By Edward D. Levin, Jerry J. Buccafusco

ISBN-10: 0849328349

ISBN-13: 9780849328343

The prices linked to a drug’s scientific trials are so major that it has develop into essential to validate either its defense and efficacy in animal types sooner than the ongoing examine of the drug in people.

Featuring contributions from exotic researchers within the box of cognitive remedy study, Animal versions of Cognitive Impairment examines probably the most well known and winning animal archetypes utilized in the context of drug discovery. It offers built-in insurance of the most recent learn referring to neuronal platforms correct to cognitive functionality and disorder, assimilating reports of this study in the context of every bankruptcy. This method is exclusive in that it brings jointly molecular and neurochemical methodologies, behavioral functions in translational types, and medical functions.

The e-book comprehensively discusses a large choice of animal types of cognitive impairment, together with genetic, lesion, pharmacological, and getting older comparable impairments. It additionally explores the importance of this learn about the remedy of varied addictions and issues comparable to stroke, autism, Alzheimer’s, schizophrenia, and ADHD.

Edited via well known specialists within the box, Animal versions of Cognitive Impairment is a well timed booklet that offers built-in insurance of state-of-the-art learn that matters neuronal structures proper to cognitive functionality and disorder.

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102, 662–677, 1988. 40. N. ), 120, 142–149, 1995. 41. , The effects of p-chlorophenylalanine-induced serotonin synthesis inhibition and muscarinic blockade on the performance of rats in a 5-choice serial reaction time task, Behav. , 51, 29–40, 1992. 42. ), 150, 112–116, 2000. 43. ), 148, 111–123, 2000. 44. ), 122, 268–280, 1995. 45. , A performance-dependent adjustment of the retention interval in a delayed non-matching-to-position paradigm differentiates effects of amnestic drugs in rats, Eur.

Nicotine and nicotinic agonists have been shown to improve cognition in rats in numerous studies [13–15, 27, 31, 59]. Similarly, nicotinic-receptor antagonists — the subject of this chapter — can cause cognitive impairments in rats. The use of nicotinic-receptor antagonists in an animal model of cognitive impairment has clinical relevance because it models the functional effect of nicotinic-receptor loss. Studies have shown that patients with Alzheimer’s disease suffer a dramatic reduction in hippocampal and cortical nicotine-receptor density that parallels the cognitive decline associated with this disease [56–58].

Of reinforcements [50] [2] [49] a IP = intraperitoneal injection; IH = intrahippocampal injection; SC = subcutaneous injection; VMH = ventromedial nucleus of the hypothalamus. b WM = working memory; RM = reference memory; IRT = interresponse time; DRL = differential reinforcement of low rate; ↑ = enhanced performance; ↓ = impaired performance; − = no effect. c Mecamylamine doses in this study refer to the base. 3-mg/kg base-wt. 17-mg/kg salt-wt. dose. fm Page 28 Tuesday, May 30, 2006 12:28 PM 28 Animal Models of Cognitive Impairment Another study tested the effects of DHBE on a win-stay version of the RAM, which is similar to the DMTS.

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Animal Models of Cognitive Impairment by Edward D. Levin, Jerry J. Buccafusco


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