Hypothalamic control of nocireceptive and other neurons in the marginal layer of the dorsal horn of the medulla (trigeminal nucleus caudalis) in the rat.

The effect of electrical stimulation of the preoptic area of the hypothalamus on the discharge of neurones in the marginal layer (lamina I) of the trigeminal nucleus caudalis was studied in the anaesthetised rat. There was a powerful suppression of the discharge evoked by noxious thermal stimuli in 49/49 specific nociceptor driven (nocireceptive) neurones. The inhibitory effect increased with graded increases in the intensity of preoptic stimulation.

Medial hypothalamic stimulation produces analgesia to facial heating in unrestrained rats.

Gradual heating of the face in unrestrained conscious rats produced a behavioural response at a mean threshold temperature of 41.9 degrees C (S.E.

Are single-unit recordings useful in understanding thermoregulation?

The data which have emerged from single-unit recordings of thermally sensitive neurons in the hypothalamus are reviewed. Although these neurons may be important components in the central control of body temperature, the interpretation of the data is fraught with uncertainties. The neurons in question could be primary thermosensors or part of an integrative network.

Is prostaglandin E the neural mediator of the febrile response? The case against a proven obligatory role.

We have reviewed the evidence in favor of a prostaglandin mediator of the thermal responses in fever and found that PGE injected into the hypothalamus does not always cause fever, that cerebrospinal fluid concentrations of PGE are not reliable reflections of hypothalamic events, and that antipyretic drugs may act in ways other than inhibiting PGE synthesis. Fever is not blocked by prostaglandin antagonists, nor by ablation of PGE-sensitive areas of the brain. There is poor correlation between the effects of pyrogens and of PGE on cerebral neurons.

Naloxone does not influence a pyrogen fever in rabbits.

Rabbits were made febrile by an intravenous injection of homologous endogenous pyrogen (Interleukin 1). When naloxone (0.1 mg/kg i.