Volume 27, Issue 2

Neurotransmitter receptors are key elements for brain function, but work so far has been focusing on the individual receptor subunits. It is, however, the receptor complexes that execute work rather than the subunits; of course, the multitude of possible combinations of the many receptors forming homomeric or heteromeric complexes is hampering studies. Moreover, not only receptors are observed in the complexes but also their corresponding protein kinases, phosphatases, and anchoring proteins, to name a few. Studying receptor complexes is still an analytical challenge. Thus far, no methods exist to unequivocally characterize or even quantify these assemblies. Major problems and limitations for the analysis exist, such as solubility, as the use of detergents is critical and may dissociate the receptor complexes as well as their separation in the native state. Gel-based techniques are able to separate and semiquantitatively quantify receptor complexes by subsequent immunochemical methods but do not allow the characterization of complex components. Immunoprecipitation methods are highly dependent on antibody availability and specificity, and the result of coimmunoprecipitation does not verify the direct physical interaction of proteins in the immunoprecipitate. Antibody shift assays are suitable to identify individual known proteins within a complex as are immunogold electron microscopic techniques and energy transfer technologies. Most techniques are simply showing the proximity of proteins rather than their physical interaction. Although fluorescence correlation spectroscopy is a promising technique, the use for quantification or comparing biological samples is limited. A lot of work remains to be done to provide tools for the characterization and quantification of receptor complexes in the brain.

Providing the critical link between the retina and visual cortex, the well-studied lateral geniculate nucleus (LGN) has stood out as a structure in search of a function exceeding the mundane ‘relay’. For many mammals, it is structurally impressive: Exquisite lamination, sophisticated microcircuits, and blending of multiple inputs suggest some fundamental transform. This impression is bolstered by the fact that numerically, the retina accounts for a small fraction of its input. Despite such promise, the extent to which an LGN neuron separates itself from its retinal brethren has proven difficult to appreciate. Here, I argue that whereas retinogeniculate coupling is strong, what occurs in the LGN is judicious pruning of a retinal drive by nonretinal inputs. These nonretinal inputs reshape a receptive field that under the right conditions departs significantly from its retinal drive, even if transiently. I first review design features of the LGN and follow with evidence for 10 putative functions. Only two of these tend to surface in textbooks: parsing retinal axons by eye and functional group and gating by state. Among the remaining putative functions, implementation of the principle of graceful degradation and temporal decorrelation are at least as interesting but much less promoted. The retina solves formidable problems imposed by physics to yield multiple efficient and sensitive representations of the world. The LGN applies context, increasing content, and gates several of these representations. Even if the basic concentric receptive field remains, information transmitted for each LGN spike relative to each retinal spike is measurably increased.

When assigning a central role to the neuronal firing, a large number of incoming postsynaptic potentials not utilized during both supra- and subthreshold neuronal activations are not given any functional significance. Local synaptic potentials at the apical dendrites get attenuated as they arrive at the soma to nearly a twentieth of what a synapse proximal to the soma produces. Conservation of these functions necessitates searching for their functional roles. Potentials induced at the postsynapses of neurons of all the neuronal orders activated by sensory inputs carry small bits of sensory information. The activation of these postsynapses by any means other than the activation from their corresponding presynaptic terminals, that also contribute to oscillating potentials, induce the semblance of the arrival of activity from their presynaptic terminals. This is a candidate mechanism for inducing the first-person internal sensory elements of various higher brain functions as a systems property. They also contribute to the firing of subthreshold-activated neurons, including motor neurons. Operational mechanism of inter-postsynaptic functional LINKs can provide necessary structural requirements for these functions. The functional independence of the distal dendritic compartment and recent evidence for in vivo dendritic spikes indicate their independent role in the formation of internal sensory elements. In these contexts, a neuronal soma is flanked by a large number of quasi-functional internal sensory processing units operated using very little energy, even when a neuron is not firing. A large number of possible combinations of internal sensory units explains the corresponding number of specific memory retrievals by the system in response to various cue stimuli.

Entorhinal cortex (EC), thought to be the location of the earliest lesions in Alzheimer’s disease (AD), has been widely studied in recent years. With the irreversible pathological changes of AD, there is an urgent need to find biomarkers that can be used to predict the presence of the disease before it is clinically expressed. The aim of this review is to summarize and analyze recent findings that are relevant to the important role of EC in the diagnosis of mild cognitive impairment (MCI) and mild AD and to describe a range of neuroimaging techniques used to define the EC boundary. A comprehensive literature search for articles published up to May 2015 was performed. Our research highlights the finding that atrophy in EC reflects the early pathological changes of AD and can be a strong predictor of prodromal AD. The early changes in EC are a good imaging biomarker that can be used to discriminate individuals with MCI from normal control subjects. A larger degree of atrophy in EC predicts increased disease severity, and the right EC in patients with mild AD exhibited greater changes than the left side. In addition, the EC seems to have an obvious advantage over the hippocampus as a biomarker when predicting future conversion to AD in individuals with MCI, and it may be of help in following the course of disease progression. In this review, we also summarize the main differences observed between the hippocampus and the EC when differentiating diseases. These findings will hopefully provide an opportunity for the effective prevention and early treatment of AD.

Mild cognitive impairment (MCI) is a transitional phase between normal cognitive aging and dementia. As the world population is aging rapidly, more MCI patients will be identified, posing significant problems to society. Normal aging is associated with cognitive and motor decline, and MCI brings additional impairments. Compared to healthy older adults, MCI patients show poorer motor control in a variety of tasks. Efficient motor control and skill learning are essential for occupational and leisure purposes; degradation of motor behaviors in MCI patients often adversely affects their health and quality of life. In this article, we first define MCI and describe its pathology and neural correlates. After this, we review cognitive changes and motor control and skill learning in normal aging. This section is followed by a discussion of MCI-related degradation of motor behaviors. Finally, we propose that multicomponent interventions targeting both cognitive and motor domains can improve MCI patients’ motor functions. Future research directions are also raised.

In recent years, a connection between psychoanalysis and neuroscience has been sought. The meeting point between these two branches is represented by neuropsychoanalysis. The goal of the relationship between psychoanalysis and neuroscience is to test psychoanalytic hypotheses in the human brain, using a scientific method. A literature search was conducted on May 2015. PubMed and Scopus databases were used to find studies for the inclusion in the systematic review. Common results of the studies investigated are represented by a reduction, a modulation, or a normalization of the activation patterns found after the psychoanalytic therapy. New findings in the possible and useful relationship between psychoanalysis and neuroscience could change the modalities of relating to patients for psychoanalysts and the way in which neuroscientists plan their research. Researchers should keep in mind that in any scientific research that has to do with people, neuroscience and a scientific method cannot avoid subjective interpretation.