Aurelia Jancsó-Gábor

Bio: Aurelia Jancsó-Gábor is an academic researcher from Hungarian Academy of Sciences. The author has contributed to research in topics: Capsaicin & Neurogenic inflammation. The author has an hindex of 11, co-authored 15 publications receiving 2240 citations.

Functional and fine structural characteristics of the sensory neuron blocking effect of capsaicin.

Abstract: In the eye of rats the long-lasting specific desensitization induced by local or systemic capsaicin treatment is characterized by three phases: 1. complete insensitivity, 2. decreased sensitivity and a tendency to rapid adaptation, 3. normal initial sensitivity with a tendency to rapid adaptation to chemical pain stimuli. A low density of microvesicles and swollen mitochondria were found after local capsaicin treatment in certain nerve endings of the cornea of rats, but no signs of axonal degeneration or alteration in fine structure of non-neural elements were seen. Systemic capsaicin desensitization induced selective mitochondrial swelling in B type of neurons of the trigeminal ganglion which was demonstrable even 60 days after the pretreatment. Actinomycin-D, 8-azaguanine, 6-azauracil, aminopterin, mannomustin or cycloheximide in high doses did not alter the desensitizing effect of systemic capsaicin treatment. However, pretreatment of rats with colchicine or vinblastine prolonged the desensitizing effect of local capsaicin application, probably by inhibiting the axonal flow. It is concluded that capsaicin is a specific sensory neuron blocking agent having a practically irreversible effect in rats and guineapigs.

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

Abstract: 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.

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

Abstract: 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.

Impaired Nociception and Pain Sensation in Mice Lacking the Capsaicin Receptor

Abstract: The capsaicin (vanilloid) receptor VR1 is a cation channel expressed by primary sensory neurons of the "pain" pathway. Heterologously expressed VR1 can be activated by vanilloid compounds, protons, or heat (>43 degrees C), but whether this channel contributes to chemical or thermal sensitivity in vivo is not known. Here, we demonstrate that sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli. VR1-/- mice showed normal responses to noxious mechanical stimuli but exhibited no vanilloid-evoked pain behavior, were impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation. Thus, VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyperalgesia.

Vanilloid (Capsaicin) Receptors and Mechanisms

Abstract: Natural products afford a window of opportunity to study important biology. If the natural product is used or abused by human beings, finding its biological target(s) is all the more significant. Hot pepper is eaten on a daily basis by an estimated one-quarter of the world’s population and

Mustard oils and cannabinoids excite sensory nerve fibres through the TRP channel ANKTM1

Abstract: Wasabi, horseradish and mustard owe their pungency to isothiocyanate compounds Topical application of mustard oil (allyl isothiocyanate) to the skin activates underlying sensory nerve endings, thereby producing pain, inflammation and robust hypersensitivity to thermal and mechanical stimuli Despite their widespread use in both the kitchen and the laboratory, the molecular mechanism through which isothiocyanates mediate their effects remains unknown Here we show that mustard oil depolarizes a subpopulation of primary sensory neurons that are also activated by capsaicin, the pungent ingredient in chilli peppers, and by Delta(9)-tetrahydrocannabinol (THC), the psychoactive component of marijuana Both allyl isothiocyanate and THC mediate their excitatory effects by activating ANKTM1, a member of the TRP ion channel family recently implicated in the detection of noxious cold These findings identify a cellular and molecular target for the pungent action of mustard oils and support an emerging role for TRP channels as ionotropic cannabinoid receptors

The Vanilloid Receptor: A Molecular Gateway to the Pain Pathway

Abstract: ▪ Abstract The detection of painful stimuli occurs primarily at the peripheral terminals of specialized sensory neurons called nociceptors. These small-diameter neurons transduce signals of a chemical, mechanical, or thermal nature into action potentials and transmit this information to the central nervous system, ultimately eliciting a perception of pain or discomfort. Little is known about the proteins that detect noxious stimuli, especially those of a physical nature. Here we review recent advances in the molecular characterization of the capsaicin (vanilloid) receptor, an excitatory ion channel expressed by nociceptors, which contributes to the detection and integration of pain-producing chemical and thermal stimuli. The analysis of vanilloid receptor gene knockout mice confirms the involvement of this channel in pain sensation, as well as in hypersensitivity to noxious stimuli following tissue injury. At the same time, these studies demonstrate the existence of redundant mechanisms for the sensation ...