RESULT AND DISCUSSION-BRIGHT LIGHT ILLUMINATION



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.

Graph 1:
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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