The Experts below are selected from a list of 39 Experts worldwide ranked by ideXlab platform
James L Meyerhoff - One of the best experts on this subject based on the ideXlab platform.
-
attack priming in female syrian golden hamsters is associated with a c fos coupled process within the Corticomedial Amygdala
Neuroscience, 1996Co-Authors: Michael Potegal, Craig F Ferris, M Hebert, James L Meyerhoff, L SkaredoffAbstract:Allowing a resident hamster a single “priming” attack on a conspecific induces a transient aggressive arousal as indicated by a reduction in the latency and increase in the probability of attack on a cecond intruder presented within the next 30 min. We present two lines of evidence identifying the Corticomedial Amygdala as an important locus mediating this effect. (1) Attack priming significantly increases the number of neurons expressing immunocytochemically identified Fos protein in the Corticomedial Amygdala, but not elsewhere. Pursuit and biting of an inanimate object does not induce Corticomedial Amygdala c-fos expression of the same pattern or magnitude. The Corticomedial Amygdala contribution to the priming effect involves more than a non-specific arousal, since Corticomedial Amygdala c-fos expression does not correlate with locomotor activity, a standard indicator of such arousal. (2) Radiofrequency lesions of the Corticomedial Amygdala reduce aggression, the greatest reduction occurring with the more anterior lesions. Other behaviors, including a priming-like locomotor practice effect in a running wheel, are unaffected by Corticomedial Amygdala lesions. These findings suggest that attack priming is an aggression-specific effect resulting from a Fos-coupled change within neural circuitry of which the Corticomedial Amygdala is a part. From a theoretical point of view, these experiments suggest a new approach to the analysis of the mechanisms underlying aggressive behavior and the persistence of aggressive arousal. We present a sketch of a quantitative neurobehavioral model which relates attack probability to neural activation within the Corticomedial Amygdala. From a methodological viewpoint, these experiments extend the utility of mapping c-fos expression as a technique for localizing endogenous, behavior-specific processes within the central nervous system.
-
brief high frequency stimulation of the Corticomedial Amygdala induces a delayed and prolonged increase of aggressiveness in male syrian golden hamsters
Behavioral Neuroscience, 1996Co-Authors: Michael Potegal, M Hebert, Mark A Decoster, James L MeyerhoffAbstract:Brief 200-Hz stimulation of the Corticomedial Amygdala (CMA) increases the aggressiveness of male Syrian golden hamsters for about 30 min; the effect peaks 10-15 min after stimulation. This effect is sensitive to stimulation amplitude and frequency. Stimulation at the parameters that reduce attack latency increases flank marking but does not affect copulation latency or general activity. Immunocytochemical analysis suggests that stimulation effects may be coupled to c-fos expression and that unilateral stimulation has bilateral effects. CMA stimulation effects appear to mimic part of the time course of behaviorally induced attack priming. The temporal persistence of aggression may result from long-term potentiation-like changes within CMA-related neural circuitry. Once sufficiently aroused, aggressive behavior in various species of fish (e.g., Heiligenberg, 1974), birds (e.g., Curio, 1975), and mammals (e.g., Potegal, 1992) tends to persist in time. Under experimental circumstances in which the aggression-provoking stimulus remains constant, temporal fluctuations in aggressive behavior imply the existence of fluctuations in central control processes. When aggression persists even after the provoking stimulus is withdrawn (e.g., Curio, 1975; Heiligenberg, 1974), such central processes must certainly play a role. We believe that these important but poorly understood internal processes contribute to a variety of phenomena within the domain of aggressive behavior and that any theory of aggression that fails to take them into account must remain incomplete (Potegal, 1994). Accordingly, we have developed an experimental model for the analysis of these processes
Michael Potegal - One of the best experts on this subject based on the ideXlab platform.
-
attack priming in female syrian golden hamsters is associated with a c fos coupled process within the Corticomedial Amygdala
Neuroscience, 1996Co-Authors: Michael Potegal, Craig F Ferris, M Hebert, James L Meyerhoff, L SkaredoffAbstract:Allowing a resident hamster a single “priming” attack on a conspecific induces a transient aggressive arousal as indicated by a reduction in the latency and increase in the probability of attack on a cecond intruder presented within the next 30 min. We present two lines of evidence identifying the Corticomedial Amygdala as an important locus mediating this effect. (1) Attack priming significantly increases the number of neurons expressing immunocytochemically identified Fos protein in the Corticomedial Amygdala, but not elsewhere. Pursuit and biting of an inanimate object does not induce Corticomedial Amygdala c-fos expression of the same pattern or magnitude. The Corticomedial Amygdala contribution to the priming effect involves more than a non-specific arousal, since Corticomedial Amygdala c-fos expression does not correlate with locomotor activity, a standard indicator of such arousal. (2) Radiofrequency lesions of the Corticomedial Amygdala reduce aggression, the greatest reduction occurring with the more anterior lesions. Other behaviors, including a priming-like locomotor practice effect in a running wheel, are unaffected by Corticomedial Amygdala lesions. These findings suggest that attack priming is an aggression-specific effect resulting from a Fos-coupled change within neural circuitry of which the Corticomedial Amygdala is a part. From a theoretical point of view, these experiments suggest a new approach to the analysis of the mechanisms underlying aggressive behavior and the persistence of aggressive arousal. We present a sketch of a quantitative neurobehavioral model which relates attack probability to neural activation within the Corticomedial Amygdala. From a methodological viewpoint, these experiments extend the utility of mapping c-fos expression as a technique for localizing endogenous, behavior-specific processes within the central nervous system.
-
brief high frequency stimulation of the Corticomedial Amygdala induces a delayed and prolonged increase of aggressiveness in male syrian golden hamsters
Behavioral Neuroscience, 1996Co-Authors: Michael Potegal, M Hebert, Mark A Decoster, James L MeyerhoffAbstract:Brief 200-Hz stimulation of the Corticomedial Amygdala (CMA) increases the aggressiveness of male Syrian golden hamsters for about 30 min; the effect peaks 10-15 min after stimulation. This effect is sensitive to stimulation amplitude and frequency. Stimulation at the parameters that reduce attack latency increases flank marking but does not affect copulation latency or general activity. Immunocytochemical analysis suggests that stimulation effects may be coupled to c-fos expression and that unilateral stimulation has bilateral effects. CMA stimulation effects appear to mimic part of the time course of behaviorally induced attack priming. The temporal persistence of aggression may result from long-term potentiation-like changes within CMA-related neural circuitry. Once sufficiently aroused, aggressive behavior in various species of fish (e.g., Heiligenberg, 1974), birds (e.g., Curio, 1975), and mammals (e.g., Potegal, 1992) tends to persist in time. Under experimental circumstances in which the aggression-provoking stimulus remains constant, temporal fluctuations in aggressive behavior imply the existence of fluctuations in central control processes. When aggression persists even after the provoking stimulus is withdrawn (e.g., Curio, 1975; Heiligenberg, 1974), such central processes must certainly play a role. We believe that these important but poorly understood internal processes contribute to a variety of phenomena within the domain of aggressive behavior and that any theory of aggression that fails to take them into account must remain incomplete (Potegal, 1994). Accordingly, we have developed an experimental model for the analysis of these processes
M Hebert - One of the best experts on this subject based on the ideXlab platform.
-
attack priming in female syrian golden hamsters is associated with a c fos coupled process within the Corticomedial Amygdala
Neuroscience, 1996Co-Authors: Michael Potegal, Craig F Ferris, M Hebert, James L Meyerhoff, L SkaredoffAbstract:Allowing a resident hamster a single “priming” attack on a conspecific induces a transient aggressive arousal as indicated by a reduction in the latency and increase in the probability of attack on a cecond intruder presented within the next 30 min. We present two lines of evidence identifying the Corticomedial Amygdala as an important locus mediating this effect. (1) Attack priming significantly increases the number of neurons expressing immunocytochemically identified Fos protein in the Corticomedial Amygdala, but not elsewhere. Pursuit and biting of an inanimate object does not induce Corticomedial Amygdala c-fos expression of the same pattern or magnitude. The Corticomedial Amygdala contribution to the priming effect involves more than a non-specific arousal, since Corticomedial Amygdala c-fos expression does not correlate with locomotor activity, a standard indicator of such arousal. (2) Radiofrequency lesions of the Corticomedial Amygdala reduce aggression, the greatest reduction occurring with the more anterior lesions. Other behaviors, including a priming-like locomotor practice effect in a running wheel, are unaffected by Corticomedial Amygdala lesions. These findings suggest that attack priming is an aggression-specific effect resulting from a Fos-coupled change within neural circuitry of which the Corticomedial Amygdala is a part. From a theoretical point of view, these experiments suggest a new approach to the analysis of the mechanisms underlying aggressive behavior and the persistence of aggressive arousal. We present a sketch of a quantitative neurobehavioral model which relates attack probability to neural activation within the Corticomedial Amygdala. From a methodological viewpoint, these experiments extend the utility of mapping c-fos expression as a technique for localizing endogenous, behavior-specific processes within the central nervous system.
-
brief high frequency stimulation of the Corticomedial Amygdala induces a delayed and prolonged increase of aggressiveness in male syrian golden hamsters
Behavioral Neuroscience, 1996Co-Authors: Michael Potegal, M Hebert, Mark A Decoster, James L MeyerhoffAbstract:Brief 200-Hz stimulation of the Corticomedial Amygdala (CMA) increases the aggressiveness of male Syrian golden hamsters for about 30 min; the effect peaks 10-15 min after stimulation. This effect is sensitive to stimulation amplitude and frequency. Stimulation at the parameters that reduce attack latency increases flank marking but does not affect copulation latency or general activity. Immunocytochemical analysis suggests that stimulation effects may be coupled to c-fos expression and that unilateral stimulation has bilateral effects. CMA stimulation effects appear to mimic part of the time course of behaviorally induced attack priming. The temporal persistence of aggression may result from long-term potentiation-like changes within CMA-related neural circuitry. Once sufficiently aroused, aggressive behavior in various species of fish (e.g., Heiligenberg, 1974), birds (e.g., Curio, 1975), and mammals (e.g., Potegal, 1992) tends to persist in time. Under experimental circumstances in which the aggression-provoking stimulus remains constant, temporal fluctuations in aggressive behavior imply the existence of fluctuations in central control processes. When aggression persists even after the provoking stimulus is withdrawn (e.g., Curio, 1975; Heiligenberg, 1974), such central processes must certainly play a role. We believe that these important but poorly understood internal processes contribute to a variety of phenomena within the domain of aggressive behavior and that any theory of aggression that fails to take them into account must remain incomplete (Potegal, 1994). Accordingly, we have developed an experimental model for the analysis of these processes
L Skaredoff - One of the best experts on this subject based on the ideXlab platform.
-
attack priming in female syrian golden hamsters is associated with a c fos coupled process within the Corticomedial Amygdala
Neuroscience, 1996Co-Authors: Michael Potegal, Craig F Ferris, M Hebert, James L Meyerhoff, L SkaredoffAbstract:Allowing a resident hamster a single “priming” attack on a conspecific induces a transient aggressive arousal as indicated by a reduction in the latency and increase in the probability of attack on a cecond intruder presented within the next 30 min. We present two lines of evidence identifying the Corticomedial Amygdala as an important locus mediating this effect. (1) Attack priming significantly increases the number of neurons expressing immunocytochemically identified Fos protein in the Corticomedial Amygdala, but not elsewhere. Pursuit and biting of an inanimate object does not induce Corticomedial Amygdala c-fos expression of the same pattern or magnitude. The Corticomedial Amygdala contribution to the priming effect involves more than a non-specific arousal, since Corticomedial Amygdala c-fos expression does not correlate with locomotor activity, a standard indicator of such arousal. (2) Radiofrequency lesions of the Corticomedial Amygdala reduce aggression, the greatest reduction occurring with the more anterior lesions. Other behaviors, including a priming-like locomotor practice effect in a running wheel, are unaffected by Corticomedial Amygdala lesions. These findings suggest that attack priming is an aggression-specific effect resulting from a Fos-coupled change within neural circuitry of which the Corticomedial Amygdala is a part. From a theoretical point of view, these experiments suggest a new approach to the analysis of the mechanisms underlying aggressive behavior and the persistence of aggressive arousal. We present a sketch of a quantitative neurobehavioral model which relates attack probability to neural activation within the Corticomedial Amygdala. From a methodological viewpoint, these experiments extend the utility of mapping c-fos expression as a technique for localizing endogenous, behavior-specific processes within the central nervous system.
Aldo Bolten Lucion - One of the best experts on this subject based on the ideXlab platform.
-
8 oh dpat in the median raphe dorsal periaqueductal gray and Corticomedial Amygdala nucleus decreases but in the medial septal area it can increase maternal aggressive behavior in rats
Psychopharmacology, 1997Co-Authors: Rosa Maria Martins De Almeida, Aldo Bolten LucionAbstract:The purpose of the present study was to analyze the role of somatodendritic autoreceptors and postsynaptic 5-HT1A receptors in the modulation of maternal aggressive behavior. The 5-HT1A receptor agonist 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin) was microinjected (0.2, 0.5 and 2.0 μg/0.2 μl) in different brain areas of female Wistar rats: median raphe nucleus (MnR); medial septal area (MS); anterior Corticomedial amygdaloid nucleus (ACoM); and dorsal periaqueductal gray (DPAG). The behaviors of lactating female rats with pups against a conspecific male intruder were recorded on day 7 post-partum. Results showed that in the median raphe nuclei, in the dorsal periaqueductal gray and in the Corticomedial amygdaloid nucleus 8-OH-DPAT decreased maternal aggression; while in the medial septum, the intermediate dose (0.5 μg/0.2 μl) of the 5-HT1A receptor agonist increased the aggressive behavior of the lactating female rat. It is concluded that the main role of the 5-HT1A somatodendritic autoreceptors and the postsynaptic receptors of the brain areas studied is to decrease maternal aggression, however, at a specific dosage, 8-OH-DPAT acting on postsynaptic receptors of the medial septal area can increase aggressiveness.
-
effect of estradiol implanted in the Corticomedial Amygdala on the sexual behavior of castrated male rats
Brazilian Journal of Medical and Biological Research, 1991Co-Authors: Alberto A Rasiafilho, T M S Peres, F H Cubillagutierrez, Aldo Bolten LucionAbstract:1. The purpose of the present investigation was to study the effect of beta-estradiol crystals implanted in the Corticomedial area of the amygdaloid body on the sexual behavior of castrated male rats. 2. The animals were divided into the following groups: group I (N = 9), castrated rats; group II (N = 4), rats which had been castrated and stereotaxically implanted with cholesterol, both groups being used as controls; group III (N = 6), castrated rats with estradiol implants. Latency to the first anogenital exploration, latency to the first mount and mount frequency were determined during the pre-castration and post-castration phases and after the material had been implanted in groups II and III in 10-min observation sessions. 3. There was diminished sexual behavior of the animals in group I without spontaneous recurrence within the period observed. Group II animals, who had undergone implantation of cholesterol, an inert substance, maintained low levels of sexual behavior (post-castration 0.8 +/- 0.7 vs 0.0 +/- 0.0 and 0.5 +/- 0.5 on the 6th and 9th day after implantation, respectively). Group III animals presented a gradual increase in the number of mounts (from post-castration 1.2 +/- 0.5 to 6.5 +/- 2.7 and 4.1 +/- 1.0 on the 6th and 9th day after implantation, respectively) and a decrease of mount latency (from post-castration 431.2 +/- 55.9 to 226.1 +/- 119.6 and 51.0 +/- 28.9 on the 6th and 9th day after implantation, respectively) reaching pre-castration levels on the 6th and 9th day after beta-estradiol implantation.(ABSTRACT TRUNCATED AT 250 WORDS)
