Prolactin fractions from lactating rats elicit effects upon sensory spinal cord cells of male rats.

Recently it has been suggested that the neurohormone prolactin (PRL) could act on the afferent nociceptive neurons. Indeed, PRL sensitizes transient receptor potential vanilloid 1 (TRPV1) channels present in nociceptive C-fibers and consequently reduces the pain threshold in a model of inflammatory pain. Accordingly, high plasma PRL levels in non-lactating females have been associated with several painful conditions (e.g. migraine). Paradoxically, an increase of PRL secretion during lactation induced a reduction in pain sensitivity. This difference could be attributed to the fact that PRL secreted from the adenopituitary (AP) is transformed into several molecular variants by the suckling stimulation. In order to test this hypothesis, the present study set out to investigate whether PRL from AP of suckled (S) or non-suckled (NS) lactating rats affects the activity of the male Wistar wide dynamic range (WDR) neurons. The WDR neurons are located in the dorsal horn of the spinal cord and receive input from the first-order neurons (Ab-, Ad- and C-fibers). Spinal administration of prolactin variant from NS rats (NS-PRL) or prolactin variant from S rats (S-PRL) had no effect on the neuronal activity of non-nociceptive Ab-fibers. However, the activities of nociceptive Ad-fibers and C-fibers were: (i) increased by NS-PRL and (ii) diminished by S-PRL. Either NS-PRL or S-PRL enhanced the post-discharge activity. Taken together, these results suggest that PRL from S or NS lactating rats could either facilitate or depress the nociceptive responses of spinal dorsal horn cells, depending on the physiological state of the rats.

Brain Na+/K(+)-ATPase regulation by serotonin and norepinephrine in normal and kindled rats.

In this work we confirmed the activation of rat brain Na+/K(+)-ATPase by norepinephrine (NE) and observed a variable response of the enzyme according to the brain region considered. In isolated neuronal or glial fractions from normal cerebral cortices, we studied the response of the enzyme to increasing concentrations of serotonin (5-HT) (10(-9)-10(-3) M). A dose-dependent response over basal values was present in glial fractions, beginning at 10(-6) M. No such response was obtained in the neuronal fractions. In amygdaloid kindled brains, the pattern of activation by NE was different than in controls: less pronounced (cortex, brainstem, and diencephalon), inhibition-activation (cerebellum), or no change (striatum). The activation of Na+/K(+)-ATPase by 5-HT observed in the control glial fraction was not present in the kindled glial fraction. In conclusion, 5-HT seems to activate Na+/K(+)-ATPase preferentially in glial cells, and the kindling process markedly modifies this regulation. The normal response to NE in brain homogenates is less altered by kindling than is the response to 5-HT in the same regions.

Serotonin-dependent (Na+,K+)ATPase in kindled rats: a study in various brain regions.

Serotonin (5-HT) modulation of brain (Na+,K+)ATPase, has recently been proposed. Activation curves of the enzyme activity dependent on 5-HT concentration have previously been observed in various brain regions of normal rats. In the present study, we report the absence of 'normal' (Na+,K+)ATPase response to 5-HT in cerebral cortex, striatum and diencephalon of kindled rats.