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17: The Stress Reaction.

A further complication arises when an individual is exposed to aversible stimuli.

Aversible stimuli induces:

* Increased activation of the Adrenal medullas by the Autonomous Nervous System (ANS) by which the catecholamine adrenalin (alt. epinephrine) and noradrenalin is released to the blood circuit.

* Increased activating of the Hypothalamus - pituitary gland - adrenal cortex axis (the HPA-axis) resulting in an increased secretion of the adrenocortical steroid hormones cortisol, corticosterone, progesterone and testosterone (the corticosteroids)

An overview of these pathways and releases of hormones is seen in Figure 5:

Figure 5

Corticotrophin-releasing factor (CRF), secreted by the Hypothalamus, travels by the portal vein system down to the Adenohypophysis initiating a release of the adrenocorticotrophe hormone (ACTH). Following this release, ACTH travels by the blood stream down to the adrenal cortex' in which the main part of the steroids is synthesized. These are subsequently released to the blood circuit.

It is believed that vasopressin (a peptide secreted by the neurohypophysis) can enhance the effect of ACTH and by that exhibiting a synergistic effect. Another effect of vasopressin is to keep the kidneys "tight" (to preserve the water balance) which is a fact well having in mind when experiments on rats exhibiting SIP (Scheduled induced polydipsia - see here) shows that the rats can have lowered levels of cortisol in their plasma.

Cortisol is a steroid, which influence the organism in many ways: Cortisol increases the gluconeogenesis and inhibits the muscles in their uptake of glucose. It stimulates the lipolysis and by doing that increases the concentration of free fatty acids. The RNA synthesis in the liver is increased by cortisol, which at the same time cause the RNA and DNA synthesis in other types of tissues to decrease. A correlation between increased levels of cortisol and immunosuppression is now broadly accepted but (maybe) the most important effect of cortisol when it comes to stereotypic behaviours is its effect on Hippocampus - one of the brain structures, which inhibits the activity in Nucleus accumbens (see here).

Increased levels of cortisol in a shorter period of time can cause reversible damages on Hippocampus (loss of dendrites) while the effect of a longer exposure (months) of increased cortisol levels is irreversible lesions of this structure (loss of neurons).

Hippocampus in a chronic stressed individual will therefore presumably not exert the same inhibiting effect on Nucleus accumbens and it is therefore possible to envision that the activity of Nucleus accumbens during "normal" dopamine-pulses could result in stereotypical behaviour. Experiments involving hippocampoectomy showed that the ectomy-induced stereotypies could be decreased by the aid of dopamine-antagonists.

Beside these above- and before mentioned factors, operating at the Environmental- and Physiological level, some observations do suggest that genetic predispositions on the Genetic level can be of importance as to the proneness for an individual to develop stereotypic behaviour.

Next topic: Evidence of genetic control of behaviour.