Galanin is a 29-amino acid peptide and widely distributed in the brain, although its significance in the control of neural activities is undefined. In the present study, we describe the effects of galanin on the electrically evoked release of dopamine in the rat central nervous system. In addition, to elucidate a possible role of galanin in the regulation of dopaminergic transmission in hypertension, we examined whether the effect of galanin on dopamine release might be altered in the central nervous system of spontaneously hypertensive rats (SHR). Galanin (1 x 10(-8) to 1 x 10(-7) mol/L) inhibited the stimulation (1 Hz)-evoked [3H]dopamine release by a comparable amount in striatal slices of Sprague-Dawley rats, although the basal release of dopamine was not affected by the peptide. In the striatum of SHR, the electrical stimulation (1 Hz)-evoked [3H]dopamine release was significantly smaller than in the striatum of Wistar-Kyoto (WKY) rats. However, the inhibitory effect of galanin on the stimulation-evoked [3H]dopamine release was significantly more pronounced in SHR than in WKY rats. These results show that galanin significantly reduced the release of dopamine in rat striatum. Furthermore, the greater inhibitory effect of galanin on dopamine release in SHR suggests that galanin might actively participate in the regulation of dopaminergic nerve activity in hypertension.

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Galanin, a 29-amino acid peptide, is widely distributed in both the central and peripheral nervous systems and is colocalized with catecholamines, although its physiological significance remains to be elucidated. In the present study we investigated the regulatory mechanisms of galanin on norepinephrine release in rat medulla oblongata. In slices of medulla oblongata of Sprague-Dawiey rats, galanin inhibited the stimulation-evoked [ 3 H] norepinephrine release in a concentration-dependent manner (fractional release ratio during electrical stimulation: control 0.937±0.043, mean±SEM, n=6; galanin lxlO" 7 M 0.501 ±0.037, n=6, p<0.05; and galanin 1x10"' M 0.299±0.018 n=6, p<0.05). Galanin potentiated inhibition of [ 3 H] norepinephrine release by the o^-agonists (UK 14,304 and clonidine). The blockade of <*,-adrenergic receptors by RX 781094 diminished the inhibition of norepinephrine release by galanin. Pretreatment of pertussis toxin, which interferes with the coupling of inhibitory guanoslne triphosphatebinding proteins to adenjiate cyclase, significantly attenuated the suppressive effects of galanin on norepinephrine release. In slices of medulla oblongata obtained from spontaneously hypertensive rats (SHR), the inhibitory effect of galanin on norepinephrine release was significantly less than in those from age-matched Wistar-Kyoto rats. These results show that galanin might inhibit the stimulation-evoked norepinephrine release in rat medulla oblongata, at least partially mediated by ofe-adrenergic receptors and the pertussis toxin-sensitive guanosine triphosphate-binding proteins. Moreover, less suppression of norepinephrine release by galanin in SHR suggests that galanin might be involved in the regulation of central sympathetic nervous activity in hypertension. Immunohistochemical studies have shown that galaninimmunoreactive neurons are present in the brain and spinal cord as well as in neuronal structures in several peripheral systems.2 Skofitsch and Jacobowitz 4 have observed the quantitative distribution of galanin-like immunoreactivity in rat central nervous system and reported that high concentrations were determined in the median eminence, hypothalamus, locus coeruleus, medulla oblongata, and the caudal spinal trigeminal nucleus. Recent evidence has suggested that galanin might actively participate in the central control of blood pressure and other cardiovascular functions because a high concentration of galanin has been found in the dorsal cardiovascular centers, particularly in the nucleus tractus solitarii of rat medulla oblongata. 4 Harfstrand et al 5 have observed that intracisternally injected galanin in the nanomolar range induced a significant hypotension in anesthetized rats and further reported that the combined treatment of galanin with neuropeptide Y resulted in a more prolonged hypotensive action.In several areas, galanin has been shown to coexist with other peptides or amines, such as -y-aminobutyric acid, norepinephrine, dopamine, serotonin, and acetylcholine.2 -6 -9 In many cases, the p...

An involvement of blood coagulation factor XIII (FXIII) in healing of burns was examined in rats with the carbon tetrachloride (CCl4)-induced hepatic injury. The oral administration of 2 and 4 ml/kg CCl4 to rats every 4 days delayed healing of the burns induced on the back skin and decreased FXIII activity. These animals showed some hepatotoxic signs (increased glutamic-oxaloacetic and glutamic-pyruvic transaminases) and accelerated blood coagulation system (increased fibrino-peptide A and fibrin degradation product). The delay in the burn healing was shortened by repeated intravenous injections with normal human placenta-derived FXIII concentrate (Fibrogammin P; 120 U/body) every 4 days. There was a negative correlation between plasma FXIII activity at the end of experiment and the time required for wound healing. These findings suggest that reduction in FXIII activity may be one of the factors inducing delayed wound healing in the CCl4-induced hepatic injury rats.

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