OLIGODENDTROCYTE STRESS PROTEIN:
Stress
proteins or heat shock proteins (HSP) play a role in normal CNS development and
function, and are enhanced after traumatic injury of the brain and during neurodegenerative
diseases (Brown, 1994; Marcucilli and Miller, 1994). Their involvement in
autoimmune diseases, such as multiple sclerosis (MS), has been suggested
(Birnbaum, 1995; Brosnan et
al., 1996; Van Noort et al., 1995). Stress
proteins are induced by a variety of stress situations, including hyperthermia, viral infection,
ischemia, anoxia and oxidative stress, and many of them are also constitutively
expressed (Birnbaum, 1995). Constitutively expressed HSP function as molecular
chaperones and participate in protein synthesis, protein folding, transport and
translocalization processes.
Stress proteins serve as biomarkers to
identify the contribution of stress situations underlying the pathogenesis of
degenerative diseases of the CNS. Oxidative stress has been implicated in the
pathogenesis of MS, and specifically, HSP32/HO-1 might indicate oxidative
stress and is involved in antioxidant defence mechanisms, but so far has not
been investigated in myelinating cells. To further characterize the stress
responses in oligodendrocytes and possible consequences for demyelinating
diseases, we have analyzed the constitutive and inducible occurrence of stress
proteins in cultured rat brain oligodendrocytes using a panel of antibodies
directed against HSP/HSC70, HSP60, HSP25, αBcrystallin and HSP32/HO-1. The data
demonstrate that oligodendrocytes differentially up-regulate HSPs after heat
shock and oxidative stress, and that oxidative stress, but not heat stress,
leads to the induction of HSP32/HO-1. Hence, HSP32/HO-1 might represent a
useful marker to further elucidate the possible involvement of oxidative stress
in inflammatory demyelinating diseases.
BRIGHT LIGHT INDUCTION OF STRESS:
Light is an important environmental
factor for regulation of mood. As rats are nocturnal and are sensitive to
extreme bright light environment, light illumination was selected in the
current study as a stressor for the stress-induced depression models. Serotonergic
neurons may play a particularly important role in the facilitation of
anxiety-related physiological or behavioural responses. A wealth of evidence
supports an association between the neuronal activity of brainstem serotonergic
neurons and the level of somatic motor activity or behavioural arousal on
exposure to uncontrollable stress or other anxiety related stimuli including
anxiogenic drugs and social defeat. Bright light can be used as an effective
aversive stimulus leading to an increase in avoidance behaviours. Exposure of
rats to the HL (1000–1200 lux) condition performed in the current study was
comparable to previous behavioural studies using a similar behavioural test
arena for an alternative anxiety paradigm, i.e. the social interaction test
which will be a suitable model for analyzing the light induced variations in
the brain.( Adriaan et al., 2007)
Light-induced modulations of
brain activity while participants are engaged in non visual cognitive tasks
were detected in numerous areas including: alertness-related subcortical
structures such as the brainstem, in a location compatible with the locus coeruleus
(LC) (Vandewalle,
et al., 2007);
the hypothalamus, in a location encompassing the SCN (Perrin, et al., 2004);
and dorsal and posterior parts of thalamus, but also in long-term memory and
emotion-related areas such as the hippocampus
and amygdale (Vandewalle, et al., 2006)
The aim of the stress research was to
develop drugs and methods able to stimulate the intrinsic adaptive mechanisms
of the organism to help it survive in situations of intense or prolonged
stress, whilst preferably maintaining the capability for physical and mental
work (Meerson, 1984).
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