TL;DR: A model based on integrate-and-fire membrane dynamics and a synaptic dynamics which produces a fixed potential jump in response to stimulation gives rise to a rich variety of behaviors and shows excellent agreement with direct numerical simulations.
Abstract: The behavior of an aggregate of neurons is followed by means of a population equation which describes the probability density of neurons as a function of membrane potential. The model is based on integrate-and-fire membrane dynamics and a synaptic dynamics which produce a fixed potential jump in response to stimulation. In spite of the simplicity of the model, it gives rise to a rich variety of behaviors. Here only the equilibrium problem is considered in detail. Expressions for the population density and firing rate over a range of parameters are obtained and compared with like forms obtained from the diffusion approximation. The introduction of the jump response to stimulation produces a delay term in the equations, which in turn leads to analytical challenges. A variety of asymptotic techniques render the problem solvable. The asymptotic resultsshow excellent agreement with direct numerical simulations.
TL;DR: Adult Drosophila is validated as a useful model to study the genetic mechanisms of thermal nociception, and the results demonstrate that, as in mammals, the latency of the jump response is inversely related to stimulus intensity, and innoxious thermosensation does not elicit this nocICEptive behavior.
Abstract: Nociception, warning of injury that should be avoided, serves an important protective function in animals. In this study, we show that adult Drosophila avoids noxious heat by a jump response. To quantitatively analyze this nociceptive behavior, we developed two assays. In the CO2 laser beam assay, flies exhibit this behavior when a laser beam heats their abdomens. The consistency of the jump latency in this assay meets an important criterion for a good nociceptive assay. In the hot plate assay, flies jump quickly to escape from a hot copper plate (> 45 degrees C). Our results demonstrate that, as in mammals, the latency of the jump response is inversely related to stimulus intensity, and innoxious thermosensation does not elicit this nociceptive behavior. To explore the genetic mechanisms of nociception, we examined several mutants in both assays. Abnormal nociceptive behavior of a mutant, painless(1), indicates that painless, a gene essential for nociception in Drosophila larvae, is also required for thermal nociception in adult flies. painless is expressed in certain neurons of the peripheral nervous system and thoracic ganglia, as well as in the definite brain structures, the mushroom bodies. However, chemical or genetic insults to the mushroom bodies do not influence the nociceptive behavior, suggesting that different painless-expressing neurons play diverse roles in thermal nociception. Additionally, no-bridge(KS49), a mutant that has a structural defect in the protocerebral bridge, shows defective response to noxious heat. Thus, our results validate adult Drosophila as a useful model to study the genetic mechanisms of thermal nociception.
TL;DR: This paper describes a jump response elicited by exposing Drosophila to chemical vapors, which provides the basis for a single-fly chemosensory assay and shows dose dependence and chemical specificity.
Abstract: Although the Drosophila visual system has been described extensively, little is known about its olfactory system. A major reason for this discrepancy has been the lack of simple, reliable means of measuring response to airborne chemicals. This paper describes a jump response elicited by exposing Drosophila to chemical vapors. This behavior provides the basis for a single-fly chemosensory assay. The behavior exhibits dose dependence and chemical specificity: it is stimulated by exposure to ethyl acetate, benzaldehyde, and propionic acid but not ethanol. Animals can respond repeatedly at short intervals to ethyl acetate and propionic acid. The response relies on the third antennal segments. To illustrate the use of this behavior in genetic analysis of chemosensory response, nine acj mutants defective in response are isolated (acj = abnormal chemosensory jump), and their responses to two chemicals are characterized. All of the acj mutants are normal in giant fiber system physiology, and two exhibit defects in visual system physiology.
TL;DR: Intracerebroventricular administration of 20, 40 and 60 nmol of dynorphin produced analgesia, as assessed by flinch/jump response to footshock, and hypothermia in the rat, and beta-endorphin showed cross-tolerance with respect to their analgesic but not their thermic effects.