Abstract
Recent evidence has suggested that the dorsal (DH) and the ventral (VH) poles of the hippocampus are structurally, molecularly and functionally different regions. While the DH is preferentially involved in the modulation of spatial learning and memory, the VH modulates defensive behaviors related to anxiety. Acute restraint is an unavoidable stress situation that evokes marked and sustained autonomic changes, which are characterized by elevated blood pressure (BP), intense heart rate (HR) increases, skeletal muscle vasodilatation and cutaneous vasoconstriction, which are accompanied by a rapid skin temperature drop followed by body temperature increases. In addition to those autonomic responses, animals submitted to restraint also present behavioral changes, such as reduced exploration of the open arms of an elevated plus-maze (EPM), an anxiogenic-like effect. In the present work, we report a comparison between the effects of pharmacological inhibition of DH and VH neurotransmission on autonomic and behavioral responses evoked by acute restraint stress in rats. Bilateral microinjection of the unspecific synaptic blocker cobalt chloride (CoCl2, 1mM) into the DH or VH attenuated BP and HR responses, as well as the decrease in the skin temperature, elicited by restraint stress exposure. Moreover, DH or VH inhibition before restraint did not change the delayed increased anxiety behavior observed 24 h later in the EPM. The present results demonstrate for the first time that both DH and VH mediate stress-induced autonomic responses to restraint but they are not involved in the modulation of the delayed emotional consequences elicited by such stress.
Highlights
Stress has been consistently shown as a risk factor for the development of cardiovascular diseases
Several responses have been traditionally associated with stressor exposure, including the neuroendocrine hypothalamo-pituitaryadrenocortical (HPA) axis activation by the release of glucocorticoids and adrenocorticotropin hormone- ACTH [1,2,3], the autonomic system, indexed by peripheral catecholamine release, heart rate, blood pressure, or core body temperature measurements [4,5,6,7,8,9,10], and several behavioral responses characterized by inhibition of locomotor activity, inhibition of feeding and drinking [2,7,11,12] and the anxiogenic effect observed in the elevated plus-maze (EPM) 24 h after the stress [9,13,14]
Acute restraint stress (RS) is a widely utilized experimental model to study the emotional and autonomic responses to stress. It is an unavoidable aversive situation where the animal is placed in a plastic tube or metal, which restricts its movements [41,42]. This stress model leads to hormonal changes [43], cardiovascular responses characterized by elevated blood pressure and heart rate [15,16] and skeletal muscle vasodilatation and cutaneous vasoconstriction, which are accompanied by a rapid skin temperature drop and followed by a rise in body temperature [9,44,45]
Summary
Stress has been consistently shown as a risk factor for the development of cardiovascular diseases. Besides the hypothalamus and brain stem, which are essential for autonomic and neuroendocrine responses to stress, higher cognitive areas of the brain that play a key role in memory, anxiety, and decision-making, may participate in the modulation autonomic and behavioral responses to stress. It has been shown, for example, that the prefrontal cortex [15], the lateral septal area [9,16] and the bed nucleus of stria terminalis [17] play important roles in the modulation of the cardiovascular and emotional components of the stress reaction. Aversive experiences, including stress, may contribute to human and animal disorders associated with major hippocampal dysfunction [32,33,34]
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