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Biomedical subjects

A Jancsó-Gábor

Publications and source records attributed to A Jancsó-Gábor.

17 recordsLinked to original sources
PubMed1980

Direct evidence for an axonal site of action of capsaicin.

Local application of capsaicin to the sciatic nerve of rats induced a long-lasting increase in the nociceptive threshold as tested by the hot-plate method, and prevented neurogenic inflammation in the lateral part of the dorsal skin of the rat's paw. Application of capsaicin to the saphenous nerve prevented the neurogenic inflammatory response, induced either by antidromic electrical stimulation of the saphenous nerve or by painting the skin with mustard oil, in the medial part of the dorsal skin of the paw. The functional impairment induced by local capsaicin treatment of saphenous or sciatic nerves was strictly confined to the skin area supplied by the corresponding nerve. It is suggested that local capsaicin treatment of peripheral nerves selectively damages the chemosensitive nerve fibres presumably by depleting their substance P content.

Administration, Topical↗
PubMed1980

Effect of capsaicin on morphine analgesia--possible involvement of hypothalamic structures.

1. Rats were treated with 50 mg/kg capsaicin on the second day of life or at the age of 2--3 months. The effect of morphine on the nociceptive threshold, as determined by the reaction time in tail withdrawal test, was measured 3--4 and 1--2 months after capsaicin pretreatment, respectively. 2. The analgesic effect of morphine was markedly attenuated in rats treated with capsaicin in the adult age, while neonatal capsaicin treatment did not affect morphine analgesia. 3. Pretreatment of adult rats with capsaicin results in the impairment of certain hypothalamic preoptic neurones, while neonatal capsaicin treatment induces selective degeneration of chemosensitive primary sensory neurones without affecting hypothalamic neurones. Therefore, it is suggested that in the analgesic effect of morphine the capsaicin-sensitive neurones of the preoptic area are involved, and the contribution of spinal mechanisms might be of minor importance. Thus, the preoptic region may be an important link in endogenous pain controlling systems.

Animals↗
PubMed1980

Tail skin vasodilatation and bath test in capsaicin-desensitized rats.

Vasodilatation in response to heat, the role of tail vasodilatation in thermolysis and the ability of the animals to use free water for evaporative cooling were studied in control and capsaicin-desensitized rats. 1) While vasodilatation in the tail began in the controls as soon as their temperatures reached 38.5-39 degrees C, in most of the desensitized rats the onset of this reaction was above a body temperature of 40 degrees C. 2) When exposed to 32 degrees C, desalivated capsaicin-treated rats showed a significant hyperthermia as compared to the controls. If the tails were amputated too, the temperatures of the controls rose to near those of the desensitized animals. 3) In the case of prolonged heat exposure or at a higher ambient temperature (38 degrees C), the desalivated tail-amputated controls still remained more tolerant to heat than the desensitized rats. 4) Even at an ambient temperature of 38 degrees C, desalivated controls without tails exhibited excellent thermoregulation when a water bath was present; they used the free water for evaporation. Capsaicin-treated rats neglected the water bath, and their temperatures rose continuously. 5) The results suggests that capsaicin treatment impaired reflex vasodilatation to heat and the behaviour of using free water for heat dissipation.

Animals↗
PubMed1979

Salivary cooling, escape reaction and heat pain in capsaicin-desensitized rats.

Salivary thermolytic mechanisms (weight of salivary glands, effect of desalivation on water intake and body temperature, grooming activity) as well as escape behaviour and reaction to heat pain were studied in capsaicin-desensitized and control rats exposed to various warm ambient temperatures. Body temperature of the desensitized rats increased more than the controls' at all the ambient temperatures studied (32, 34 and 36 degrees C); however, significant differences in the mechanism of salivary cooling were obtained only at 34 and 36 degrees C. Central impairment of saliva spreading in desensitized rats seems evident. Complete surgical desalivation did not increase hyperthermia of control and desensitized animals in warm environments. Therefore other mechanisms, primarily vasodilatatory, must also be involved in the rat's thermolytic normal response. Although desensitized rats did not show a tendency to escape from the warm environment their response to heat pain was normal. In conclusion, it is suggested that heat perception in desensitized animals is impaired; however, the existence of some capsaicin-insensitive thermolytic mechanisms (prone extension of the body) cannot be excluded.

Animals↗
PubMed1976

Sensory effects of capsaicin congeners. Part II: Importance of chemical structure and pungency in desensitizing activity of capsaicin-type compounds.

The characteristic insensitivity of sensory nerve endings to chemically induced pain brought about by capsaicin could be reproduced on the rat's eye by pungent vanillylamides, homovanilloyl-alkylamides and piperine, while homovanilloyl-cycloalkylamides, -azacycloalkylamides, - alkylesters, -alkyl-homovanillylamides, undecenoyl-3-aminopropranololand zingerone were practically ineffective in this respect. Desensitizing potency was not parallel with the stimulating effect of the compounds, e.g. the strongly pungent homovanilloyl-octylester failed to desensitize the receptors, while the less pungent homovanilloyl-dodecylamide proved to be a more potent desensitizing agent than capsaicin itself. It is concluded that the inverse position of the acylamide linkage does not modify, while its replacement by an esteric group completely abolishes the desensitizing activity. In contrast to the stimulating effect, in desensitizing action the presence of an alkyl chain is essential and its optimal length corresponds to 10-12 C atoms. On the basis of these results the possible molecular interactions at the site of action are discussed.

Animals↗
PubMed1975

Sensory effects of capsaicin congeners I. Relationship between chemical structure and pain-producing potency of pungent agents.

A quantitative method for measuring the efficiency of pungent agents of capsaicin-type by the pain reaction elicited on the eye of rats is described. About 50 derivatives -- most of them amides or esters of homovanillic acid -- were tested by this method and the share of different chemical groups of the molecule in the pungent action was analyzed. It turned out that the presence of an acylamide linkage or alkyl chain is not essential for pungency, since acylamide linkage can be replaced by an esteric group and the alkyl chain by cycloalkyl rings. The importance of OH group on the aromatic ring is confirmed. On the basis of the findings a hypothetical pharmacological receptor for capsaicin on pain sensory nerve endings is presented.

Animals↗
PubMed1970

Irreversible impairment of thermoregulation induced by capsaicin and similar pungent substances in rats and guinea-pigs.

1. In rats and guinea-pigs a subcutaneous or intraperitoneal injection of capsaicin, the substance responsible for the pungency of red pepper, produces profound hypothermia associated with skin vasodilatation.2. After large doses of capsaicin rats and guinea-pigs become insensitive to the hypothermic action of capsaicin. This densensitization is apparently irreversible since it is present months after the capsaicin treatment.3. Capsaicin-desensitized animals are no longer able to protect themselves against overheating but respond with pronounced hyperthermia to high ambient temperatures (32-40 degrees C). Temperature regulation against cold exposure, however, is not impaired.4. They also respond with an enhanced hyperthermia to painful stimuli such as repeated pinching of the tail or repeated introduction of the thermometer probe into the rectum.5. The enhanced hyperthermias are not due to increased heat production but to impairment of the heat dissipating mechanisms, which in rats and guinea-pigs acts mainly through evaporation of saliva, and skin vasodilatation.6. Acylamides with pungent action related to capsaicin such as piperine, caprinoyl-p-aminophenol and propionyl vanillylamide also cause hypothermia followed by desensitization and their efficacy is dependent on their pungency. The non-pungent nonenoyl benzylamide produces neither hypothermia nor desensitization.7. Capsaicin and its related pungent acylamides appear first to stimulate and then to desensitize the hypothalamic warmth detectors. By stimulating them the acylamides evoke reflexly the hypothermic response, whereas after desensitization the protective thermoregulatory reflexes for heat dissipation are no longer activated in response to high ambient temperature and to painful stimuli.

Alkaloids↗
PubMed1970

Stimulation and desensitization of the hypothalamic heat-sensitive structures by capsaicin in rats.

1. In rats the injection of capsaicin into the pre-optic area of the anterior hypothalamus produces a prompt fall in body temperature and abolishes shivering. With repeated injections of capsaicin the hypothermic effect gradually diminishes and finally vanishes (local desensitization).2. Rats desensitized by hypothalamic injections exhibit a behaviour similar to rats pre-treated parenterally with capsaicin: put in a heat box at 37-39 degrees C they lose their ability to regulate against overheating of their bodies and respond with an enhanced hyperthermia to strong sensory stimuli such as repeated pinching of the tail.3. Parenteral desensitization strongly inhibits the effect of capsaicin given into the hypothalamus. On the other hand in intrahypothalamically desensitized rats the hypothermic response to subcutaneously given capsaicin is also reduced.4. The hypothermic response to local heating of the anterior hypothalamus by diathermy (from 1 to 4 degrees C above the initial temperature) was markedly reduced or even abolished in rats pre-treated parenterally with large doses of capsaicin.5. It is concluded that the hypothalamic warmth detectors are stimulated and subsequently desensitized by capsaicin. Thus, in the thermoregulatory disturbances caused by capsaicin the impairment of the hypothalamic warmth detectors plays an important role.6. Capsaicin is proposed as a tool in studying the function of the hypothalamic warmth detectors.

Alkaloids↗
PubMedDate not supplied

Effects of elevated ambient temperatures on the sleep-waking activity of rats with impaired warm reception.

The sleep-waking activities of intact and of capsaicin-desensitized rats (animals with damaged peripheral and central warm receptors) were studied at room temperature and at the warm ambient temperatures of 32 and 34 degrees C. At 32 degrees C, the time spent in sleep increased significantly in the desensitized animals, while a decrease in the amount of deep slow wave sleep was found in the controls. At 34 degrees C, the amount of the sleep-waking stages returned to the levels observed at room temperature in the desensitized rats. A further decrease in sleep and a significantly increased wakefulness was found in the controls. At both warm ambient temperatures, the body temperature of the desensitized rats was significantly higher than that of the controls. We suggest that warm environments exert a dual effect on the sleep-waking activity. The activating effect abolished by desensitization seems to be in connection with capsaicin-sensitive thermoreceptors, while the deactivation brought about by heat is not influenced by capsaicin.

Animals↗