BRIGHT LIGHT ILLUMINATION:
It
is believed that serotonin levels cycle over a 24-h period, be entrainable by
light and maintain a fixed phase relationship with the rhythm of neurogenesis
(Wildt et al., 2004). This finding suggests that stress induction using bright
light may be involved in the light-activated cascade of events that culminates
in the circadian regulation of a variety of physiological functions in rodents,
including the rate of neuronal proliferation, biochemical factors and
behavioral interruption in the brain.
As
several reports indicated that bright light-illumination affects synaptic
plasticity, dendritic morphology and neurogenesis in animals (Adriaan
Bouwknecht et al., 2007) and induces both clinical and anatomical features of
neurotoxic damage in humans (i.e. posttraumatic stress disorders). The precise
mechanism by which stress induces brain damage is still a matter of debate.
Moreover, the understanding as well as interpretation of the effects observed
in this paradigm requires further examination, ideally approaching from various
disciplines.
BEHAVIORAL
CHANGES ON EXPOSURE TO BRIGHT LIGHT ILLUMINATION:
Exposure of rats
to the high light condition increased multiple measures of anxiety-related
behavior of group II rats. Increasing the intensity of illumination of the
open-field arena reduced locomotors activity and increased avoidance of the
center of the arena. In addition, rearing and grooming were reduced under the
condition while the duration of time spent in the corners of the apparatus and
the frequency of a stereotypical behavior of facing the corners of the
apparatus were increased. Facing the corner is interpreted as a copying style
to avoid the exposure to the bright light and the open surface of the arena Fig
2. The locomotion and sleep cycle deprivation was observed in the rats exposed
to light. Further, stress exposed group II rats exhibited decreased ambulation
and rearing which indicated reduced exploration and apathy respectively in
these animals. Increased immobility period and grooming activity depicted a
higher level of anxiety.
During
the period of the study, food intake and body weight were recorded (Table.1).
The deficits of both food intake and growth rate were found to be decreased on
stress induction.5-HT has been in the implicated in the control of eating
behavior and body weight. Enhanced activity at postsynaptic serotonergic
receptors reduces the amount of food eaten during a meal, decreases the rate of
eating and weight gain, and increases energy expenditure, both in animals and
in humans (Simansky 1996, Leibowitz 1998). It is well established that
monoamines and corticotropin-releasing hormone (CRH) (Krahn et al.,
1990, 1986) influence feeding behavior and mediate behavioral and physiological
response to stress (Kenett et al., 1986).Several investigators have attributed.
Stress induced anorexia to activation of CRH and/or serotonin
(5-hydroxytryptamine, 5-HT) pathways. However, rate of fecal pellet excretion
seemed to be increased during stress exposure period.
Table 1:
Effect of 1200 lux light induced
stress induction during consecutive days on body weight.
(Body weight changes represented in %)
PARTICULARS
|
DAY 1
|
DAY 3
|
DAY 5
|
DAY 7
|
DAY 9
|
DAY 11
|
DAY14
|
GROUP I
|
120.0±5.8
|
121.0±5.7
|
120.8±5.03
|
121.5±5.6
|
122.5±0.5
|
123.8±5.68
|
124.5±5.4
|
GROUP II
|
120.0±5.7
|
117.7±6.4
|
114.7±6.1
|
109.5±5.7**c
|
107.3±5.02
|
103.1±5.6
|
100.7±5.45**a***c
|
Values are expressed as mean ±
SD (n=6).
Statistical representation was
expressed * p<0.05.
*a Day 1 compared with Day 14.
*c Group I compared with Group II.
Effect of 1200 lux light–induced
stress induction during consecutive days on body weight:
(Body weight changes represented in %)
Values are expressed as mean ±
SD (n=6).
Statistical
representation was expressed * p<0.05.
*a Day 1 compared with Day 14.
*c Group I compared with Group II.
Figure
2: A version towards stress
A
number of clinical surveys suggest that life event stresses may have a role in
the onset of various mental illnesses including depression and pshychiatrical
disorders (Brown et al., 1978). The
severity of depressive disorders and its high prevalence in the modern society
increases the need of valid reliable animal models tor depression for the
study. Parallel studies on experimental animal show that an uncontrollable
stress situation produces neurochemical changes and behavior deficits (e.g.
deficit of food intake or exploratory activity) in experimental animals are
often taken as animal model of depression (Curzon et al., 1989).
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