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bicuculline/лихорадка
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Страница 1 от 26 полученные результаты
Involvement of transmitters in pituitary adenylate cyclase-activating polypeptide-induced hyperthermia.
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The involvement of transmitters in the hyperthermic effect of centrally administered pituitary adenylate cyclase-activating polypeptide (PACAP-38) was studied. Rats were treated with different receptor antagonists or agonists in doses that per se proved to be ineffective. The following agonists and
Previous heat shock treatment attenuates bicuculline-induced convulsions in rats.
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Exposure to elevated temperature provokes a sequence of events (heat shock response) in all living organisms. Through this response, heat shock proteins (HSPs) are induced and protect the cells against subsequent injury. We investigated the effect of heat treatment on bicuculline-induced
GABAergic system inducing hyperthermia in the rat preoptic area: its independence of prostaglandin E2 system.
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Brain temperature of conscious freely moving rats was recorded during perfusion of the preoptic area (POA) with neuroactive compounds using the microdialysis technique. Unilateral perfusion of the POA with the sodium channel blocking agent, tetrodotoxin (1 microM), induced a pronounced hyperthermia.
Gamma oscillation underlies hyperthermia-induced epileptiform-like spikes in immature rat hippocampal slices.
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BACKGROUND
Recently a hyperthermic rat hippocampal slice model system has been used to investigate febrile seizure pathophysiology. Our previous data indicates that heating immature rat hippocampal slices from 34 to 41 degrees C in an interface chamber induced epileptiform-like population spikes
Disinhibition of RVLM neural circuits and regulation of sympathetic nerve discharge at peak hyperthermia.
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Hyperthermia is a potent activator of visceral sympathetic nerve discharge (SND), and the functional integrity of the rostral ventral lateral medulla (RVLM) is critically important for sustaining sympathoexcitation at peak hyperthermia. However, RVLM mechanisms mediating SND activation to acute heat
Alpha2-adrenergic receptor agonists prevent emotional hyperthermia.
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Emotionally significant stimuli, including potential threats from the external environment, trigger an increase in body temperature, a response known as emotional hyperthermia. Sympathetically-mediated brown adipose tissue (BAT) thermogenesis contributes substantially to this hyperthermic response.
Prostaglandin E(2) fever mediated by inhibition of the GABAergic transmission in the region immediately adjacent to the organum vasculosum of the lamina terminalis.
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Unilateral microinjection of prostaglandin (PG)E(2) into a region immediately adjacent to the organum vasculosum of the lamina terminalis (peri-OVLT) in the preoptic area elicited thermogenic, tachycardic, cutaneous vasoconstrictive, and hyperthermic responses simultaneously in
Medullary regulation of visceral sympathetic nerve discharge at peak hyperthermia in aged F344 rats.
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Heat stress provides a potent stimulus for the activation of visceral sympathetic nerve discharge (SND) in young but not aged rats. Central mechanisms mediating attenuated SND responses to heating in aged rats have not been investigated. Because the GABAergic system in the rostral ventral lateral
Transient hyperthermia protects against subsequent seizures and epilepsy-induced cell damage in the rat.
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Many mild preconditioning stress conditions, including physical and metabolic injuries, increase the resistance of neurons to subsequent more severe stresses of the same or different type. This "tolerance phenomenon" lasts one to several weeks, providing a unique opportunity to investigate
Changes of body temperature and thermoregulatory responses of freely moving rats during GABAergic pharmacological stimulation to the preoptic area and anterior hypothalamus in several ambient temperatures.
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Action of gamma-aminobutyric acid (GABA) in the preoptic area and anterior hypothalamus (PO/AH) has been implicated to regulate body temperature (T(b)). However, its precise role in thermoregulation remains unclear. Moreover, little is known about its release pattern in the PO/AH during active
Does GABA act through dopaminergic/cholinergic interaction in the regulation of higher environmental temperature-induced change in body temperature?
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Acute exposure of adult male albino rats to higher ambient temperature (40 degrees C) for 2 h significantly increased body temperature (BT). Administration of either bicuculline (1 mg/kg, i.p.), a GABA antagonist, or physostigmine (0.1 mg/kg, i.p.), an inhibitor of acetylcholinesterase,
Higher environmental temperature-induced increase of body temperature: involvement of central opioidergic-GABAergic interaction.
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Exposure (2 h) of male albino rats to higher environmental temperature (HET, 40 degrees C) significantly increased the body temperature (BT). Administration of bicuculline (1 mg/kg, i.p.), physostigmine (0.2 mg/kg, i.p.), or their combination significantly raised the BT of normal rats (kept at 28
Opioid and prostaglandin mechanisms involved in the effects of GABAergic drugs on body temperature.
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1. Intraperitoneal (i.p.) injection to restrained rats of GABA (250-1000 mg/kg) or the GABAA-receptor agonist muscimol (0.05-1 mg/kg) induced a dose-dependent decrease in body temperature (BT). 2. Intraperitoneal injection of low doses of the GABAB-receptor agonist (+/-)-baclofen (1-10 mg/kg) did
Hypothermia induced in rabbits by intracerebroventricular taurine: specificity and relationships with central serotonin (5-HT) systems.
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The intracerebroventricular (i.c.v.) injection of taurine produced a fall in core temperature, the extent of which was dependent on the thermal gradient between the body and the environment. Concurrently, a sudden rise in ear skin temperature, which was maximal in the cold and negligible at 30
Higher environmental temperature-induced increase in body temperature: involvement of serotonin in GABA mediated interaction of opioidergic system.
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Exposure (2 h) of adult male albino rats to higher environmental temperature (HET, 40 degrees C) significantly increased body temperature (BT). Administration of (a) 5-HTP (5 mg/kg, i.p.) or morphine (1 mg/kg, i.p.) or physostigmine (0.2 mg/kg, i.p.) alone significantly increased and (b)
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