Glutamatergic systems in the bed nucleus of the stria terminalis, effects on cardiovascular system

Abstract

The bed nucleus of the stria terminalis (BST) is a part of the limbic system. Two studies have shown that microinjection of L: -glutamate in the BST elicited cardiovascular depressive and bradycardic responses, but in one study, both pressor and depressor responses were observed in the chemical stimulation of BST by glutamate in the urethane-anesthetized rats. Also, the roles of glutamate receptor subtypes have not been investigated yet. The aim of this study was to find the effects of glutamate and its receptors on the blood pressure and heart rate in the BST of urethane-anesthetized rats. The drugs (50 nl) were microinjected into the BST of anaesthetized rats. The blood pressure and heart rate were recorded throughout each experiment. The average changes in the mean arterial pressure and heart rate at different intervals were compared both within each case group and between the case and the control groups, using repeated measures ANOVA. Microinjection of L: -glutamate (0.25 M) into the BST resulted in the decrease of the mean arterial pressure (-18.85 +/- 3.84 mmHg) and heart rate (-18 +/- 4 beats/min). Injection of AP5, antagonist of glutamate NMDA receptor (2.5 , 5 mM) and CNQX, antagonist of glutamate AMPA receptor (0.5, 1 mM) had no significant effect on the mean arterial pressure and heart rate. Either Ap5 or CNQX, when co-injected with glutamate, abolished the depressor and bradycardic effects of glutamate, suggesting that simultaneous activation of both glutamate receptors is necessary for the effect of glutamate system to emerge.

Neural regulation of endocrine and autonomic stress responses

“…In anesthetized rats, chemical or electrical stimulation of the BST produces predominantly depressor actions, particularly when the stimulation is directed to the anteromedial subregion 77–79 . However, in awake animals, pharmacological activation of this region elicits a rapid pressor response, followed by bradycardia 80, 81 , whereas inactivation exacerbates restraint-induced increases in heart rate 82 .…”

Central Autonomic System

“…Several subdivisions, including the dorsolateral (or oval), dorsomedial, anteromedial, and ventral magnocellular subnuclei, have extensive autonomic projections to sites such as the paraventricular and arcuate nuclei, lateral hypothalamic area and ventrolateral periaqueductal gray matter. There is some evidence that neurons in the bed nucleus of the stria terminalis respond to cardiovascular stimuli (Hilton and Spyer, 1971), and stimulation of the bed nucleus can cause increased gastric motility (Hermann et al, 1990), and decreased blood pressure and heart rate (Hatam and Nasimi, 2007). On the other hand, there has been no systematic attempt to relate the subnuclei of the bed nucleus of the stria terminalis, or their connections with specific autonomic responses.…”

Role of the bed nucleus of the stria terminalis in the cardiovascular responses to acute restraint stress in rats

“…In anesthetized rats, BST stimulation, either electrical or chemical with excitatory amino acids, causes cardiovascular responses (Gelsema and Calaresu 1987;Ciriello and Janssen 1993;Gelsema et al 1993;Dunn and Williams 1995;Hatam and Nasimi 2007). Microinjection of noradrenaline or carbachol into the BST evokes a BP increase associated with reflex bradycardia in unanesthetized rats Crestani et al 2007Crestani et al , 2008.…”