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The Global ETD Search service is a free service for researchers
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Showing 1 to 6 of 6 (0.017 seconds)| 1 |
Induction of Grooming Behavior in Male Rats by M-Chlorphenylpiperazine, a Central 5-Hydroxytryptamine Receptor AgonistBrus, Ryszard, Nowak, Przemyslaw, Szkilnik, Ryszard, Kostrzewa, Richard M., Shani, Jashovam 01 December 1997 (has links)
Grooming behavior in rats has so far been known to be induced mainly by dopamine agonists type D1. In order to explore the involvement of serotonine (5-HT) and its receptors in such a behavior, rats were exposed to two phases of treatment: to the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT), injected intraventricularly three days after birth, and to the serotonin partial agonist m-chlorophenylpiperazine (mCPP), administered in two dose levels, two months later. Grooming behavior was monitored immediately before and after the higher dose of mCPP, while brain levels of 5-HT and its major metabolite 5-HIAA were assayed one week after mCPP administration. It is documented that while a low dose of mCPP in the non-lesioned rats increased the grooming-time by 5.7-fold, the higher mCPP dose in the non-lesioned non-primed rats increased grooming behavior by 3.6-fold. The 5,7-DHT lesions caused a 6.7-fold increase in the non-primed rats, and a 4.2-fold increase in the primed ones. These increases were noticeable only in male rats. When a higher dose of mCPP followed its lower dose in the 5,7-DHT-lesioned rats, a 3.6-fold decrease was recorded only in the female rats. A 88% and 94% drop in 5-HT and 5-HIAA levels in the brain neostriatum of the 5,7-DHT-lesioned rats was noticed in both sexes, one week after mCPP administration. These findings are the first to demonstrate that the 5-HT2 partial agonist mCPP is capable of modifying grooming behavior, and that 5,7,-DHT brain lesions increase basal grooming time, suggesting that 5-HT neurons and receptors are involved in grooming behavior in rats.
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Ontogenetic Serotoninergic Lesioning Alters Histaminergic Activity in Rats in AdulthoodJośko, Jadwiga, Drab, Jacek, Jochem, Jerzy, Nowak, Przemyslaw, Szkilnik, Ryszard, Korossy-Mruk, Eva, Boron, Dariusz, Kostrzewa, Richard M., Brus, Halina, Brus, Ryszard 01 August 2011 (has links)
The aim of this study was to determine histamine content in the brain and the effect of histamine receptor antagonists on behavior of adult rats lesioned as neonates with the serotonin (5-HT) neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). At 3 days after birth Wistar rats were pretreated with desipramine (20 mg/kg ip) before bilateral icv administration of 5,7-DHT (37.5 μg base on each side) or saline-ascorbic (0.1%) vehicle (control). At 10 week levels of 5-HT and its metabolite 5-hydroxyindole acetic acid (5-HIAA) were determined in frontal cortex, striatum, and hippocampus by an HPLC/ED technique. In the hypothalamus, frontal cortex, hippocampus and medulla oblongata, the level of histamine was analyzed by an immunoenzymatic method. Behavioral observations (locomotion, exploratory-, oral-, and stereotyped activity) were performed, and effects of DA receptor agonists (SKF 38393, apomorphine) and histamine receptor antagonists S(+)chlorpheniramine (H1), cimetidine (H2), and thioperamide (H3) were determined. We confirmed that 5,7-DHT profoundly reduced contents of 5-HT and 5-HIAA in the brain in adulthood. Histamine content was also reduced in all examined brain regions. Moreover, in 5,7-DHT-lesioned rats the locomotor and oral activity responses to thioperamide were altered, and apomorphineinduced stereotype was intensified. From the above, we conclude that an intact central serotoninergic system modulates histamine H3 receptor antagonist effects on the dopaminergic neurons in rats.
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Thioperamide, an H <sub>3</sub> Receptor Antagonist Prevents [ <sup>3</sup> H]Glucose Uptake in Brain of Adult Rats Lesioned as Neonates With 5,7-DihydroxytryptamineJośko, Jadwiga, Drab, Jacek, Nowak, Przemysław, Szkilnik, Ryszard, Körőssy, Èva, Boroń, Dariusz, Brus, Halina, Kostrzewa, Richard M., Brus, Ryszard 01 January 2011 (has links)
As a first attempt at exploring an association between histaminergic and serotoninergic neuronal phenotypes in glucose regulation, the influence of the histamine H 3 receptor antagonist thioperamide on glucose uptake by brain was determined in rats in which the serotoninergic innervations of brain was largely destroyed perinatally. Male Wistar rats were initially treated on the 3rd day after birth with the serotoninergic neurotoxin 5,7- dihydroxytryptamine (5,7-DHT) (75 μg icv) or saline vehicle (10 μl icv). At 8 weeks lesioned and control rats were terminated in order to validate the effectiveness of 5,7-DHT: reduction in 5-HT and 5-HIAA by 83-91% and 69-83% in striatum, frontal cortex, and hippocampus (HPLC/ED method). Other groups of rats were pretreated with thioperamide (5.0 mg/kg ip) or saline vehicle 60 min prior to 6-[ 3 H]-D-glucose (500 μCi/kg ip). Fifteen-min later rats were decapitated and brains were excised and dissected to remove frontal cortex, striatum, hippocampus, thalamus/hypothalamus, pons, and cerebellum. Liquid scintillation spectroscopy was used to determine that [ 3 H]glucose uptake, which was enhanced in 5,7-DHT lesioned rats in cortex (by 88%), hippocampus, thalamus/hypothalamus, pons and cerebellum (each by 47-56%), and in striatum (by 35%). In contrast, thioperamide prevented the enhancement in [ 3 H]glucose uptake in all brain regions of 5,7-DHT neonatally lesioned rats; and [ 3 H]glucose levels were significantly different in all brain regions (except thalamus/hypothalamus) in thioperamide-versus saline-treated rats. These findings indicate a functional association between histaminergic and serotoninergic systems in brain in relation to glucose regulation.
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Neonatal Co-Lesion by DSP-4 and 5,7-DHT Produces Adulthood Behavioral Sensitization to Dopamine D<sub>2</sub> Receptor AgonistsNowak, Przermysław, Nitka, Dariusz, Kwieciński, Adam, Jośko, Jadwiga, Drab, Jacek, Pojda-Wilczek, Dorota, Kasperski, Jacek, Kostrzewa, Richard M., Brus, Ryszard 01 January 2009 (has links)
To assess the possible modulatory effects of noradrenergic and serotoninergic neurons on dopaminergic neuronal activity, the noradrenergic and serotoninergic neurotoxins DSP-4 N-(2-chlorethyl)-N-ethyl-2-bromobenzylamine (50.0 mg/kg, sc) and 5,7- dihydroxytryptamine (5,7-DHT) (37.5 μg icv, half in each lateral ventricle), respectively, were administered to Wistar rats on the first and third days of postnatal ontogeny, and dopamine (DA) agonist-induced behaviors were assessed in adulthood. At eight weeks, using an HPLC/ED technique, DSP-4 treatment was associated with a reduction in NE content of the corpus striatum (> 60%), hippocampus (95%), and frontal cortex (> 85%), while 5,7-DHT was associated with an 80-90% serotonin reduction in the same brain regions. DA content was unaltered in the striatum and the cortex. In the group lesioned with both DSP-4 and 5,7-DHT, quinpirole-induced (DA D2-agonist-agonist) yawning, 7-hydroxy-DPAT-induced (DA D3 agonist) yawning, and apomorphine-induced (non-selective DA agonist) stereotypies were enhanced. However, SKF 38393-induced (DA D1 agonist) oral activity was reduced in the DSP-4 + 5,7-DHT group. These findings demonstrate that DA D2- and D3-agonist-induced behaviors are enhanced while DA D1-agonist-induced behaviors are suppressed in adult rats in which brain noradrenergic and serotoninergic innervation of the brain has largely been destroyed. This study indicates that noradrenergic and serotoninergic neurons have a great impact on the development of DA receptor reactivity (sensitivity).
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Neuroteratology and Animal Modeling of Brain DisordersArcher, Trevor, Kostrzewa, Richard M. 09 February 2016 (has links)
Over the past 60 years, a large number of selective neurotoxins were discovered and developed, making it possible to animal-model a broad range of human neuropsychiatric and neurodevelopmental disorders. In this paper, we highlight those neurotoxins that are most commonly used as neuroteratologic agents, to either produce lifelong destruction of neurons of a particular phenotype, or a group of neurons linked by a specific class of transporter proteins (i.e., dopamine transporter) or body of receptors for a specific neurotransmitter (i.e., NMDA class of glutamate receptors). Actions of a range of neurotoxins are described: 6-hydroxydopamine (6-OHDA), 6-hydroxydopa, DSP-4, MPTP, methamphetamine, IgG-saporin, domoate, NMDA receptor antagonists, and valproate. Their neuroteratologic features are outlined, as well as those of nerve growth factor, epidermal growth factor, and that of stress. The value of each of these neurotoxins in animal modeling of human neurologic, neurodegenerative, and neuropsychiatric disorders is discussed in terms of the respective value as well as limitations of the derived animal model. Neuroteratologic agents have proven to be of immense importance for understanding how associated neural systems in human neural disorders may be better targeted by new therapeutic agents.
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NeurotoxinsKostrzewa, Richard M. 01 January 2016 (has links)
The era of selective neurotoxins arose predominately in the 1960s with the discovery of the norepinephrine (NE) isomer 6-hydroxydopamine (6-OHDA), which selectively destroyed noradrenergic sympathetic nerves in rats. A series of similarly selective neurotoxins were later discovered, having high affinity for the transporter site on nerves and thus being accumulated and able to disrupt vital intraneuronal processes, to lead to cell death. The Trojan Horse botulinum neurotoxins (BoNT) and tetanus toxin bind to glycoproteins on the neuronal plasma membrane, then these stealth neurotoxins are taken inside respective cholinergic or glycinergic nerves, producing months-long functional inactivation but without overtly destroying those nerves. The mitochondrial complex I inhibitor rotenone, while lacking total specificity, still destroys dopaminergic nerves with some selectivity; and importantly, results in the neural accumulation of synuclein-to model Parkinson’s disease (PD) in animals. Other neurotoxins target specific subtypes of glutamate receptors and produce excitotoxicity in nerves with that receptor population. The dopamine D2 receptor agonist quinpirole, termed a selective neurotoxin, produces a behavioral state replicating some of the notable features of schizophrenia, but without overtly destroying nerves. These processes, mechanisms or treatment-outcomes account for the means by which neurotoxins are classified as such, and represent some of the means by which neurotoxins as a group are able to destroy or functionally inactivate nerves; or replicate an altered neurological state. Selective neurotoxins have proven to be important in gaining insight into biochemical processes and mechanisms responsible for survival or demise of a nerve. Selective neurotoxins are useful also for animal modeling of human neural disorders such as PD, Alzheimer disease, attention-deficit hyperactivity disorder (ADHD), Lesch-Nyhan disease, tardive dyskinesia, schizophrenia and others. The importance of neurotoxins in neuroscience will continue to be ever more important as even newer neurotoxins are discovered.
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