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Rats exposed to extreme heat stress (40°C) neither sweat nor pant. Instead they activate other heat loss mechanisms such as skin vasodilation, especially of the tail, and they also salivate and spread the saliva on their skin and fur to remove heat by evaporation. For saliva-spreading, the submandibular and the sublingual glands are primary thermoregulatory effector organs under such conditions. Saliva lost under heat stress has severe implications for the rats' body fluid economy and contributes to thermal dehydration and subsequent thirst. The importance of the rostral hypothalamus in particular the anteroventral wall of the third ventricle (lamina terminalis) in the control of body fluid homeostasis has been clearly demonstrated. Far less data are available concerning a possible role of the lamina terminalis in the control of body temperature. However, lesioning studies in the rat, that included the lamina terminalis and parts of the preoptic area or the anterior hypothalamus, led to severe deficits in regulating body temperature under heat stress and clearly affected the thermoregulatory secretory function of salivary glands. In order to neuroanatomically demonstrate central efferent pathways controlling heat-induced salivation, including those arising from the rostral hypothalamus, we employed the viral tracing technique, that uses the transsynaptic retrograde transport of an attenuated strain of pseudorabies virus (PRV-Bartha) for neuronal tract tracing. In an attempt to further distinguish the central efferent outflow towards the salivary gland innervation, viral inoculations were combined with ipsilateral chorda tympani destruction (parasympathectomy), removal of the ipsilateral superior cervical ganglion (sympathectomy) and total ipsilateral efferent denervation (parasympathectomy and sympathectomy). In addition, the immunohistochemical detection of the neuronal activation marker c-Fos was used as a more functional approach to neuroanatomically demonstrate central structures activated in the heat (2h, 40°C). Unilateral injections of PRV-Bartha into as well as surgical denervation of the left submandibular or sublingual gland were performed in male Sprague-Dawley rats (250-350 g) under general anaesthesia with sodium pentobarbitone (60 mg/kg, i.p.). For the histological brain analysis rats were (re-)anaesthetized (100 mg/kg pentobarbitone, i.p.) after a 1-4 day tracing period or after 2 h heat stress, respectively, and then transcardially perfused with 0.9% saline followed by 4% paraformaldehyde/phosphate buffer. Inoculation of the glands revealed multisynaptic neuronal pathways arising from various forebrain regions including the entire lamina terminalis. The denervation experiments suggested that the first wave of lamina terminalis infection was due to efferent connections directed towards the parasympathetic submandibular gland innervation. Heat stress induced a clear Fos-activation in many brain structures when compared to the controls and again the lamina terminalis and in particular its median preoptic nucleus showed an intense Fos-response. These data suggest that one efferent forebrain pathway influencing salivary secretion under heat stress may originate in the lamina terminalis and may be used especially under heat stress-induced hyperthermic and hyperosmolal conditions. Therefore a key to the understanding of the central regulation of heat induced salivation in the rat may be the unravelling of the integrative role of the lamina terminalis in processing thermoregulatory and osmoregulatory information.