Changing the strength of connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. In its most general form, the synaptic plasticity and memory hypothesis states that "activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation and is both necessary and sufficient for the information storage underlying the type of memory mediated by the brain area in which that plasticity is observed." We outline a set of criteria by which this hypothesis can be judged and describe a range of experimental strategies used to investigate it. We review both classical and newly discovered properties of synaptic plasticity and stress the importance of the neural architecture and synaptic learning rules of the network in which it is embedded. The greater part of the article focuses on types of memory mediated by the hippocampus, amygdala, and cortex. We conclude that a wealth of data supports the notion that synaptic plasticity is necessary for learning and memory, but that little data currently supports the notion of sufficiency.

WHh a continuum electromechanical model, the electrical admittance has been derived for an AT-cut quartz crystal microbalance (QCM) simultaneously loaded by a surface mass layer and a contacting Newtonian liquid. This admittance expression Is used to derive a lumped-element equivalent circuit model that describes the near-resonance electrical characteristics of the QCM under these loading conditions. The resulting model Is a modified Butterworth-Van Dyke equivalent circuit, having circuit elements that are explicitly related to physical properties of the quartz, perturbing mass layer, and contacting liquid. The effects of mass and liquid loading on the fundamental and third harmonic resonances are predicted from the model and compared with experimental Impedance analyzer measurements. Surface mass accumulation causes a simple translation In frequency of the resonance peak, while Increasing the density-viscosity product of the contacting solution causes both a translation and a damping of the resonance peak. With the model, changes In surface mass can be differentiated from changes In solution properties.

Mice that overexpress the human mutant amyloid precursor protein (hAPP) show learning deficits, but the apparent lack of a relationship between these deficits and the progressive beta-amyloid plaque formation that the hAPP mice display is puzzling. In the water maze, hAPP mice are impaired before and after amyloid plaque deposition. Here we show, using a new water-maze training protocol, that PDAPP mice also exhibit a separate age-related deficit in learning a series of spatial locations. This impairment correlates with beta-amyloid plaque burden and is shown in both cross-sectional and longitudinal experimental designs. Cued navigation and object-recognition memory are normal. These findings indicate that A beta overexpression and/or A beta plaques are associated with disturbed cognitive function and, importantly, suggest that some but not all forms of learning and memory are suitable behavioural assays of the progressive cognitive deficits associated with Alzheimer's-disease-type pathologies.

At excitatory synapses, the postsynaptic scaffolding protein postsynaptic density 95 (PSD-95) couples NMDA receptors (NMDARs) to the Ras GTPase-activating protein SynGAP. The close association of SynGAP and NMDARs suggests that SynGAP may have an important role in NMDAR-dependent activation of Ras signaling pathways, such as the MAP kinase pathway, and in synaptic plasticity. To explore this issue, we examined long-term potentiation (LTP), p42 MAPK (ERK2) signaling, and spatial learning in mice with a heterozygous null mutation of the SynGAP gene (SynGAP(-/+)). In SynGAP(-/+) mutant mice, the induction of LTP in the hippocampal CA1 region was strongly reduced in the absence of any detectable alteration in basal synaptic transmission and NMDAR-mediated synaptic currents. Although basal levels of activated ERK2 were elevated in hippocampal extracts from SynGAP(-/+) mice, NMDAR stimulation still induced a robust increase in ERK activation in slices from SynGAP(-/+) mice. Thus, although SynGAP may regulate the ERK pathway, its role in LTP most likely involves additional downstream targets. Consistent with this, the amount of potentiation induced by stimulation protocols that induce an ERK-independent form of LTP were also significantly reduced in slices from SynGAP(-/+) mice. An elevation of basal phospho-ERK2 levels and LTP deficits were also observed in SynGAP(-/+)/H-Ras(-)/- double mutants, suggesting that SynGAP may normally regulate Ras isoforms other than H-Ras. A comparison of SynGAP and PSD-95 mutants suggests that PSD-95 couples NMDARs to multiple downstream signaling pathways with very different roles in LTP and learning.

Very rapidly after Varroa destructor invaded apiaries of Apis mellifera, the devastating effect of this mite prompted an active research effort to understand and control this parasite. Over a few decades, varroa has spread to most countries exploiting A. mellifera. As a consequence, a large number of teams have worked with this organism, developing a diversity of research methods. Often different approaches have been followed to achieve the same goal. The diversity of methods made the results difficult to compare, thus hindering our understanding of this parasite. In this paper, we provide easy to use protocols for the collection, identification, diagnosis, rearing, breeding, marking and measurement of infestation rates and fertility of V. destructor. We also describe experimental protocols to study orientation and feeding of the mite, to infest colonies or cells and measure the mite’s susceptibility to acaricides. Where relevant, we describe which mite should be used for bioassays since their behaviour is influenced by their physiological state. We also give a method to determine the damage threshold above which varroa damages colonies. This tool is fundamental to be able to implement integrated control concepts. We have described pros and cons for all methods for the user to know which method to use under which circumstances. These methods could be embraced as standards by the community when designing and performing research on V. destructor

Summary1. The ecto-parasitic mite Varroa destructor is a serious world-wide pest of the honeybee Apis mellifera and has being linked with the death of millions of colonies, although its role in colony death has remained elusive. 2. A simulation model was developed to explain the link between the mite and collapse of the host bee colony, given that colony death does not always occur. We investigated the effects of two pathogens, deformed wing virus (DWV) and acute paralysis virus (APV), vectored by the mite, on the host colony. 3. Two previously published simulation models, a bee and a mite, were combined and adapted for use in temperate climates with a variety of bee diseases. The model was constructed using Modelmaker® software, which allows the progression of a disease in the host colony to be followed daily. 4. The population dynamics generated by the model were similar to those observed in a natural honeybee colony. When DWV-or APV-transmitting mites were introduced into the colony, its adult worker bee population collapsed either during winter or spring for DWV, or autumn to spring for APV. This corresponds well with field observations of colony death in Europe. 5. The model revealed that DWV initially had little effect on the colony but during late summer, as the population of DWV-transmitting mites increased, the virus caused a reduction in the number of healthy young bees entering the overwintering population. This imbalance in the age structure of the overwintering bees resulted in the eventual death of the colony during the winter or spring. As few as 2000-3600 mites in autumn could kill a colony. 6. In contrast, APV transmitted by Varroa was only able to kill the honeybee colony if a large (10 000+) mite population was already present when an overt APV infection occurred. It was difficult for APV to become established within the bee population due to it causing rapid host death. 7. The model predicts that the less virulent DWV will become more widely established than the highly virulent APV, and that mite control measures need to be taken prior to the production of overwintering bees.

Studies of patients and animals with brain lesions have implicated the hippocampal formation in spatial, declarative/relational and episodic types of memory. These and other types of memory consist of a series of interdependent but potentially dissociable memory processes-encoding, storage, consolidation and retrieval. To identify whether hippocampal activity contributes to these processes independently, we used a novel method of inactivating synaptic transmission using a water-soluble antagonist of AMPA/kainate glutamate receptors. Once calibrated using electrophysiological and two-deoxyglucose techniques in vivo, drug or vehicle was infused chronically or acutely into the dorsal hippocampus of rats at appropriate times during or after training in a water maze. Our findings indicate that hippocampal neural activity is necessary for both encoding and retrieval of spatial memory and for either trace consolidation or long-term storage.

The response of polymer-coated surface acoustic wave (SAW) devices to temperature changes and polymer vapor absorption is examined. A perturbational approach is used to relate velocity and attenuation responses to film translational and strain modes generated by the SAW. Two distinct regimes of Aim behavior