Kranick SM, & Duda JE. Olfactory dysfunction in Parkinson’s disease. Neurosignals. 2008; 16(1): 35-40.
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Prior to the onset of the cardinal motor features of idiopathic Parkinson’s disease (PD), other manifestations of neurodegeneration such as olfactory dysfunction are often apparent. Characterizing these potential biomarkers of preclinical PD is particularly important in identifying individuals who will go on to develop disabling symptoms, and thus be good candidates for new neuroprotective strategies. As shown by the Braak neuropathologic staging of PD, the olfactory system is among the first neuronal populations to display Lewy body pathology. Clinically, loss of smell can be easily tested in the office using several validated techniques and is often helpful to the physician in distinguishing idiopathic PD from other forms of parkinsonism. Recent findings have indicated that a decline in olfaction may be observed in selected at-risk patients, which has significant implications for identifying potential study populations. Ongoing studies of olfactory dysfunction may also reveal potential for use as a medication-independent biomarker of disease progression in addition to use as a biomarker for the diagnosis of PD.
A new study points to rare gene duplications and deletions that are believed to play a significant role in the psychological disorder
By Nikhil Swaminathanin Scientific American
A new study indicates that the genetic culprits behind schizophrenia may be much less common than previously believed. Researchers report this week in Science that a rare but devastating change in one of several different genes may dramatically increase the risk of developing the debilitating brain disorder affecting 1 percent of the world’s population and marked by psychotic behavior, hallucinations and delusions. Until now, most scientists believed that it was likely that a cluster of relatively common genetic mutations was to blame.
Nature Reviews Neuroscience 9, 78. February 2008
A single action potential in a single neuron can induce a behavioral response.
Conventional wisdom holds that the brain analyses patterns of activity in multiple cortical neurons in order to interpret incoming stimuli; however, the question of how many neurons must be active in order to generate a perception has remained unresolved. Two new studies indicate that the neural code that underlies sensory perceptions might be sparser than previously estimated and that activity in single neurons can contribute significantly to behavioural responses.
in Nature Reviews Neuroscience 9, 82 – 83. February 2008
Extended periods of synaptic plasticity involve activation of both NMDA and metabotropic glutamate receptors.
One of the main cellular mechanisms assumed to underlie learning is long-term potentiation (LTP), an experimental form of synaptic plasticity that results in a long-lasting increase in the strength of synaptic transmission. However, prolonged synaptic stimulation in vitro eventually stops producing further LTP (also known as ‘LTP occlusion’). So, how does ongoing experience result in further learning? Clem et al. now show that the opposing actions of activated N-methyl-D-aspartate receptors (NMDARs) and metabotropic glutamate receptors (mGluRs) allow progessive synaptic strengthening during sensory-induced plasticity.– Leonie Welberg
An actual and full review about synaptic plasticity can be found in the book Synaptic Plasticity: Molecular, Cellular, and Functional Aspects by Richard F. Thompson
Neuroscience Gateway. February 2008
Researchers physically separate neuron cell bodies and neurites to determine signaling pathways important in process extension.
What does it take for one neuron to reach out and touch another? In neuritogenesis, neurons develop the long, thin projections that eventually become axons and dendrites. Because these neurites are so small, it has been difficult to differentiate them biochemically from neuron cell bodies. Now Pertz et al. report proteomic analysis of separate populations of neurites and somas in a recent article in Proceedings of the National Academy of Sciences…
Link to the full review.
A grid cell is a type of neuron found in the entorhinal cortex (EC) that fires strongly when an animal is in specific locations in an environment. Grid cells were discovered in 2005 and it is hypothesized that a network of these cells constitute a mental map of the spatial environment (Hafting et al., 2005).
A good introduction to the concept of grid cells can be found in Phineas Cage Fun Club
While the Blue Brain folk want to construct an incredibly detailed model of a single cortical column, a recent paper by Izhikevich and Edelman (Large-scale model of mammalian thalamocortical systems) reports on a less detailed model of the entire human thalamocortical system.
Some of the details of their model (roughly from large-scale to lower scale) include:
1. The cortical sheet’s geometry was constructed from human MRI data.
2. Projections among cortical regions were modeled using data from diffusion tensor MRI of the human brain (above image is Figure 1 of the paper showing a subset of such connections).
3. Synaptic connectivity patterns among neurons within and between cortical layers are based on detailed studies of cat visual cortex (and iterated to all of cortex).
4. Individual neurons are not modelled using the relatively computationally intensive Hodgkin-Huxely models, but a species of integrate-and-fire neuron that included a variable threshold, short-term synaptic plasticity, and long term spike-timing dependent plasticity.
5. The only subcortical structure included in the model is the thalamus, but the model does include simple simulated neuromodulatory influences (dopamine, acetylcholine).
Link to the full post BY ERIC THOMSON IN NEUROCHANNELS BLOG AT 2/25/2008 03:20:00 PM
Nature: A synaptic memory trace for cortical receptive field plasticity
Froemke RC, Merzenich MM, Schreiner CE
This is an excellent paper revealing how cholinergic modulation (by stimulating nucleus basalis, or basal forebrain) transiently changes the balance between excitation and inhibition within the cortical circuit, thus mediating specific circuit plasticity in the primary auditory cortex…
Full post in SCLin’s Neuroscience blog.