et al., 1992; Avila-Costa et al.,
1998; Fiala et al., 2002; Avila-Costa et al., 2004; Avila-Costa et al., 2005b and others),
presynaptic ending edema (Ingham et al., 1991; Pickel et al., 1992; Avila-Costa et al., 2005b)
an addition of postsynaptic receptors to the postsynaptic density (Lüscher et al., 2000; Zhu et
al., 2000) and modifications of the pre and postsynaptic membranes -perforations— (Vrensen
and Nunez, 1981; Sirevaag and Greenough, 1985; Geinisman et al., 1988; Calverley and
Jones, 1987; Meshul and Casey, 1989; Geinisman et al., 1992; Toni et al., 2001 and others).
The presence of the perforated synapses suggests an increase in activity of that synaptic
terminal. However, despite the compelling evidence relating structural modification, the
mechanisms by which perforated synapses contribute to synaptic plasticity remain unknown.
In this way, in our laboratory we investigated whether the dopamine depletion produces
changes in the synaptology of the corpus striatum of rats after unilateral injection of 6-
OHDA. In this chapter our focus is to describe briefly the characteristics of perforated
synapses, synaptic organization of the corpus striatum, structure which plays an important
role in Parkinson's disease, and to analyze the synaptic changes after dopamine depletion,
focusing mainly in the formation of perforated synapses.
P
ERFORATED
S
YNAPSES
A synapse is an intercellular junction defined ultrastructurally as a postsynaptic electron
density (PSD) in direct opposition to a presynaptic profile associated with synaptic vesicles
that is referred to as an active zone. The synaptic cleft is a tight intercellular junction that is
resistant to biochemical disruption. The intervening space at the synapse is termed the
synaptic cleft (10 to 20 nm wide) (figure 1).
The chemical synapse is by far the most common type of synapse in the central nervous
systems of mammals. Because an axon terminal can form a synapse with any part of the
surface of another neuron, synapses in which an axon forms the presynaptic component may
be designated as being:
‐
axo-dendritic
‐
axo-somatic
‐
axo-axonal
