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The opiate antagonist naloxone hydrochloride was employed in order to determine whether endogenous opioids play a role in the control of affective defense behavior elicited from the medial hypothalamus in the cat. The effects of naloxone upon quiet biting attack behavior elicited from the lateral hypothalamus were also assessed. A comparison of the differences in response latencies or thresholds before and after naloxone (i.p.) administration was made. Naloxone (1, 4 and 10 mg/kg) was found to significantly facilitate affective defense behavior in a dose- and time-dependent manner. The duration of facilitation ranged from 30 min after a 1 mg/kg injection to 180 min after a 10 mg/kg injection. The data also suggest that the effects of naloxone upon affective defense behavior are opposite to those seen with quiet biting attack. In two animals, quiet biting attack behavior was suppressed for 30 min following a 10 mg/kg injection of naloxone. Naloxone was also administered to cats in which hypothalamic stimulation elicited predatory responses coupled with components of affective defense behavior. In these cases, naloxone was ineffective in altering latencies for this 'mixed' response. These findings suggest that the opiate peptide system selectively inhibits affective defense behavior elicited from the medial hypothalamus of the cat.

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The effects of D-Ala2-Met5-enkephalinamide (DAME) upon the hissing component of hypothalamically elicited affective defense behavior in the cat were examined in this study. Microinjections of DAME placed into the nucleus accumbens significantly suppressed this response in a dose and time dependent manner. This dose dependent suppression of affective defense decreased toward baseline levels at 60 and 90 min following delivery of 1 and 10 micrograms/0.5 microliters of DAME, respectively. Similar injections placed into the caudate nucleus had no effects upon this response. Neither vehicle control nor naloxone placed into nucleus accumbens was found to significantly alter latencies for hissing. Naloxone injected into nucleus accumbens prior to administration of either a 1-microgram or a 10-micrograms dose of DAME blocked the suppressive effects of DAME that were observed when this drug was administered alone. These findings suggest that opioid receptors in the nucleus accumbens play an important role in the regulation of the hissing component of hypothalamically elicited affective defense behavior in the cat.

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This study examined the effects of intracerebral injections of D-Ala2-Met5-enkephalinamide (DAME) upon hypothalamically elicited hissing behavior in the cat. The bed nucleus of the stria terminalis (BNST) was selected for investigation because of its anatomical connections with the medial hypothalamus, its relatively high concentrations of enkephalins and opiate receptors and its demonstrated ability to modulate hypothalamically elicited aggressive reactions in the cat. DAME microinjected into the BNST in 1.0 or 10.0 micrograms/0.5 microliter quantities resulted in significant dose dependent increases in mean latencies for elicitation of the hissing response. Suppression of hissing following the 1.0 microgram dose of DAME was selectively diminished by prior administration of naloxone. These findings suggest that the opiate receptors within the BNST play a role in the regulation of the hissing component of hypothalamically elicited affective defense behavior.

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PIP: Many believe that the political and economic motivations of Haitian migrants can not be separated. Since Haiti 1st became an independent nation small numbers of its citizens have emigrated, but after France's Duvalier took power in 1957, the flow of migrants reached major proportions. For several reasons, the approximate 100,000 Haitians who arrived between 1960 and 1972 identified themselves as members of an immigrant population rather than as refugees. The new Haitian organizations that arose from 1965-1972 tried to organize Haitians as an ethnic interest group in the U.S. When Haitians 1st arrived by boat there was no strong political movement in the U.S., 1st to popularize the possibility of identifying oneself as a political refugee, and then to nurture and encourage such as stance. Even at the height of the movement to support the boat people and win then status as political refugees, perhaps the majority of the Haitian population and ertainly the majority of the Haitian organizations in New York stayed away from open discussion of Haitian politics. Today, some Haitian leaders tend to put aside the issue of Haitians as members of the Haitian diaspora, while others focus on the continuation of political repression in Haiti. The self-definitions of the Haitian population in the US in the future will continue to be shaped by and in turn help shape, political and economic conditions both in the US and Haiti.^ieng

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An experiment was performed in order to determine the effects of temporal lobe seizures upon hypothalamically elicited aggressive behavior in the cat. Seizures were induced by electrical stimulation of the pyriform cortex or those subnuclei of the amygdala which had previously been shown to modulate aggressive responses at subseizure current levels. The results clearly indicate that a significant modification of affective defense thresholds following seizures was a direct function of the locus of stimulation. Specifically, seizures generated from the pyriform cortex and medial aspects of the amygdala (sites associated with prior facilitation of affective defense as determined by subseizure electrical stimulation) were followed by a reduction in threshold for this response. In contrast, an elevation in affective defense thresholds occurred when seizures were generated from the central or lateral nuclei of the amygdala (sites associated with prior suppression of affective defense as determined by subseizure electrical stimulation). The primary pathway utilized in the facilitation of affective defense appears to involve the stria terminalis, its bed nucleus, and the anterior medial hypothalamus. Preliminary data suggest that seizures generated from the pyriform cortex or amygdala can also modify quiet biting attack behavior, but in a manner opposite to that demonstrated for affective defense.

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The purpose of this experiment was to study the possible modulatory role of the bed nucleus of stria terminalis (BNST) in the regulation of affective defense and quiet biting attack reactions in the cat. The experimental paradigm employed concurrent electrical stimulation of the hypothalamic attack sites and of the BNST. The results of the present study demonstrate that concurrent electrical stimulation of the BNST can differentially modulate the two different forms of aggressive behavior by facilitating affective defense and by suppressing quiet biting attack.

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The purpose of the present study was to determine the role of the midbrain periaqueductal gray (PAG) and thalamic centrum medianum-parafascicular complex (CM-Pf) in the regulation of hypothalamically elicited flight behavior in the cat. The experimental paradigm involved a comparison of the differences in response latencies between single stimulation of the hypothalamus and concurrent stimulation of the hypothalamus and sites in the PAG or the CM-Pf. Dual stimulation of the ventral and dorsal aspects of the PAG resulted in differential modulation of flight behavior. Stimulation of the dorsal PAG suppressed hypothalamically elicited flight behavior while stimulation of the ventral aspects of the PAG facilitated flight behavior. Facilitation of flight behavior was also found from stimulation of ventral portions of the CM-Pf.

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Hypothalamic sites from which quiet biting attack and affective defense were elicited, were concurrently stimulated with others in the midbrain from which modulation of these behaviors was attempted. Stimulation of medial and lateral aspects of the tegmentum differentially modulated quiet biting attack and affective defense behavior. Facilitation of quiet attack and suppression of affective defense resulted from stimulation of the lateral tegmentum, while suppression of quiet attack and facilitation of affective defense followed stimulation of its medial aspect.

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The present study was conducted to determine the role of the bed nucleus of the stria terminalis (BNST) and preoptic region in the regulation of hypothalamically elicited flight behavior in the cat. The general paradigm involved concurrent electrical stimulation of sites in the hypothalamus from which flight responses were elicited and of the BNST or preoptic region from which modulation of flight behavior was attempted. Electrical stimulation of the dorsal and ventral preoptic region modulated flight behavior in opposing ways. Suppression of flight behavior resulted from stimulation of the BNST and ventral aspect of the preoptic region, while facilitation of the behavioral response followed stimulation of the dorsal aspect of the preoptic region.

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This experiment was performed in order to examine several of the underlying mechanisms by which the septal area and adjacent regions regulate quiet biting attack behavior elicited from electrical stimulation of the hypothalamus in the cat. The results clearly indicate that stimulation of the septal area and anterior cingulate gyrus increased the latency for the occurrence of quiet biting attack behavior. Those sites within the septal area from which inhibition of attack can be produced are linked to sensory mechanisms associated with trigeminal reflexes activated during hypothalamic stimulation. Stimulation of these septal area sites decreased the lateral extent of the 'effective sensory fields' of the lipline established during hypothalamic stimulation, but did not appear to have any affect upon the latency of the hypothalamically elicited jaw-opening response. Deoxyglucose autoradiography revealed that the inhibition resulting from stimulation of the lateral septal area may be due to either the monosynaptic activation of the lateral hypothalamus or the disynaptic activation of this area utilizing a circuit involving the nuclei of the diagonal band of Broca.

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The present study utilized the [14C]2-deoxyglucose (2-DG) cell labeling procedure to characterize a functional pathway from the prefrontal cortex (Pfc) and mediodorsal thalamic nucleus (MD) to the hypothalamus. Rats were injected with 2-DG prior to a 45 min experimental paradigm consisting of alternating 30 s on-off periods of electrical brain stimulation. Standard procedures were utilized for the removal and processing of brain tissue for X-ray autoradiography. In the first phase of this study, stimulation applied to the prefrontal cortex generally yielded a pattern of 2-DG distribution consistent with the findings of classical anatomical studies. Stimulation of the dorsomedial and ventromedial prefrontal cortex or the infralimbic cortex produced the most effective activation of the diencephalon. This activation was primarily limited to MD, with no involvement of any region of the hypothalamus. In the second phase of this study, brain regions activated following stimulation of sites along the rostro-caudal axis of MD were examined. Stimulation of MD resulted in the activation of the nucleus reuniens and other midline and non-specific thalamic nuclei. Stimulation of this nucleus also activated the ventromedial thalamic nucleus, medial aspects of the nucleus accumbens and the medial and sulcal prefrontal cortices. Again, in each of these cases, labeling within any region of the hypothalamus could not be detected. Since MD stimulation activated the midline thalamus, and the nucleus reuniens in particular, the last phase of this experiment involved stimulation of the nucleus reuniens in order to determine the source of medial thalamic inputs to the hypothalamus. Stimulation of the nucleus reuniens activated fibers which were distributed to both the medial and lateral hypothalamus. In addition, stimulation also activated the descending periventricular system, which could be followed to the level of the midbrain central gray and such limbic structures as the hippocampal formation, septal area, amygdala and prefrontal cortex. These findings indicate that Pfc-MD activation of the hypothalamus is achieved indirectly via interneurons within the nucleus reuniens.

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Electrical stimulation of the midbrain tegmentum can produce differential modulation of quiet biting attack and affective defense behavior elicited from the hypothalamus of the cat. Stimulation of the lateral half of the tegmentum facilitated quiet biting attack and suppressed affective defense. Conversely, stimulation of the medial tegmentum suppressed quiet biting attack and facilitated affective defense. These results clearly indicate a topographic organization of modulatory sites controlling hypothalamic aggression within the midbrain tegmentum.

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Pairs of bipolar electrodes were stereotaxically aimed at two of three sites: the locus coeruleus (LC), the substantia nigra, pars compacta (SNC), and the median forebrain bundle (MFB). Rats were shaped to bar-press for trains of intracranial electrical stimulation presented as pairs of monophasic pulses. The first pulse of a pair (the C, conditioning pulse) was followed by a second pulse (the T, test pulse) after a parametrically varied interval. The effects of chronic morphine administration were tested in a paradigm of 7 days saline, 7 days morphine, 1 day morphine+naloxone, and 6 days post-drug saline. High doses of morphine (5 mg/kg) depressed response rates for intracranial self-stimulation (ICSS). LC placements and those just lateral or ventral to the LC showed large increases in ICSS rates under morphine (2.5 mg/kg). This area was delimited on either side by tips that showed response rate depressions under morphine. MFB placements yielded response rate facilitations under morphine. Sites medial to the MFB and ventral within the MFB showed rate depressions under morphine. Dorsal substantia nigra placements showed facilitated rates, whereas placements ventral within the SNC and substantia nigra, pars reticulata (SNR) produced more variable results, with rates tending to be depressed by morphine. The ICSS procedure may be a useful animal model for detecting the abuse potential of drugs.

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Acute exposure to severe stressors induce profound analgesia as well as depleting catecholamine levels. The present study examined whether d-amphetamine and apomorphine, agents which increase catecholamine availability, would alter the analgesic effectiveness of cold-water swims (CWS) and 2-deoxy-D-glucose (2-DG) as measured by an operant liminal escape procedure. Two groups of 10 rats each were tested to determine alterations in liminal escape threshold functions following amphetamine at doses of 0.25, 0.5, 1, 2 mg/kg and following apomorphine at doses of 0.025, 0.05, 0.1, 0.2 mg/kg. Half of the amphetamine and half of the apomorphine groups were tested across their respective dose ranges for the drug effects upon CWS analgesia. The remaining animals in each group received 2-DG (600 mg/kg IP) alone followed by 2-DG paired with each stimulant dose. No dose of amphetamine or apomorphine alone altered escape thresholds. While amphetamine produced slight potentiations of 2-DG analgesia at the two low doses, apomorphine at the 0.05 and 0.1 mg/kg doses returned CWS and 2-DG analgesia to within normal placebo values. These results provide indirect evidence for a role for brain norepinephrine and dopamine in stress-induced analgesia, and these data are discussed with respect to catecholamine involvement in pain-inhibitory processes.

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During a severe drought Port-au-Prince, Haiti, lost hydroelectric power for 10 weeks. This led to water shortages in areas of the city dependent on water supplied from electrically driven pumps. In a study of the impact of water restriction on disease, 400 families were randomly selected from two urban areas differentially affected by the water shortage. Disease in children was found to be related to quantity of water used, socioeconomic status, employment of head of household, and family size. The methods used in this study are recommended for the investigation of the relationship between water quantity and health.

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Chlordiazepoxide (CDP) has been previously shown to possess antinociceptive properties that are resistant, except at high doses, to the opiate antagonist naloxone. The present study evaluated whether CDP's antinociceptive effects were subject to tolerance following repeated injections and whether cross-tolerance might develop between the antinociceptive action of CDP and that of either morphine or cold water swins. CDP increased flinch-jump thresholds following acute administration and exhibited tolerance following repeated injections. Neither morphine-tolerant nor cold water swim-adapted rats displayed an antinociceptive effect when tested with CDP. On the other hand, chronic pretreatment with CDP attenuated the antinociceptive effects of cold water swims, but did not produce any clear effect upon morphine analgesia.

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Extensive evidence has indicated that distinct neural systems specifically designed to inhibit sensitivity to painful stimuli exist. Recent advances suggest that the endorphins, enkephalins and the opiate receptor interact with a descending serotonergic bulbospinal system to mediate the analgesic responses to opiates and electrical stimulation. In assessing the evolutionary and behavioral significance of this pain-inhibitory system, several laboratories discovered that acute exposure to a wide variety of stressful events results in a transient analgesia. Chronic exposure to a number of these stressors results in adaptation of the analgesic response. The purpose of this review is to identify and characterize the mechanisms by which these stressors activate pain-inhibition. The relationship of stress-induced analgesia to each of the following is reviewed: (a) the role of endorphins, enkephalins and the opiate receptor; (b) the role of the descending serotonergic bulbospinal system; (c) the role of the pituitary gland; and (d) the role of hypothalamic mechanisms. Data will be discussed in terms of "opiate" and "non-opiate" pain-inhibitory mechanisms, in which some stressors act through the former and other stressors act through the latter.

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In addition to the well-known activation of the pituitary-adrenal axis, acute exposure to severe stressors includes a temporary analgesia in rats. Thus, the present study investigates whether the pituitary was involved in the mediation of analgesia induced by severe cold-water swim (CWS) stress. Flinch-jump thresholds were measured 30 min following 3.5-min swims in water temperatures ranging from 2-35 degrees C. Compared with untreated normal rats, hypophysectomized rats, receiving corticosterone and thyroxin, displayed significantly less CWS-induced analgesia, while similarly-supplemented normal rats exhibited significantly more CWS-induced analgesia. In a second experiment, operant liminal escape pain thresholds were determined following acute and chronic CWS. Whereas normal rats exhibited profound analgesia following the initial swims, the hypophysectomized rats never displayed any CWS-induced operant escape shifts. Stress-induced alterations in general activity levels and/or thermoregulation were shown to be unrelated to the diminished effectiveness of CNS to produce analgesia in hypophysectomized rats. These data imply that the pituitary is involved in the mediation of CWS-induced analgesia.

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