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  • 1
    Electronic Resource
    Electronic Resource
    The effects of intrahippocampal ibotenate on resistance to extinction after continuous or partial reinforcement (1986)
    Springer
    Experimental brain research 61 (1986), S. 519-530 
    Details
    ISSN: 1432-1106
    Keywords: Hippocampus ; Subiculum ; Partial reinforcement extinction effect ; Partial reinforcement acquisition effect ; Entorhinal cortex ; botenate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracerebral injections of ibotenate were used to produce, in rats, extensive cell loss in the hippocampus and dentate gyrus (complete hippocampal, CH), in the CH plus subiculum (SUB + CH), or in the subiculum plus entorhinal cortex (SUB + EC). These rats and sham-operated controls were trained to run in a straight alley for food reward delivered on a continuous (CR) or partial (PR) reinforcement schedule. In controls PR training gave rise to the well-known partial reinforcement extinction effect (PREE), i.e., greater resistance to extinction than that observed in CR-trained animals. Previous work had shown that large aspiration lesions of the hippocampal formation eliminate the PREE by increasing resistance to extinction in CR-trained animals and decreasing resistance to extinction in PR-trained animals. In the present experiments the PREE survived CH lesions, which increased resistance to extinction in both CR and PR training conditions; these effects were observed in the start and run (but not goal) sections of the alley. In contrast, subicular cell loss (in both SUB + CH and SUB + EC groups) abolished the PREE (but in the goal section only) by increasing resistance to extinction in the CR condition and decreasing resistance to extinction in the PR condition. In addition, some of the effects of PR training on start and run speeds during acquisition were altered by the CH and SUB + CH lesions. These results confirm previous data showing that the hippocampal formation plays a role in mediating the behavioural effects of PR training, but require modification of the model previously proposed to account for these data.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00237577
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  • 2
    Electronic Resource
    Electronic Resource
    An iontophoretic study of the effects of α-amino-hydroxy-5-methyl-4-isoxazole propionic acid lesions of the nucleus basalis magnocellularis on cholinergic and GABAergic influences on frontal cortex neurones of rats (1994)
    Springer
    Experimental brain research 98 (1994), S. 441-456 
    Details
    ISSN: 1432-1106
    Keywords: α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid lesion ; Cholinergic ; GABAergic ; Nucleus basalis ; Iontophoresis ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Unilateral lesions of the nucleus basalis magnocellularis (NBM) produced by α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid in rats caused, 8–10 weeks after the lesion, a 94% reduction in cortical acetylcholinesterase fibres and reduced activities of acetylcholinesterase and choline acetyltransferase by 70–80% in the frontal cortex ipsilateral to the lesion. In anaesthetized unlesioned control rats, iontophoretic administration of acetylcholine and carbachol produced atropine-sensitive inhibition and excitation of frontal cortical neurones, effects similar to those produced by electrically stimulating the NBM. The lesion reduced cortical neuronal firing rates but increased the percentage and sensitivity of neurones responding to acetylcholine, the predominant response changing from inhibition to excitation; response duration increased but latency was unaffected. The size of the response of individual neurones to carbachol, but not the percentage of sensitive neurones, was also increased in lesioned animals. The proportion of neurones responding to bicuculline and their individual sensitivities were increased by the lesion, suggesting that the lesion increased GABAergic tone; responses to glutamate were unchanged. The lesion did not affect the proportion of neurones in which acetylcholine modulated neuronal responses but reversed the nature of the modulation to predominantly excitatory; excitation was the predominant response to electrical forepaw stimulation in unlesioned control animals. This suggests a possible interaction between GABAergic and cholinergic mechanisms in selective attention and processing of cognitive information. Acute administration of di-isopropyl fluorophosphate to unlesioned animals significantly increased the number of frontal cortical neurones responding to acetylcholine, without affecting individual neuronal sensitivity or responses to carbachol and glutamate. The similarity of these effects to those of acetylcholine in lesioned animals suggests that the increased sensitivity to acetylcholine in the latter was due to loss of acetylcholinesterase, enabling diffusion of acetylcholine to more distant neurones. However, acetylcholinesterase does not hydrolyse carbachol and therefore it is necessary to postulate a different post-synaptic mechanism to explain the lesion-induced increases in the sensitivities of individual neurones to carbachol and to acetylcholine; interpretation of experimental findings should take these two mechanisms into account.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233982
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  • 3
    Electronic Resource
    Electronic Resource
    The effects of intra-subicular ibotenate on resistance to extinction after continuous or partial reinforcement (1988)
    Springer
    Experimental brain research 73 (1988), S. 315-319 
    Details
    ISSN: 1432-1106
    Keywords: Subiculum ; Partial reinforcement ; Extinction effect ; Ibotenate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracerebral injections of ibotenate were used to produce, in rats, extensive cell loss in the subiculum. These rats and sham-operated controls were trained to run in a straight alley for food reward delivered on a continuous (CR) or partial (PR) reinforcement schedule. In controls PR training gave rise to the well-known partial reinforcement extinction effect (PREE), i.e., greater resistance to extinction than that observed in CR-trained animals. Previous experiments have shown that large aspiration lesions of the hippocampal formation eliminate the PREE; and that ibotenate-induced lesions of the subicular region plus either the hippocampus or the entorhinal cortex disrupt it. In contrast to these previous results, the PREE was unaltered in the present experiment by damage largely restricted to the subiculum. This lesion caused only relatively small changes in running speeds during acquisition. Thus the critical region(s) of damage within the hippocampal formation for disruption of the PREE remains uncertain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00248223
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    The selective 5-HT3 receptor antagonist, WAY100289, enhances spatial memory in rats with ibotenate lesions of the forebrain cholinergic projection system (1995)
    Springer
    Psychopharmacology 117 (1995), S. 318-332 
    Details
    ISSN: 1432-2072
    Keywords: WAY100289 ; Spatial learning ; Memory Rats ; 5HT3 Receptor antagonist
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of three doses (0.003, 0.03 and 1.0 mg/kg sc) of the 5-HT3 receptor antagonist, WAY 100289, on spatial learning and memory in the water maze were examined in rats before and after ibotenate lesions to the nucleus basalis and medial septal brain regions at the source of cholinergic projections to cortex and hippocampus. The representative cholinergic nicotinic and muscarinic receptor agonists nicotine (0.1 mg/kg) and arecoline (1.0 mg/kg) were also tested for comparison. Both arecoline and nicotine improved initial acquisition in rats before lesioning, in terms of latency to find a hidden platform and accuracy of search strategy. WAY100289 did not affect the performance of normal rats significantly, apart from some non-significant trends towards improvement with the highest dose. However, in animals showing transient navigational deficits in retention and relearning after lesioning, WAY100289 improved performance at all three doses, though ameliorative effects of nicotine and arecoline were more marked also in lesioned rats. These results show that WAY100289 improved spatial learning in animals impaired after lesions to cholinergic projection nuclei, which may reflect an interaction with cholinergic transmission to enhance cognitive function. However, in the present study, WAY100289 appeared to be less effective than direct cholinergic agonists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02246107
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  • 5
    Electronic Resource
    Electronic Resource
    Relationship between up-regulation of nicotine binding sites in rat brain and delayed cognitive enhancement observed after chronic or acute nicotinic receptor stimulation (1996)
    Springer
    Psychopharmacology 124 (1996), S. 323-331 
    Details
    ISSN: 1432-2072
    Keywords: Nicotine ; Water maze ; Nicotinic receptor up-regulation ; Cognitive enhancement ; Delayed acute effect
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract (−)-Nicotine tartrate (2 mg/kg), and a nicotinic agonist, RJR 2403 (1.4 mg/kg), and antagonist, mecamylamine (1 mg/kg), were administered to separate groups of rats SC twice daily for 10 days. Two other groups received the same doses of nicotine or RJR 2403 for 1 day followed by saline for 9 days. Twenty-four hours after the final injection, the rats were compared to a 10-day saline-injected group on acquisition of a hidden platform position in the Morris water maze (20 trials, 30-min inter-trial interval). The rats were killed 48 h after the last drug injection and frontal, entorhinal and posterior cingulate cortex and dorsal and ventral hippocampus assayed for [3H]-nicotine binding density. Chronic nicotine significantly increased the number of frontal and entorhinal cortical and dorsal hippocampal, but not posterior cingulate cortical or ventral hippocampal, nicotinic receptors, and improved rate of learning. Chronic mecamylamine and RJR 2403 also significantly increased the number of nicotinic receptors in frontal cortex, though not other regions, but retarded rate of learning. Nicotine given for 1 day 11 days earlier marginally increased nicotinic receptors in entorhinal cortex (but not other regions) and significantly increased rate of learning, though significantly less than 10-day nicotine. Entorhinal cortical and dorsal hippocampal nicotinic receptor numbers were positively associated with rate of learning but not performance at asymptote. Thus cognitive enhancement after chronic nicotine is in part a delayed consequence of nicotine administration 11 days earlier, and may reflect regional changes in nicotinic receptor up-regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02247437
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  • 6
    Electronic Resource
    Electronic Resource
    Chronic treatments with cholinoceptor drugs influence spatial learning in rats (1993)
    Springer
    Psychopharmacology 111 (1993), S. 508-511 
    Details
    ISSN: 1432-2072
    Keywords: Spatial learning ; Rat ; Muscarinic ; Nicotinic ; Receptors ; Chronic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nicotine, scopolamine, oxotremorine, diisopropyl-fluorophosphate (DFP) and tetrahydroaminoacridine (THA) were administered chronically to different groups of rats in doses reported to alter central muscarinic and/or nicotinic receptro numbers. Beginning 24 h after final drug injection, the groups were compared to a vehicle control group on acquisition of a hidden platform position in the Morris water maze over 20 trials with a 30-min inter-trial interval. Chronic treatment with either nicotine or scopolamine significantly improved the rate of learning, but oxotremorine and DFP retarded learning and THA had no effect on learning. The chronic drug effects on behaviour were consistent with known effects of the injected drugs on muscarinic and nicotinic binding in the forebrain and on the sensitivity of frontal cortex neurones to iontophoretically applied cholinoceptor agonists. However, alternative explanations for the observed changes cannot be ruled out, since the drugs used are known to have a wide range of effects on other neurotransmitters.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253544
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