Neuroscience
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The interaction between excitatory and inhibitory inputs is critical to neuronal signal processing. However, little is known about this fundamental property, largely due to the inability to clearly isolate the respective inputs. Here we took advantage of the characteristic stereotypical architecture of synaptic connections in the main olfactory bulb, which enabled us to entirely separate excitatory and inhibitory inputs. ⋯ Unexpectedly, these forms of plasticity depend on activity of somatic (mainly non-synaptic) NMDA receptors (NMDARs). In contrast, the same repetitive stimulation induced the LTP of excitatory inputs in strongly activated MCs (MC2) that require activity of synaptic NMDARs. These distinct forms of plasticity in the developing olfactory circuit may represent a novel rule of modification in convergent inputs that leads to decorrelation of inputs and facilitates odor discrimination.
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Neuro-glucostasis is required for normal expression of the steroid positive-feedback-induced preovulatory pituitary luteinizing hormone (LH) surge, a critical element of female reproduction. Glucoprivic signals from the caudal hindbrain restrain this surge, but the cellular source of this stimulus is unclear. Norepinephrine (NE) exerts well-defined stimulatory effects on the reproductive neuroendocrine axis. ⋯ The present studies demonstrate that hindbrain glucoprivation inhibits the LH surge, in part, by reducing preoptic noradrenergic input, and furthermore implicate A2 neurons as a source of this altered signal. Results also suggest that AMPK sensor deactivation does not supersede the impact of pharmacological inhibition of glucose catabolism on A2 cell function nor afferent signaling of hindbrain glucopenia on GnRH neurons. Further studies are needed to determine if decreased AMPK activation in these cell populations reflect compensatory gain in positive energy balance and/or direct effects of estrogen on AMPK.
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The molecular and cellular mechanisms, which coordinate the critical stages of brain development to reach a normal structural organization with appropriate networks, are progressively being elucidated. Experimental and clinical studies provide evidence of the occurrence of developmental alterations induced by genetic or environmental factors leading to the formation of aberrant networks associated with learning disabilities. Moreover, evidence is accumulating that suggests that also late-onset neurological disorders, even Alzheimer's disease, might be considered disorders of aberrant neural development with pathological changes that are set up at early stages of development before the appearance of the symptoms. ⋯ In the present review we focus on (1) aspects of neurogenesis with relevance to aging; (2) neurodegenerative disease (NDD)-associated proteins/pathways in the developing brain; and (3) further pathways of the developing or neurodegenerating brains that show commonalities. Elucidation of complex pathogenetic routes characterizing the earliest stage of the detrimental processes that result in pathological aging represents an essential first step toward a therapeutic intervention which is able to reverse these pathological processes and prevent the onset of the disease. Based on the shared features between pathways, we conclude that prevention of NDDs of the elderly might begin during the fetal and childhood life by providing the mothers and their children a healthy environment for the fetal and childhood development.
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Oligodendrocyte precursor cells (OPC) are glial cells that metamorphose into myelinating oligodendrocytes during embryogenesis and early stages of post-natal life. OPCs continue to divide throughout adulthood and some eventually differentiate into oligodendrocytes in response to demyelinating lesions. ⋯ In this review, we summarize the interwoven factors and cascades that promote the activation, recruitment and differentiation of OPCs into myelinating oligodendrocytes in the adult brain based mostly on results found in the study of demyelinating diseases. The goal of the review was to draw a complete picture of the transformation of OPCs into mature oligodendrocytes to facilitate the study of this transformation in both the normal and diseased adult brain.
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The rapid release of prepared movements by a loud acoustic stimulus capable of eliciting a startle response has been termed the StartReact effect (Valls-Solé et al., 1999), and premotor reaction times (PMTs) of <70 ms are often observed. Two explanations have been given for these short latency responses. The subcortical storage and triggering hypothesis suggests movements that can be prepared in advance of a "go" signal are stored and triggered from subcortical areas by a startling acoustic stimulus (SAS) without cortical involvement. ⋯ In Experiment 2, we examined the StartReact effect in a highly cortically represented action involving speech of a consonant-vowel (CV) syllable. Similar to previous work examining limb movements, a robust StartReact effect was found. Collectively, these experiments provide evidence for cortical (M1) involvement in the StartReact effect.