Neuroscience
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Review Biography Historical Article
Cajal's first steps in scientific research.
More than 125 years ago, Santiago Ramón y Cajal was able to draft and prove the neuron doctrine, and later, to develop prophetic theories about neural function and plasticity, many of which have been proven by current neuroscience. It was chance that made Cajal, during his doctorate studies, have his first contact with histology and force him to study the then current theories about pathogenesis of inflammation. Thus, he gained knowledge of the vascular hypothesis, by Julius Cohnheim, a German pathologist who, opposing the opinion of his teacher and father of cellular pathology, Rudolf Virchow, made leukocytes the protagonists of inflammation, given their ability to develop ameboid movements directed by chemical signals. ⋯ So, the basic postulates of chemotaxis can be identified at different moments in Cajal's research, from the description of the "growth cone" in embryonic neuroblasts, the origin of the neurotrophic theory, to the proposal of the pathophysiological mechanisms of neuronal plasticity. From Cajal's point of view, the neurons move during their development and also adapt to different external circumstances. Chemical endogenous substances can stimulate this movement in a similar way to leukocytes during the process of inflammation.
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Sensory perception can be influenced by cognitive functions like attention and expectation. An emblematic case of this is the placebo effect, where a reduction in pain perception can be obtained by inducing expectation of benefit following a treatment. The current study assessed the behavioural and brain activity correlates of a placebo procedure inducing an enhancement of non-noxious somatic sensation. ⋯ Although the intensity of stimulation was physically identical in the two sessions, the experimental group reported stronger tactile sensation after cream treatment than before. In parallel, the experimental group showed enhanced somatosensory cortical responses (N140, P200) after treatment, whereas subcortical and early-cortical SEP components did not change. We suggest that these findings reflect top-down modulation on tactile perception probably due to an interplay between expectation and attention and might rely on interactions between prefrontal and parietal brain regions.
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Studies of puberty have focused primarily on changes in hormones and on observable physical bodily characteristics. Little is known, however, about the nature of the relation between pubertal status and brain physiology. This is particularly important given findings that have linked the onset of puberty with both changes in cognitive functioning and increases in the incidence of depression and anxiety. ⋯ In addition, puberty was related to right hippocampus and amygdala volumes, after controlling for ICV. In contrast, no significant associations were found between age and hippocampal and amygdala volumes after controlling for pubertal status and ICV. These findings highlight the importance of the relation between pubertal status and morphometry of the hippocampus and amygdala, and of limbic and subcortical structures that have been implicated in emotional and social behaviors.
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The firing properties of dopamine (DA) neurons in the substantia nigra (SN) pars compacta are strongly influenced by the activity of apamin-sensitive small conductance Ca(2+)-activated K(+) (SK) channels. Of the three SK channel genes expressed in central neurons, only SK3 expression has been identified in DA neurons. ⋯ Electrophysiological recordings of the effects of the SK channel blocker apamin on DA neurons from wild type and SK(-/-) mice show that SK2-containing channels contributed to the precision of action potential (AP) timing, while SK3-containing channels influenced AP frequency. The expression of SK2 in DA neurons may endow distinct signaling and subcellular localization to SK2-containing channels.
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Several lines of evidence indicate group III metabotropic glutamate receptors (mGluRs) have systemic anti-hyperalgesic effects. We hypothesized this could occur through modulation of transient receptor potential vanilloid 1 (TRPV1) receptors on nociceptors. To address this question we performed anatomical studies to determine if group III mGluRs were expressed on cutaneous axons and if they co-localized with TRPV1. ⋯ Finally, the anti-hyperalgesic effect of group III in this paradigm was local and not systemic since intraplantar administration of L-AP-4 in one hind paw did not attenuate nociceptive behaviors following CAP injection in the contralateral hind paw. Adenyl cyclase/cyclic AMP/PKA may be the second messenger pathway linking these two receptor families because intraplantar injection of forskolin (FSK, 10 μM) reduced PWL to heat and L-AP-4 reversed this FSK effect. Taken together, these results suggest group III mGluRs can negatively modulate TRPV1 through inhibition of adenyl cyclase and downstream intracellular activity, blocking TRPV1-induced activation of nociceptors.