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socially transmitted food preference and declarative memory

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Research with experimental rats carried out by the Institute of Neuroscience of the UAB describes the brain region connected to how our declarative memory functions. According to this experiment, part of the prefrontal cortex plays a key role in the social transmission of food preference. Results from the research could be useful to find new treatment for diseases that affect the memory, such as Alzheimer’s disease.Declarative memory is described as a flexible, conscience and associative type of memory (i.e., it is based on relations between different stimuli). It differs from other types of memories that allow us to recall effective or emotionally-charged data, or carry out processes such as riding a bicycle or playing an instrument. Declarative memory allows us to remember things such as specific moments of our lives, names of people, what we ate for lunch, the capitals of the world, etc. The malfunctioning of this type of memory is one of the most common symptoms found in those suffering from Alzheimer’s disease.

A useful model from which to learn about how declarative memory functions is the social transmission of food preference. In other species, this task is connected to the survival of the species and plays a crucial role in their evolution. In this research, the social transmission of food preference was carried out with experimental rats.

When one rodent sniffs another rodent’s snout right after the second one has eaten, the first one will later choose to eat the same exact food. Animals learn to remember what their congeners eat and, in that way, lower the risk of eating new foods that could be harmful to them. In addition, they must later use this information acquired during a brief episode of social interaction in very different circumstances. Therefore, they need the flexible expression of memory, which is one of the main traits of declarative memory.

This task depends on learning how to associate smells, a function that is commanded by a specific region of the brain, the nucleus basalis magnocellularis (NBM), which produces acetylcholine (a neurotransmitter that “transfers information” from one neurone to another through synapses). This chemical substance is essential in making the memory work correctly. The nucleus basalis magnocellularis equivalent in humans is the nucleus basalis Meynert. Precisely this is one of the regions of the brain that shown signs of degeneration among those who suffer from Alzheimer’s (and who are often treated with drugs that help to produce acetylcholine).

The acetylcholine produced by the nucleus basalis is transferred to other regions of the brain, where it is “recognised” by receptor molecules. The research team examined the possibility of one part of the brain, the prelimbic prefrontal cortex, being linked to the social transmission of food preference. To do so, they applied a chemical compound to the experimental rats that neutralised the acetylcholine receptors (muscarinic cholinergic receptor) of this region. By blocking the receptor, the effect of the neurotransmitter was also neutralised and the changes in the animals’ behaviour were observed.

The results demonstrated that the social transmission of food preference was clearly affected after neutralising the acetylcholine receptors. Researchers also verified that the effects were not due to other aspects that could alter the experiment, such as lack of olfactory perception, motivation or social interaction. The results therefore suggest that the prelimbic prefrontal cortex, via the use of acetylcholine, regulates cognitive operations (e.g. flexibility in behaviour, attention or strategic planning) that could be needed to correctly express social transmission of food preference, and therefore necessary for our declarative memory.

Learn Mem. 2006 Nov-Dec;13(6):783-93. Epub 2006 Nov 13.

Effects of nucleus basalis magnocellularis stimulation on a socially transmitted food preference and c-Fos expression.

Boix-Trelis N, Vale-Martínez A, Guillazo-Blanch G, Costa-Miserachs D, Martí-Nicolovius M.

Departament de Psicobiologia i Metodologia de les Ciències de la Salut Institut de Neurociències, Universitat Autònoma de Barcelona, Barcelona 08193, Spain.

Experiment 1 examined the effects of electrical stimulation of nucleus basalis magnocellularis (NBM) on a relational odor-association task–the social transmission of food preference (STFP). Rats were stimulated unilaterally in the NBM for 20 min (100 microA, 1 Hz) immediately before the social training. They were tested on their ability to remember preference for the trained food either immediately or following a 24-h delay. Stimulation of NBM improved retention regardless of delay, and additional behavioral measures (social interaction, motor activity, or exploration) did not account for such effects. Experiment 2 investigated brain regions activated after NBM electrical stimulation by examining the induction of c-Fos. This treatment led to bilateral increased c-Fos expression in prefrontal regions, such as orbitofrontal, prelimbic, and infralimbic cortices, and some hippocampal subregions (dorsal CA and ventral dentate gyrus). In contrast, no differences between groups in c-Fos expression were found in basolateral amygdala, dorsal dentate gyrus, ventral CA, or ventral subiculum. Present findings indicate that pretraining NBM electrical stimulation facilitates the acquisition of STFP, supporting a role of NBM in the early stages of memory formation, and suggest that the treatment might cause such effects by inducing neural changes, related to transcription factors such as c-Fos, in the prefrontal cortex or the hippocampal formation.

PMID: 17101878 [PubMed – indexed for MEDLINE]

see also:

Neuroscience. 2007 Jun 28; [Epub ahead of print]

Behavioral and immunohistological effects of cholinergic damage in immunolesioned rats: Alteration of c-Fos and polysialylated neural cell adhesion molecule expression.

Chambon C, Paban V, Manrique C, Alescio-Lautier B.

Université d’Aix-Marseille I, Laboratoire de Neurobiologie Intégrative et Adaptative, UMR/CNRS 6149, 3 Place Victor Hugo, 13331 Marseille Cedex 03, France.

The aim of this study was to determine the brain structures as well as the plasticity events associated with the behavioral effects of cholinergic damage. Rats were submitted to injection of 192 IgG-saporin in the medial septum/diagonal band of Broca complex and the nucleus basalis magnocellularis. The immunohistochemical expression of c-Fos protein and PSA-NCAM (polysialylated neural cell adhesion molecule) and the behavioral performances in the nonmatching-to-position task were assessed at various post-lesion times. Thus, 3 days after injection of the immunotoxin, increased c-Fos labeling was observed in the areas of infusion, indicating these cells were undergoing some plastic changes and/or apoptotic processes. A drastic increase was observed in the number of PSA-NCAM positive cells and in their dendritic arborization in the dentate gyrus. At 7 days post-lesion, no behavioral deficit was observed in immunolesioned rats despite the drastic loss of cholinergic neurons. These neurons showed decreased c-Fos protein expression in the piriform and entorhinal cortex and in the dentate gyrus. In the latter, PSA-NCAM induction was high, suggesting that remodeling occurred, which in turn might contribute to sustaining some mnemonic function in immunolesioned rats. At 1 month, cholinergic neurons totally disappeared and behavioral deficits were drastic. c-Fos expression showed no change. In contrast, the increased PSA-NCAM-labeling observed at short post-lesion times was maintained but the plastic changes due to this molecule could not compensate the behavioral deficit caused by the immunotoxin. Thus, as the post-lesion time increases, a gradual degeneration process should occur that may contribute to mnemonic impairments. This neuronal loss leads to molecular and cellular alterations, which in turn may aggravate cognitive deficits.

PMID: 17601671 [PubMed – as supplied by publisher]


Written by huehueteotl

July 18, 2007 at 8:58 am

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