Local modifications to small numbers of connections can result in global changes in brain connectivity. In the new study, Santiago Canals of the Max Planck Institute for Biological Cybernetics in Tübingen and his colleagues used the same protocol to induce LTP. But while the vast majority of researchers have investigated LTP in slices of hippocampal tissue, this study involved observing LTP in live animals. To do this, the researchers first anaesthetized 14 rats, then made small openings in the animals' skulls so that electrodes could be implanted into the hippocampus. The electrodes were fixed to the sides of the opening in the skull with dental cement and plastic screws. The rats were then fitted into a custom-made fMRI-compatible frame which prevented them from moving their heads, and placed in the scanner. In this way, the researchers could induce LTP in their experimental animals and simultaneously monitor the global changes in brain activity induced by it. Following induction of LTP, stimulation of neurons in the perforant path was found to activate cells in the hippocampus which receive inputs from them, as measured by an increase in blood flow to that region of the brain. Unexpectedly though, it also led to increased activity in the subiculum and entorhinal cortex, areas which surround the hippocampus, and to activation of these same regions in the opposite hemisphere. In fact, the acitivty in the opposite hemisphere was found to be higher than that of the activity of cells in the hemisphere in which LTP had been induced. But the effects went even further afield than the hippomcampus and adjacent regions - activation of neurons in the prefrontal cortex, nucleus accumbens and olfactory nucleus was also observed. Application of MK-801, a compound which blocks the NMDA receptor, inhibited this activity, confirming that it was occurring in response to the LTP induced in the perforant path-hippocampus synapses. Earlier studies have shown that LTP induces a series of biochemical changes within individual neurons. These can eventually lead to structural changes in the microscopic organization of neurons which enable the potentiated connections to persist for longer periods of time. Cells can not only strengthen existing synapses, but they can form de novo connections, by sprouting new dendritic spines, the tiny finger-like projections at which synapses are located. However, these changes have until now been thought to occur only at the level of single potentiated synapses. This new research provides the first evidence that the local modifications in synaptic connections induced by LTP lead to long-lasting changes in the activity of a diffuse network of brain regions, and even to facilitated communication between the two hemispheres. The fMRI data showed that hippocampal LTP recruits higher order association areas, as well as regions involved in emotions and others subserving different sensory modalities, all of which are known to be involved in memory formation.

Reduced MET signaling (c allele) may contribute to a syndrome that includes ASD with co-occurring gastrointestinal conditions. 214-family sample, the MET rs1858830 C allele was associated with both autism spectrum disorder and gastrointestinal conditions. Stratification by the presence of gastrointestinal conditions revealed that the MET C allele was associated with both autism spectrum disorder and gastrointestinal conditions in 118 families containing at least 1 child with co-occurring autism spectrum disorder and gastrointestinal conditions. In contrast, there was no association of the MET polymorphism with autism spectrum disorder in the 96 families lacking a child with co-occurring autism spectrum disorder and gastrointestinal conditions

The ERK MAP kinase signaling cascade plays critical roles in brain development, learning, memory, and cognition. It has recently been appreciated that mutation or deletion of elements within this signaling pathway leads to developmental syndromes in humans that are associated with impaired cognitive function and autism. Here, we review recent studies that provide insight into the biological roles of the ERKs in the brain that may underlie the cognitive deficits seen in these syndromes

Review of types and neuroanatomy of memory.