Memory animal models

Alzheimer s disease (AD) 2. In the hippocampus of p-amylo id-treated rats, an animal model of AD, 2-AG levels are elevated and exert neuroprotection but also participate in memory retention loss 2. Inhibitors of cellular re-uptake or CB-, antagonists, possibly depending on the phase of the disorder... 

Morgan, D., Diamond, D. M., Gottschall, P. E. et al. A(3 peptide vaccination prevents memory loss in an animal model of Alzheimer s disease. Nature 408 982-985, 2000. 

The clinical consequences of the currently used benzodiazepines range from sedation, muscle relaxation, seizure reduction, anxiolysis, and hypnosis. Clearly, it would be highly desirable to be able to separate some of these effects. In addition, it would be useful to reduce other undesirable consequences such as development of tolerance and dependence, abuse, synergistic interaction with ethanol, and memory impairment (for a comprehensive review see [22]). Animal models for some of the aforementioned conditions, in combination with transgenic mouse technology, have recently led to a deeper understanding of the contribution some of the individual a subunits make to these behaviors. 

An acute dose of lobeline impairs attention in one animal model, but not as much as mecamylamine (Turchi et al. 1995). Lobeline improves memory when administered after a passive avoidance paradigm (Decker et al. 1993). Pretreatment with lobeline improves performance in rats with septal lesions on a spatial discrimination water maze. Lobeline is about one-tenth as potent as nicotine in the passive avoidance memory task, but equivalent to nicotine in the water maze. 

Cognitive effects Animal studies There is an extensive literature that deals with the effects of ginseng on memory, learning, and behavior (Gillis 1997 Wang et al. 1995). However, ginseng extract (G115) failed to show anxiolytic effects in an animal model (Petkov et al. 1987)... 

Opioid effects on memory are consistent in humans and animal models (Braida et al. 1994 Saha et al. 1991). Verbal and visual memory are impaired by morphine one hour after oral administration (Hanks et al. 1995 Kerr et al. 1991). These could be due to direct neuronal effects of opioids, or perhaps through indirect effects on cholinergic transmission. However, in some animal paradigms morphine can enhance memory consolidation through indirect dopaminergic mechanisms (Castellano et al. 1994). 

West PA (1990) Neimobehavioral studies of forced swimming. The role of learning and memory in the forced swim test ProgNeimopsychopharmacol Biol Psychiatry 14 863-875 WUlner P (1997) Validity, reliability and utility of the chronic mild stress model of depression a 10-year review and evaluation. Psychopharmacology (Berl) 134 319-329 WUlner P, Muscat R, Papp M (1992) Chronic mUd stress-induced anhedonia a realistic animal model of depression. Neimosci Biobehav Rev 16 525-534 WUson JH (2000) A conspecific attenuates prolactin responses to open-field exposure in rats. Horm Behav 38 39-43... 

Several brain functions have been linked to specific glutamate receptor subtypes in selected brain regions. For example, glutamatergic neurons and NMDA receptors in the hippocampus are important for longterm potentiation (FTP), a crucial component in the formation of memory (Wilson and Tonegawa, 1997). Animal models with selective lesioning or strengthen-... 

Norepinephrine may also play a role in the induction of immediate early genes in response to pup exposure (Thomas and Palmiter, 1997). Norepinephrine has been linked to maternal behavior in certain other animal models, such as sheep and rats. It may also play a role in olfactory recognition and memory in rats. Intraventricular administration of 6-OHDA prior to birth has been noted to impair postpartum maternal behavior administration after birth had no such effect. 

If the functional deficit in AD is the result of neuronal and synapse loss, the ideal strategy would be to use techniques to reestablish neuronal and synaptic viability. In this sense, trophic factors are very promising. The positive results obtained in animal models of AD with brain tissue implantations with NGF and the memory enhancement and learning from laboratory animals treated with NGF have opened new windows to the possibility of the clinical use of NGF to treat AD. However, the potential benefits of the NGF may be counterbalanced by its capacity to increase the P-APP synthesis, consequently having an adverse effect in the progression of the illness. The increase of the APP synthesis may not necessarily affect all APP isoforms equally. The possibility of aberrant synapses and of alterations in the metabolism of the t- and P-amyloid protein exists [F. Hefti et al. 1995). 

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