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Uptake, replication, and transneuronal passage of a swine neurotropic herpesvirus (pseudorabies virus, PRV) was evaluated in the rat CNS. PRV was localized in neural circuits innervating the tongue, stomach, esophagus and eye with light microscopic immunohistochemistry. In each instance, the distribution of PRV-immunoreactive neurons was entirely consistent with that observed following injection of cholera toxin- horseradish peroxidase conjugate (CT-HRP). Injections of the tongue resulted in retrograde transport of PRV and CT-HRP to hypoglossal motor neurons, while preganglionic neurons in the dorsal motor vagal nucleus or somatic motor neurons in the nucleus ambiguus were labeled following injections of the stomach or esophagus, respectively. At longer times after infection, viral antigens were found in astrocytes adjacent to infected neurons and their efferent axons and second-order neuron labeling became apparent. The distribution of second-order neurons was also entirely dependent upon the site of PRV injection. Following tongue injection, second-order neurons were observed in the trigeminal complex, the brain-stem tegmentum and in monoaminergic cell groups. Injection of the stomach or esophagus led to second-order neuron labeling confined to distinct subdivisions of the neucleus of the solitary tract and monoaminergic cell groups. Comparative quantitative analysis of the number of PRV immunoreactive neurons present in the diencephalon and brain stem following injection of virus into both the eye and stomach musculature of the same animal demonstrated that retrograde transport of PRV from the viscera was more efficient and occurred at a much faster rate than anterograde transport of virus. These data demonstrate projection-specific transport of PRV in the nervous system and provide further insight into the means through which this neurotropic virus infects the nervous system.

Lesions of the area postrema/caudal medial nucleus of the solitary tract (AP/cmNTS), located on the surface of the dorsal medulla of the rat, cause a transient syndrome of hypophagia and body weight loss, with the establishment of a new growth curve at a lower body weight set point. The regulatory responses to prolonged food deprivation, glucoprivic stimulation, and chronic access to a palatable diet are left largely intact. However, there is an overconsumption of highly palatable foods during acute exposure to supermarket and high-fat diets. Intestinal transit and gastric retention are unaffected by the lesion, indicating normal motor function within the gastrointestinal system. The hypophagia and chronic depression of body weight by the AP/cmNTS lesion demonstrate that this area is an important part of the larger neurocircuitry subserving feeding behavior and energy balance.

Lesions of the area postrema (AP) and adjacent caudal medial nucleus of the solitary tract (cmNTS) cause significant changes in water and sodium balance. Lesioned rats display a permanent polydipsia, which in part is due to a primary polyuria. Water-to-food ratios are elevated chronically. Lesioned rats are unable to concentrate their urine as well as controls. In addition, lesioned rats overdrink in response to 24-h water deprivation. This lesion also causes a natriuresis and an overconsumption of 3% NaCl solution. These findings establish the AP-cmNTS as an important part of the neurocircuitry underlying water and sodium balance.

Chronic decerebrate rats fitted with oral fistulas for remote injection of water or nutrient were tested for their capacity to behaviorally compensate for dehydration by increasing their ingestion of water. Decerebrates and their controls were given water for ingestion via the oral fistula in 50-microliter aliquots following various challenges. The rats' ejection of water from the mouth marked behavioral termination of the drinking. The volume of water was measured 1 and 24 h after an intragastric meal of regular diet; 0.5, 4, 8, and 24 h following subcutaneous isotonic or hypertonic NaCl injection; and 1, 4, 8, and 24 h following an intragastric meal of regular or 3% NaCl adulterated diet. Unlike controls, decerebrates failed to increase the amount of water ingested following intracellular dehydration regardless of the means of producing dehydration or the duration of time permitted for a response. However, both control and decerebrate rats increased their ingestion of a sweet solution (0.03 M sucrose) demonstrating their capacity to respond and confirming their ability to compensate for food deprivation. This lack of increased water intake in response to dehydration for decerebrate rats favors the existence of at least some aspects of the regulatory circuitry for this behavioral control of water balance to lie in the forebrain.