I have developed "tennis elbow" from lugging this book around the past four weeks, but it is worth the pain, the effort, and the aspirin. It is also worth the (relatively speaking) bargain price. Including appendixes, this book contains 894 pages of text. The entire panorama of the neural sciences is surveyed and examined, and it is comprehensive in its scope, from genomes to social behaviors. The editors explicitly state that the book is designed as "an introductory text for students of biology, behavior, and medicine," but it is hard to imagine any audience, interested in any fragment of neuroscience at any level of sophistication, that would not enjoy this book. The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or

Principles of Neural Science

http://n-acetylaspartate.com/PDF%20files/NAA%20Review.pdf

N-Acetylaspartate in the CNS: From neurodiagnostics to neurobiology

Neuroscience is contributing to an understanding of the biological bases of human intelligence differences. This work is principally being conducted along two empirical fronts: genetics — quantitative and molecular — and brain imaging. Quantitative genetic studies have established that there are additive genetic contributions to different aspects of cognitive ability — especially general intelligence — and how they change through the lifespan. Molecular genetic studies have yet to identify reliably reproducible contributions from individual genes. Structural and functional brain-imaging studies have identified differences in brain pathways, especially parieto-frontal pathways, that contribute to intelligence differences. There is also evidence that brain efficiency correlates positively with intelligence.

/pdf/the-neuroscience-of-human-intelligence-differences-2mdlx5it3p.pdf

The Neuroscience of Human Intelligence Differences

Graph analysis has become an increasingly popular tool for characterizing topological properties of brain connectivity networks. Within this approach, the brain is modeled as a graph comprising N nodes connected by M edges. In functional magnetic resonance imaging (fMRI) studies, the nodes typically represent brain regions and the edges some measure of interaction between them. These nodes are commonly defined using a variety of regional parcellation templates, which can vary both in the volume sampled by each region, and the number of regions parcellated. Here, we sought to investigate how such variations in parcellation templates affect key graph analytic measures of functional brain organization using resting-state fMRI in thirty healthy volunteers. Seven different parcellation resolutions (84, 91, 230, 438, 890, 1314 and 4320 regions) were investigated. We found that gross inferences regarding network topology, such as whether the brain is small-world or scale-free, were robust to the template used, but that both absolute values of, and individual differences in, specific parameters such as path length, clustering, small-worldness and degree distribution descriptors varied considerably across the resolutions studied. These findings underscore the need to consider the effect that a specific parcellation approach has on graph analytic findings in human fMRI studies, and indicate that results obtained using different templates may not be directly comparable.

/pdf/network-scaling-effects-in-graph-analytic-studies-of-human-54g0hwzu4r.pdf

Network scaling effects in graph analytic studies of human resting-state fMRI data

The relationship between a reported history of trauma and dissociative symptoms has been explained in 2 conflicting ways. Pathological dissociation has been conceptualized as a response to antecedent traumatic stress and/or severe psychological adversity. Others have proposed that dissociation makes individuals prone to fantasy, thereby engendering confabulated memories of trauma. We examine data related to a series of 8 contrasting predictions based on the trauma model and the fantasy model of dissociation. In keeping with the trauma model, the relationship between trauma and dissociation was consistent and moderate in strength, and remained significant when objective measures of trauma were used. Dissociation was temporally related to trauma and trauma treatment, and was predictive of trauma history when fantasy proneness was controlled. Dissociation was not reliably associated with suggestibility, nor was there evidence for the fantasy model prediction of greater inaccuracy of recovered memory. Instead, dissociation was positively related to a history of trauma memory recovery and negatively related to the more general measures of narrative cohesion. Research also supports the trauma theory of dissociation as a regulatory response to fear or other extreme emotion with measurable biological correlates. We conclude, on the basis of evidence related to these 8 predictions, that there is strong empirical support for the hypothesis that trauma causes dissociation, and that dissociation remains related to trauma history when fantasy proneness is controlled. We find little support for the hypothesis that the dissociation–trauma relationship is due to fantasy proneness or confabulated memories of trauma.

/pdf/evaluation-of-the-evidence-for-the-trauma-and-fantasy-models-3i92em6xwl.pdf

Evaluation of the Evidence for the Trauma and Fantasy Models of Dissociation

MRS) was used to acquire in vivo spectra from the bilateral anterior cingulate of 10 healthy subjects while they received a subanesthetic dose of either placebo or ketamine, an NMDAR antagonist. Assessments given before and after ketamine or placebo administration included the Brief Rating Psychiatric Rating Scale, the Scale for the Assessment of Negative Symptoms, the Clinician-Administered Dissociative States Scale, and the Stroop task. Results: As predicted, there was a significant increase in anterior cingulate glutamine, a putative marker of glutamate neurotransmitter release, with ketamine administration. This increase was not related to schizophrenia-like positive or negative symptoms but was marginally related to Stroop performance. Conclusions: In humans as in animals, an acute hypofunctional NMDAR state is associated with increased glutamatergic activity in the anterior cingulate. (Am J Psychiatry 2005; 162:394–396) A ccording to the N-methyl-D-aspartate receptor (NMDAR) hypofunction model of schizophrenia (1, 2), NMDAR blockade results in inhibition of γ-aminobutyric acid neurons, causing disinhibition of glutamatergic neurons that converge onto pyramidal neurons in widely distributed cortical regions. NMDAR hypofunction and/or the downstream surge of glutamate in corticolimbic regions may be related to positive and negative symptoms in schizophrenia. Directly supporting this hypothesis, extracellular glutamate concentrations in the prefrontal cortex were found to increase in awake rats when they were given ketamine, an NMDAR antagonist (3). However, to our knowledge, no studies assessing the effects of NMDAR antagonism on glutamatergic activity in humans have been reported. The current study investigated the effects of ketamine on anterior cingulate glutamatergic activity and the relationship to ketamine-induced schizophrenia-like features in healthy humans. Glutamine, the major metabolite of synaptic glutamate (4, 5), was measured with 4-T 1 H proton magnetic resonance spectroscopy ( 1 H-MRS). We hypothesized that there would be a significant increase in anterior cingulate glutamine with ketamine administration, and that this increase would be directly related to schizophrenia-like positive and negative symptoms.

https://ajp.psychiatryonline.org/doi/pdf/10.1176/appi.ajp.162.2.394

Effects of ketamine on anterior cingulate glutamate metabolism in healthy humans: a 4-T proton MRS study.

Long-term treatment of rats with haloperidol: lack of an effect on brain N-acetyl aspartate levels.

Imaging Intelligence with Proton Magnetic Resonance Spectroscopy.

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Effects of ketamine on anterior cingulate glutamate metabolism in healthy humans: a 4-T proton MRS study.

Long-term treatment of rats with haloperidol: lack of an effect on brain N-acetyl aspartate levels.

Imaging Intelligence with Proton Magnetic Resonance Spectroscopy.