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  • 1
    Electronic Resource
    Electronic Resource
    Genetic ablation of tumor necrosis factor-alpha (TNF-α) and pharmacological inhibition of TNF-synthesis attenuates MPTP toxicity in mouse striatum (2004)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 89 (2004), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The impact of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) in the pathology of Parkinson's disease (PD) and in MPTP neurotoxicity remains unclear. Here, male TNF-α (–/–) deficient mice and C57bL/6 mice were treated with MPTP (4 × 15mg/kg, 24 h intervals) and in one series, thalidomide was administered to inhibit TNF-α synthesis. Real-time RT-PCR revealed that the striatal mRNA levels of TNF-α, of the astrocytic marker glial fibrillary acidic protein (GFAP) and of the marker for activated microglia, macrophage antigen complex-1 (MAC-1), were significantly enhanced after MPTP administration. Thalidomide (50 mg/kg, p.o.) partly protected against the MPTP-induced dopamine (DA) depletion, and TNF-α (–/–) mice showed a significant attenuation of striatal DA and DA metabolite loss as well as striatal tyrosine hydroxylase (TH) fiber density, but no difference in nigral TH and DA transporter immunoreactivity. TNF-α deficient mice suffered a lower mortality (10%) compared to the high mortality (75%) seen in wild-type mice after acute MPTP treatment (4 × 20mg/kg, 2 h interval). HPLC measurement of MPP+ levels revealed no differences in TNF-α (–/–), wild-type and thalidomide treated mice. This study demonstrates that TNF-α is involved in MPTP toxicity and that inhibition of TNF-α response may be a promising target for extending beyond symptomatic treatment and developing anti-parkinsonian drugs for the treatment of the inflammatory processes in PD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2004.02399.x
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  • 2
    Electronic Resource
    Electronic Resource
    Double dissociation of the effects of selective nucleus accumbens core and shell lesions on impulsive-choice behaviour and salience learning in rats (2005)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 22 (2005), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The nucleus accumbens can be subdivided into at least two anatomically distinct subregions: a dorsolateral ‘core’ and a ventromedial ‘shell’, and this distinction may extend to a functional dissociation. Here, we contrasted the effects of selective excitotoxic core and medial shell lesions on impulsive-choice behaviour using a delayed reward choice paradigm and a differential reward for low rates of responding (DRL) test, against a form of salience learning known as latent inhibition (LI). Core lesions led to enhanced impulsive choices as evidenced by a more pronounced shift from choosing a continuously reinforced lever to a partially reinforced lever, when a delay between lever press and reward delivery was imposed selectively on the former. The core lesions also impaired performance on a DRL task that required withholding the response for a fixed period of time in order to earn a reward. Medial shell lesions had no effect on these two tasks, but abolished the LI effect, as revealed by the failure of stimulus pre-exposure to retard subsequent conditioning to that stimulus in an active avoidance procedure in the lesioned animals. As expected, selective core lesions spared LI. The double dissociations demonstrated here support a functional segregation between nucleus accumbens core and shell, and add weight to the hypothesis that the core, but not the shell, subregion of the nucleus accumbens is preferentially involved in the control of choice behaviour under delayed reinforcement conditions and in the inhibitory control of goal-directed behaviour.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2005.04388.x
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  • 3
    Electronic Resource
    Electronic Resource
    Dissociation of function between the dorsal and the ventral hippocampus in spatial learning abilities of the rat: a within-subject, within-task comparison of reference and working spatial memory (2004)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 19 (2004), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Lesions restricted to the dorsal, but not the ventral, hippocampus severely impair the formation of spatial memory. This dissociation was first demonstrated using the water maze task. The present study investigated whether the dorsal and the ventral hippocampus are involved differentially in spatial reference and spatial working memory using a four-baited/four-unbaited version of the eight-arm radial maze task. This test allows the concurrent evaluation of reference and working memory with respect to the same set of spatial cues, and thereby enables a within-subjects within-task comparison between the two forms of memory functions. Rats with N-methyl-d-aspartic acid-induced excitotoxic lesions of the dorsal hippocampus, ventral hippocampus or both were compared with sham and unoperated controls. We showed that dorsal lesions were as effective as complete lesions in severely disrupting both reference and working spatial memory, whereas rats with ventral lesions performed at a level comparable with controls. These results lend further support to the existence of a functional dissociation between the dorsal and the ventral hippocampus, with the former being preferentially involved in spatial learning.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0953-816X.2004.03170.x
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  • 4
    Electronic Resource
    Electronic Resource
    Postnatal ontogeny of hippocampal expression of the mineralocorticoid and glucocorticoid receptors in the common marmoset monkey (2005)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 21 (2005), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) are nuclear transcription factors that mediate many of the basal and stress functions and effects of the corticosteroid hormones, including those related to brain development. Despite this, relatively little is known about the postnatal ontogeny of MR and GR gene and protein expression in the central nervous system, and this is particularly true of the primates, including humans. Here we describe the postnatal ontogeny of central MR and GR gene and protein expression in the common marmoset monkey. By developing marmoset-specific riboprobes and using in situ hybridization, it was demonstrated that MR mRNA expression in the dentate gyrus and Ammon's horn was significantly greater in marmoset infants (aged 4–6 weeks) than in neonates (1–2 days), juveniles (4–5 months) and adults (3–6 years), with expression in the latter three ontogenetic stages being broadly similar. In the same subjects and ontogenetic stages, GR mRNA expression was developmentally consistent in the marmoset dentate gyrus and Ammon's horn, as well as in the paraventricular nucleus of the hypothalamus. Qualitative immunohistochemical comparison of infants and adults demonstrated that MR protein expression in the hippocampus was, as for mRNA, also greater in infants than adults, and that hippocampal GR protein was, as for mRNA, also similar in infants and adults. The increase in MR mRNA expression between the stages of neonate and infant co-occurred with a reduction in basal plasma ACTH and cortisol titres. The ontogenetic profiles of MR and GR gene expression in the marmoset monkey are therefore fundamentally different from those described for the rat and the mouse. This evidence for the postnatal ontogeny of central corticosteroid nuclear receptor expression in a primate is important for understanding both the developmental stage-specific significance of stress exposure and its potential long-term effects on health and disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2005.04003.x
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  • 5
    Electronic Resource
    Electronic Resource
    GABAA receptors containing the α5 subunit mediate the trace effect in aversive and appetitive conditioning and extinction of conditioned fear (2004)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 20 (2004), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A reduction in α5 subunit-containing γ-aminobutyric acid (GABA)A receptors has been reported to enhance some forms of learning in mutant mouse models. This effect has been attributed to impaired α5 GABAA receptor-mediated inhibitory modulation in the hippocampus. The introduction of a point mutation (H105R) in the α5 subunit is associated with a specific reduction of α5 subunit-containing GABAA receptors in the hippocampus. The present study examined the modulation of associative learning and the extinction of conditioned response in these animals. The strength of classical conditioning can be weakened when a trace interval is interposed between the conditioned stimulus and unconditioned stimulus. Here we report that this ‘trace effect’ in classical conditioning was absent in the mutant mice − they were insensitive to the imposition of a 20-s trace interval. This effect of the mutation was most clearly in the female mice using an aversive conditioning paradigm, and in the male mice using an appetitive conditioning paradigm. These gender-specific phenotypes were accompanied by a resistance to extinction of conditioned fear response in the mutant mice that was apparent in both genders. Our results identify neuronal inhibition in the hippocampus mediated via α5 GABAA receptors as a critical control element in the regulation of the acquisition and expression of associative memory.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2004.03642.x
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  • 6
    Electronic Resource
    Electronic Resource
    Decreased Density of Forebrain Cholinergic Neurons and Disintegration of the Spatial Organization of Behavior in Experimental Autoimmune Dementia (EAD) (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Experimental autoimmune dementia (EAD) is a rat model designed to examine the potential role of anti-cholinergic neurons antibodies (Abs) in the neuropathology of Alzheimer's disease (AD) and dementia. We have previously shown that sera of AD and Down's syndrome patients contain Abs which bind specifically to the high molecular weight neurofilament protein (NF-H) of the purely cholinergic electromotor neurons of Torpedo. Production of such Abs in EAD rats by prolonged immunization with Torpedo cholinergic NF-H results in the accumulation of IgG in the septum and hippocampus of the immunized rats and in memory deficits.In the present study, we examined immunohistochemically whether the anti-cholinergic NF-H immune response of the FAD rats affects their brain cholinergic neurons. In addition, since dementia is associated with severe deterioration in the spatio-temporal organization of behavior, we examined whether EAD rats also mimic this important feature of dementia. The results obtained show that production in EAD rats of anti-cholinergic NF-H Abs similar to those found in AD patients results in a marked decrease in the density of forebrain cholinergic neurons and in derangements in the spatio-temporal organization of their behavior. These findings may replicate pathogenic processes in AD and support a role for anti-cholinergic NF-H Abs in the degeneration of cholinergic neurons in the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23061.x
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  • 7
    Electronic Resource
    Electronic Resource
    The latent inhibition model of schizophrenic attention disorder and of antipsychotic drug action: comment on Dunn, Atwater and Kilts (Psychopharmacology, 1993, 112:315–323) (1994)
    Springer
    Psychopharmacology 116 (1994), S. 379-380 
    Details
    ISSN: 1432-2072
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02245344
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  • 8
    Electronic Resource
    Electronic Resource
    Antagonism of amphetamine-induced disruption of latent inhibition in rats by haloperidol and ondansetron: Implications for a possible antipsychotic action of ondansetron (1994)
    Springer
    Psychopharmacology 114 (1994), S. 657-664 
    Details
    ISSN: 1432-2072
    Keywords: Latent inhibition ; Dopamine ; Ondansetron ; 5HT3 antagonists ; Amphetamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Latent inhibition (LI) is a behavioural phenomenon whereby preexposure to a stimulus without reinforcement interferes with the formation of subsequent associations to that stimulus. Using preexposure to a tone stimulus which subsequently serves as a conditioned stimulus for suppression of licking, we have confirmed that LI is disrupted by a low dose of amphetamine. Haloperidol was able to prevent this effect of amphetamine. Ondansetron, a selective and potent 5HT3 receptor antagonist, was also shown to be effective at blocking the amphetamine-induced disruption of LI at a dose of 0.01 mg/kg, but not at 0.1 mg/kg. In addition, it was demonstrated that ondansetron could enhance LI; using only ten preexposures, no LI was obtained in the saline group, but was apparent in animals given ondansetron, an effect which has been previously shown with haloperidol. Haloperidol, at the higher dose used, reduced suppression of licking, however, ondansetron at the effective dose had no such effect. It is concluded that ondansetron is able to attenuate increases in dopamine activity, produced pharmacologically with amphetamine without affecting baseline dopamine activity. The implications of these findings for a possible antipsychotic action of ondansetron are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02244998
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  • 9
    Electronic Resource
    Electronic Resource
    The partial reinforcement extinction effect after treatment with chlordiazepoxide (1981)
    Springer
    Psychopharmacology 73 (1981), S. 269-275 
    Details
    ISSN: 1432-2072
    Keywords: Chlordiazepoxide ; Partial reinforcement ; Resistance to extinction ; Conditioned frustration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two experiments are reported, in which rats were run in a straight alley for food reward with or without injections of the anti-anxiety drug, chlordiazepoxide (CDP). The experiments were directed to two questions. (1) Can one predict the effects of CDP from knowledge of the effects of a second anti-anxiety drug, sodium amylobarbitone (SA)? (2) Can the effects of CDP be predicted from the hypothesis that anti-anxiety drugs attenuate responses to conditioned frustrative stimuli? The experiments examined the effects of CDP on the partial reinforcement extinction effect (PREE) at one trial a day. CDP injected throughout acquisition and extinction reduced the PREE. This effect was probably due to the presence of the drug during acquisition. Injected during extinction only, CDP increased resistance to extinction in both continuous and partial reinforcement groups. These effects of CDP were closely similar to those previously reported for SA, thus answering question (1) in the affirmative. The effects of CDP on the PREE were also consistent with the conditioned-frustration hypothesis (question 2).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00422416
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  • 10
    Electronic Resource
    Electronic Resource
    The partial reinforcement extinction effect: Influence of chlordiazepoxide in septal lesioned rats (1981)
    Springer
    Psychopharmacology 74 (1981), S. 280-289 
    Details
    ISSN: 1432-2072
    Keywords: Lateral septal lesions ; Medial septal lesions ; Chlordiazepoxide ; Partial reinforcement ; Resistance to extinction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats sustained electrolytic lesions either in the medial septal (MS) or lateral septal (LS) area or they were sham-operated. They were tested in the straight alley with food reward on either continuous (CRF) or partial (PRF) reinforcement at one trial a day and were injected with either 5 mg/kg chlordiazepoxide HCl (CDP) or with saline before the daily trial throughout acquisition and extinction. The effects of the drug on resistance to extinction interacted with those of the LS lesion in ways which were consistent with the hypothesis that CDP acts via the lateral septal area if it is injected during acquisition on a PRF schedule. MS lesions produced only small changes in the effects of CDP. In general, CDP acted to reverse the effects produced by each lesion: Under those conditions in which MS lesions produced faster running speeds, CDP caused the lesioned animals to run slower; and under those conditions in which LS lesions produced slower running speeds, CDP caused the lesioned animals to run faster.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427111
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