To eat unidentified or misidentified mushrooms taken from the wild can be very dangerous. In the vast majority of toxic mushroom ingestions in Korea, the mushroom was incorrectly identified. In general, poisoning of toxic mushrooms can be classified into seven types according to the toxins that they contain; amatoxin, gyromitrin, coprine, muscarine, ibotenic acid-muscimol, psilocybin-psilocin and gastrointestinal irritants. When clinicians care for a patient who ingested a toxic mushroom, it is very important to identify what kind of mushroom may have caused a patient's illness. But, in clinical practice, accurate botanical identification of the mushroom can be very difficult. Therefore, for estimating the caused mushroom and adequate treatment of poisoning, clinicians should know the type and treatment of toxic mushroom poisoning.
Agaricales* ; Edetic Acid ; Humans ; Irritants ; Korea* ; Muscarine ; Mushroom Poisoning* ; Poisoning

Our previous report demonstrated that chick myoblasts are equipped with Ca2+-permeable stretch- activated channels and Ca2+-activated potassium channels (KCa), and that hyperpolarization-induced by KCa channels provides driving force for Ca2+ influx through the stretch-activated channels into the cells. Here, we showed that acetylcholine (ACh) also hyperpolarized the membrane of cultured chick myoblasts, suggesting that nicotinic acetylcholine receptor (nAChR) may be another pathway for Ca2+ influx. Under cell-attatched patch configuration, ACh increased the open probability of KCa channels from 0.007 to 0.055 only when extracellular Ca2+ was present. Nicotine, a nAChR agonist, increased the open probability of KCa channels from 0.008 to 0.023, whereas muscarine failed to do so. Since the activity of KCa channel is sensitive to intracellular Ca2+ level, nAChR seems to be capable of inducing Ca2+ influx. Using the Ca2+ imaging analysis, we were able to provide direct evidence that ACh induced Ca2+ influx from extracellular solution, which was dramatically increased by valinomycin-mediated hyperpolarization. In addition, ACh hyperpolarized the membrane potential from -12.5+/-3 to -31.2+/-5 mV by generating the outward current through KCa channels. These results suggest that activation of nAChR increases Ca2+ influx, which activates KCa channels, thereby hyperpolarizing the membrane potential in chick myoblasts.
Acetylcholine* ; Membrane Potentials ; Membranes ; Muscarine ; Myoblasts* ; Nicotine ; Potassium Channels ; Receptors, Nicotinic

Cholinergic modulation of GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) by the activation of muscarine receptors was investigated in mechanically dissociated rat nucleus basalis of the Meynert neurons using the conventional whole-cell patch recording configuration. Muscarine (10microM) reversibly and concentration-dependently decreased mIPSC frequency without affecting the current amplitude distribution. Muscarine action on GABAergic mIPSCs was completely blocked by 1microM methoctramine, a selective M2 receptor antagonist, but not by 1microM pirenzepine, a selective M1 receptor antagonist. NEM (10microM), a G-protein uncoupler, attenuated the inhibitory action of muscarine on GABAergic mIPSC frequency. Muscarine still could decrease GABAergic mIPSC frequency even in the Ca2+-free external solution. However, the inhibitory action of muscarine on GABAergic mIPSCs was completely occluded in the presence of forskolin. The results suggest that muscarine acts presynaptically and reduces the probability of spontaneous GABA release, and that such muscarine-induced inhibitory action seems to be mediated by G-protein-coupled M2 receptors, via the reduction of cAMP production. Accordingly, M2 receptor-mediated disinhibition of nBM neurons might play one of important roles in the regulation of cholinergic outputs from nBM neurons as well as the excitability of nBM neurons themselves.
Animals ; Cholinergic Neurons ; Colforsin ; gamma-Aminobutyric Acid ; GTP-Binding Proteins ; Inhibitory Postsynaptic Potentials ; Muscarine* ; Neurons* ; Pirenzepine ; Rats*

BACKGROUND: Evidence has accumulated that tramadol hydrochloride can produce relief of moderate to severe pain across the range of acute and chronic pain states by combining a synergistically weak opioid and a monoaminergically mediated antinociceptive mechanism. Neostigmine can produce antinociceptive effects by interacting with muscarine receptors in peripheral tissues. This study was designed to determine whether intraarticular tramadol results in better analgesic effect and whether tramadol and neostigmine would provide superior analgesia to tramadol alone, after knee arthroscopic surgery. METHODS: Forty-five ASA class 1 or 2 patients undergoing arthroscopic knee surgery were randomly allocated to three treatment groups. All patients received general anesthesia with nitrous oxide, O2 and inhalational agents. When the surgical procedure was completed, the study drug was injected into the patient's knee joint through the arthroscope. Patients in group 1 (n = 15) received 30 ml of 0.5% mepivacaine; patients in group 2 (n = 15) received tramadol 50 mg and 30 ml of 0.5% mepivacaine; patients in group 3 (n = 15) received a combination of tramadol 50 mg, neostigmine 100 micro gram and 30 ml of 0.5% mepivacaine. Postoperative pain was assessed using the visual analogue scale (VAS) at 1, 2, 4, 6, 12 and 24 hours after the intraarticular injection. RESULTS: There were no significant differences among the three groups in the 1 to 2 hour postoperative period and groups 2 and 3 showed significantly lower VAS score than group 1 from 4 to 24 hours postoperatively. CONCLUSIONS: It is concluded that after knee arthroscopy, intraarticular injection of tramadol had a good analgesic effect, whereas neostigmine added to tramadol did not show superior analgesic effects over tramadol alone.
Analgesia ; Anesthesia, General ; Arthroscopes ; Arthroscopy* ; Chronic Pain ; Humans ; Injections, Intra-Articular ; Knee Joint ; Knee* ; Mepivacaine ; Muscarine ; Neostigmine* ; Nitrous Oxide ; Pain, Postoperative ; Postoperative Period ; Tramadol*

BACKGROUND: Evidence has accumulated that tramadol hydrochloride can produce relief of moderate to severe pain across the range of acute and chronic pain states by combining a synergistically weak opioid and a monoaminergically mediated antinociceptive mechanism. Neostigmine can produce antinociceptive effects by interacting with muscarine receptors in peripheral tissues. This study was designed to determine whether intraarticular tramadol results in better analgesic effect and whether tramadol and neostigmine would provide superior analgesia to tramadol alone, after knee arthroscopic surgery. METHODS: Forty-five ASA class 1 or 2 patients undergoing arthroscopic knee surgery were randomly allocated to three treatment groups. All patients received general anesthesia with nitrous oxide, O2 and inhalational agents. When the surgical procedure was completed, the study drug was injected into the patient's knee joint through the arthroscope. Patients in group 1 (n = 15) received 30 ml of 0.5% mepivacaine; patients in group 2 (n = 15) received tramadol 50 mg and 30 ml of 0.5% mepivacaine; patients in group 3 (n = 15) received a combination of tramadol 50 mg, neostigmine 100 micro gram and 30 ml of 0.5% mepivacaine. Postoperative pain was assessed using the visual analogue scale (VAS) at 1, 2, 4, 6, 12 and 24 hours after the intraarticular injection. RESULTS: There were no significant differences among the three groups in the 1 to 2 hour postoperative period and groups 2 and 3 showed significantly lower VAS score than group 1 from 4 to 24 hours postoperatively. CONCLUSIONS: It is concluded that after knee arthroscopy, intraarticular injection of tramadol had a good analgesic effect, whereas neostigmine added to tramadol did not show superior analgesic effects over tramadol alone.
Analgesia ; Anesthesia, General ; Arthroscopes ; Arthroscopy* ; Chronic Pain ; Humans ; Injections, Intra-Articular ; Knee Joint ; Knee* ; Mepivacaine ; Muscarine ; Neostigmine* ; Nitrous Oxide ; Pain, Postoperative ; Postoperative Period ; Tramadol*