The Experts below are selected from a list of 14187 Experts worldwide ranked by ideXlab platform
J A Zwart - One of the best experts on this subject based on the ideXlab platform.
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the blink reflex in chronic tension type headache migraine and cervicogenic headache
Cephalalgia, 1994Co-Authors: Trond Sand, J A ZwartAbstract:R1 and R2 blink reflex latencies were investigated blind in 10 patients with cervicogenic headache, 11 patients with chronic tension-type headache, 11 patients with migraine, and 9 headache-free controls. There were no R1 or R2 latency differences between the four groups. The latency of R1 increased significantly with headache duration in tension-type headache patients. Shorter R1 latencies were found on the symptomatic side than on the non-symptomatic side in cervicogenic headache patients. The results suggest that a state of hyperactivity may be present in the ipsilateral trigeminal nucleus in cervicogenic headache. Hypoactivity, however, may develop over time in tension-type headache.
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The blink reflex in chronic tension‐type headache, migraine, and cervicogenic headache
Cephalalgia, 1994Co-Authors: Trond Sand, J A ZwartAbstract:R1 and R2 blink reflex latencies were investigated blind in 10 patients with cervicogenic headache, 11 patients with chronic tension-type headache, 11 patients with migraine, and 9 headache-free controls. There were no R1 or R2 latency differences between the four groups. The latency of R1 increased significantly with headache duration in tension-type headache patients. Shorter R1 latencies were found on the symptomatic side than on the non-symptomatic side in cervicogenic headache patients. The results suggest that a state of hyperactivity may be present in the ipsilateral trigeminal nucleus in cervicogenic headache. Hypoactivity, however, may develop over time in tension-type headache.
Trond Sand - One of the best experts on this subject based on the ideXlab platform.
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the blink reflex in chronic tension type headache migraine and cervicogenic headache
Cephalalgia, 1994Co-Authors: Trond Sand, J A ZwartAbstract:R1 and R2 blink reflex latencies were investigated blind in 10 patients with cervicogenic headache, 11 patients with chronic tension-type headache, 11 patients with migraine, and 9 headache-free controls. There were no R1 or R2 latency differences between the four groups. The latency of R1 increased significantly with headache duration in tension-type headache patients. Shorter R1 latencies were found on the symptomatic side than on the non-symptomatic side in cervicogenic headache patients. The results suggest that a state of hyperactivity may be present in the ipsilateral trigeminal nucleus in cervicogenic headache. Hypoactivity, however, may develop over time in tension-type headache.
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The blink reflex in chronic tension‐type headache, migraine, and cervicogenic headache
Cephalalgia, 1994Co-Authors: Trond Sand, J A ZwartAbstract:R1 and R2 blink reflex latencies were investigated blind in 10 patients with cervicogenic headache, 11 patients with chronic tension-type headache, 11 patients with migraine, and 9 headache-free controls. There were no R1 or R2 latency differences between the four groups. The latency of R1 increased significantly with headache duration in tension-type headache patients. Shorter R1 latencies were found on the symptomatic side than on the non-symptomatic side in cervicogenic headache patients. The results suggest that a state of hyperactivity may be present in the ipsilateral trigeminal nucleus in cervicogenic headache. Hypoactivity, however, may develop over time in tension-type headache.
Paul R Sanberg - One of the best experts on this subject based on the ideXlab platform.
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hyperactivity and Hypoactivity in a rat model of huntington s disease the systemic 3 nitropropionic acid model
Brain Research Protocols, 1997Co-Authors: Cesario V Borlongan, T K Koutouzis, Thomas B Freeman, David W Cahill, Robert A Hauser, Paul R SanbergAbstract:Abstract The present study proposes the use of systemic 3-nitropropionic acid (3-NP) treatment in rats as a model of Huntington's disease (HD). The systemic 3-NP model involves chronic injection of low dose intraperitoneal (i.p.) injections of 3-NP to rats once every 4 days over a period of time. Evidence from our experimental studies suggests that manipulating the number of injections can result in either increased nocturnal spontaneous locomotor activity (hyperactivity) or nocturnal akinesia (Hypoactivity) [1] . For example, two injections of 3-NP (using the treatment of one injection every 4 days) result in hyperactivity, while four injections or more of 3-NP lead to Hypoactivity [1] . The locomotor activity is recorded by Digiscan locomotor activity monitors [11] . The observation of these two types of locomotor activity is unique since no excitotoxin model has replicated a two-stage progression of a HD-like behavioral alteration. Most studies using excitotoxins like quinolinic acid (QA) and kainic acid (KA) have only reproduced the hyperactivity stage 4 , 5 , 7 . With the systemic 3-NP model, investigations into at least two stages of the disease are made possible. This allows for better assessment of intervention strategies such as neural transplants across different stages of the disease. The systemic 3-NP rat model is believed to be an improved animal model of HD.
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systemic 3 nitropropionic acid behavioral deficits and striatal damage in adult rats
Brain Research Bulletin, 1995Co-Authors: Cesario V Borlongan, T K Koutouzis, Timothy S Randall, Thomas B Freeman, David W Cahill, Paul R SanbergAbstract:Abstract Previous animal studies have demonstrated that systemic administration of 3-nitropropfonic acid 3-NP) leads to neuropathological changes similar to those seen in Huntington's disease (HD). Recently, we reported hypeactivity in 6- and 10-week old rats treated with systemic 3-NP OP, 10 mg/kg/day) once every 4 days for 28 days. Although these behavioral results seem to differ from the observed hyperactivity in most excitotoxic models of HD, 3-NP may provide a better model of juvenile onset and advanced HD. In the present study, older rate were similarly treated with 3-NP to further characterize the reported age dependency of striatai neuronal death caused by 3-NP. Hypoactivtty was observed In 14- and 28-week old rats with the latter demonstrating more profound features. The present study also provided the first direct evidence of a 3-NP affect on passive avoidance behavior. Experimental and control animals showed no sigraficant difference in daytime acquisition and retention of a passive avoidance task. However, when the retention tests were conducted during the night time (in contrast to previous daytime tests), 3-NP-treated animals exhibited significant retention deficits. M addition, the neuropathological effects of 3-NP were determined by Nissi, ACNE and NADPH-diaphorase histochemistry. Metabolic activity was studied using cytochroms oxidase activity as an index. Results revealed striatal glial infiltration, lose of intrinsic striatai Cholingergic neurons, but some sparing of large ACNE positive neurons, minimal damage of NADPH-disphorase-containing neurone, and very slight, if any, alterations in cytochrome oxidese activity. In summary, the present results revealed that long-term systemic administration of 3-NP leads to a) an age-dependent Hypoactivity, b) a contextual retention deficit in paasive avoidance, and c) a selective destruction of striatal neuronal populations.
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nicotine potentiates haloperidol induced catalepsy and locomotor Hypoactivity
Pharmacology Biochemistry and Behavior, 1991Co-Authors: Dwaine F Emerich, Marie D Zanol, Andrew B Norman, Brian J Mcconville, Paul R SanbergAbstract:Abstract Nicotine was found to potentiate the catalepsy and reduced locomotion following the administration of haloperidol. The ability of various doses of nicotine (0.1, 0.2, or 0.3 mg/kg) to potentiate the catalepsy produced by haloperidol (0.1, 0.2, or 0.4 mg/kg) was investigated. Nicotine potentiated the cataleptic effects of both the 0.2 and 0.4 mg/kg doses of haloperidol, but had no effect following the lowest (0.1 mg/kg) dose of haloperidol. The nicotine potentiation of catalepsy produced by the highest dose of haloperidol was independent of the dose of nicotine used. Nicotine alone did not produce catalepsy. A second experiment evaluated the ability of nicotine to potentiate the decreases in spontaneous locomotor activity produced by haloperidol. Animals received nicotine (0.1 mg/kg) alone or in conjunction with haloperidol (0.1 or 0.4 mg/kg) and were tested in Digiscan Animal Monitors. Haloperidol produced a dose-related decrease in locomotion. Nicotine significantly potentiated the Hypoactivity produced by both doses of haloperidol. These results indicated that: 1) nicotine produces a significant potentiation of both the catalepsy and locomotor decreases following haloperidol and 2) the Digiscan Animal Activity Monitors may provide a more sensitive assessment of the interaction between nicotine and haloperidol than the catalepsy bat test. These data suggest that adjunct treatment with nicotine may prove useful for treating neuroleptic responsive disorders such as Tourette Syndrome, schizophrenia and Huntington's disease.
Antonello Bonci - One of the best experts on this subject based on the ideXlab platform.
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rescuing cocaine induced prefrontal cortex Hypoactivity prevents compulsive cocaine seeking
Nature, 2013Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello BonciAbstract:A study of compulsive drug-seeking behaviour in rats reveals that prolonged cocaine self-administration decreases prelimbic cortex activity resulting in increased compulsive drug-seeking actions; conversely, increasing activity in the prelimbic cortex decreases drug-seeking behaviour, a finding relevant to addiction treatment. Antonello Bonci and colleagues use a rodent model for compulsive cocaine usage to show that in animals expressing the strongest drug-seeking behaviours, there is a prolonged reduction in activity in the deeper layers of the prelimbic cortex, part of the brain thought to be associated with compulsive drug seeking. Correcting this Hypoactivity using optogenetic strategies prevents cocaine-seeking behaviours. In addition, optogenetic inhibition of prelimbic activity was sufficient to drive compulsive drug seeking. This work identifies prelimbic stimulation as a possible therapy in compulsive drug users. Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences1. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control2,3,4 could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking5,6,7,8 in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the prelimbic cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive prelimbic cortex neurons with in vivo optogenetic prelimbic cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic prelimbic cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in prelimbic cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic prelimbic cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal cortex could serve as a promising therapy for treating compulsive drug use.
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rescuing cocaine induced prefrontal cortex Hypoactivity prevents compulsive cocaine seeking
Nature, 2013Co-Authors: Billy T Chen, Christina Hatch, Ikue Kusumotoyoshida, Woodward F Hopf, Antonello Bonci, Hau Jie Yau, Saemi L ChoAbstract:Loss of control over harmful drug seeking is one of the most intractable aspects of addiction, as human substance abusers continue to pursue drugs despite incurring significant negative consequences. Human studies have suggested that deficits in prefrontal cortical function and consequential loss of inhibitory control could be crucial in promoting compulsive drug use. However, it remains unknown whether chronic drug use compromises cortical activity and, equally important, whether this deficit promotes compulsive cocaine seeking. Here we use a rat model of compulsive drug seeking in which cocaine seeking persists in a subgroup of rats despite delivery of noxious foot shocks. We show that prolonged cocaine self-administration decreases ex vivo intrinsic excitability of deep-layer pyramidal neurons in the prelimbic cortex, which was significantly more pronounced in compulsive drug-seeking animals. Furthermore, compensating for hypoactive prelimbic cortex neurons with in vivo optogenetic prelimbic cortex stimulation significantly prevented compulsive cocaine seeking, whereas optogenetic prelimbic cortex inhibition significantly increased compulsive cocaine seeking. Our results show a marked reduction in prelimbic cortex excitability in compulsive cocaine-seeking rats, and that in vivo optogenetic prelimbic cortex stimulation decreased compulsive drug-seeking behaviours. Thus, targeted stimulation of the prefrontal cortex could serve as a promising therapy for treating compulsive drug use.
Dennis L Murphy - One of the best experts on this subject based on the ideXlab platform.
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Are serotonin transporter knockout mice 'depressed'?: Hypoactivity but no anhedonia.
Neuroreport, 2006Co-Authors: Allan V. Kalueff, Pamela S. Gallagher, Dennis L MurphyAbstract:Although the serotonin transporter is a key target for antidepressants, its exact role in depression etiology remains unclear. While serotonin transporter knockout mice are a potential model to examine this problem, their depression pro¢le is unclear in several ‘despair’ tests, and may be confounded by their Hypoactivity phenotype (con¢rmed here by marble-burying and bedding tests). To assess depression in these mice, we evaluated wild-type, heterozygous, and serotonin transporter knockout C57BL/6 male mice on a well-validated, anhedonia-based depression paradigm, the sucrose preference test. Overall, all three genotypes showed similar sucrose preference, indicating an unaltered hedonic state. These results demonstrate that depression-like behavior (unlike Hypoactivity) is not a baseline phenotypic feature of serotonin transporter knockout mice, suggesting anew that these mice do not represent a genetic model of depression. NeuroReport 17:1347^1351 � c 2006 Lippincott Williams & Wilkins.
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Are serotonin transporter knockout mice 'depressed'?: Hypoactivity but no anhedonia.
Neuroreport, 2006Co-Authors: Allan V. Kalueff, Pamela S. Gallagher, Dennis L MurphyAbstract:Although the serotonin transporter is a key target for antidepressants, its exact role in depression etiology remains unclear. While serotonin transporter knockout mice are a potential model to examine this problem, their depression profile is unclear in several 'despair' tests, and may be confounded by their Hypoactivity phenotype (confirmed here by marble-burying and bedding tests). To assess depression in these mice, we evaluated wild-type, heterozygous, and serotonin transporter knockout C57BL/6 male mice on a well-validated, anhedonia-based depression paradigm, the sucrose preference test. Overall, all three genotypes showed similar sucrose preference, indicating an unaltered hedonic state. These results demonstrate that depression-like behavior (unlike Hypoactivity) is not a baseline phenotypic feature of serotonin transporter knockout mice, suggesting anew that these mice do not represent a genetic model of depression.
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are serotonin transporter knockout mice depressed Hypoactivity but no anhedonia
Neuroreport, 2006Co-Authors: Allan V. Kalueff, Pamela S. Gallagher, Dennis L MurphyAbstract:Although the serotonin transporter is a key target for antidepressants, its exact role in depression etiology remains unclear. While serotonin transporter knockout mice are a potential model to examine this problem, their depression profile is unclear in several 'despair' tests, and may be confounded by their Hypoactivity phenotype (confirmed here by marble-burying and bedding tests). To assess depression in these mice, we evaluated wild-type, heterozygous, and serotonin transporter knockout C57BL/6 male mice on a well-validated, anhedonia-based depression paradigm, the sucrose preference test. Overall, all three genotypes showed similar sucrose preference, indicating an unaltered hedonic state. These results demonstrate that depression-like behavior (unlike Hypoactivity) is not a baseline phenotypic feature of serotonin transporter knockout mice, suggesting anew that these mice do not represent a genetic model of depression.