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Results for “Neuronal Plasticity”

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At least 217 records · Page 12Linked to original sources
PubMed2001

[Experience guided neuronal plasticity. Significance for pathogenesis and therapy of psychiatric diseases].

Whereas the basic wiring of the mammalian central nervous system is genetically predefined, its fine tuning throughout different phases of infancy, childhood, and adulthood are highly experience-dependent. There is growing evidence from a variety of experimental data that juvenile experience and learning events modulate the functional maturation of the brain, thereby shaping the neuronal substrate for the development of intellectual and socioemotional capacities. Since early experiences occur during phases of elevated neuronal and synaptic plasticity, they induce an "imprinting" of synaptic connectivity and neural circuitry in the infant brain. Results from experimental research support the hypothesis that impoverished intellectual stimulation and traumatic socioemotional experience during early childhood may impair the formation of functional brain pathways, in particular of the limbic circuits, which play a major role in emotional behavior and learning. Such defective systems, representing functional "scars" in the brain, may be the neuronal basis of a variety of mental disorders and clinical symptoms caused by early stressful psychosocial environments. A basic thesis of this paper is that mechanisms involved in neuronal learning and memory are not only used and reused in structuring the CNS during the initial establishment of connections in the immature brain but also can be employed in molding personality and behavior during psychotherapy in adulthood.

Adult↗
PubMed2004

Effects of conditioning during amygdalar inactivation on training-induced neuronal plasticity in the medial geniculate nucleus and cingulate cortex in rabbits (Oryctolagus cuniculus).

This study addressed the amygdala's role in avoidance conditioning in rabbits (Oryctolagus cuniculus). Intra-amygdalar muscimol infusion before 60 or 120 conditioning trials blocked training-induced neuronal activity (TIA) in the medial geniculate (MG) nucleus. One hundred twenty trials with muscimol blocked TIA permanently, during conditioning with muscimol and then later without muscimol; 60 trials with muscimol blocked TIA only when muscimol was present. Cingulate cortical TIA was blocked only when muscimol was present. Behavioral learning did not occur with muscimol, but later learning was facilitated (i.e., savings occurred) in rabbits initially given muscimol plus training. These results define the time period wherein amygdalar processes initiate TIA in the MG nucleus and suggest that distinct forms of amygdalar processes induce TIA in the MG nucleus and cingulate cortex.

Action Potentials↗
PubMed1985

Intertectal neuronal plasticity in Xenopus laevis: persistence despite catecholamine depletion.

In normal Xenopus, the tectum receives a direct projection from the contralateral retina and an indirect projection, via the intertectal system, from the ipsilateral eye. The two maps of binocular visual space, at each tectum, are in register. If one eye is rotated during larval development, the ipsilateral visuotectal projection compensates by changing its orientation. Rearrangement of the intertectal system brings the ipsilateral map back into register with the contralateral map. We sought to determine whether this intertectal plasticity required normal levels of brain monoamines. Animals received an eye rotation between stages 55-63 of larval life and were then placed in one of 3 groups. A first control group received no further treatment. A second control group was given intraventricular injections of ascorbate vehicle. The experimental group was given intraventricular injections of 6-hydroxydopamine in ascorbate vehicle. Two to 3 months after metamorphosis, visuotectal projections were mapped electrophysiologically and the brains were assayed for monoamines. Intertectal plasticity occurred in all 3 groups of animals, including animals in which brain catecholamine levels were severely reduced. We conclude that normal levels of brain catecholamines are not required for this form of neural plasticity.

Animals↗
PubMed2002

Santiago Ramón y Cajal's concept of neuronal plasticity: the ambiguity lives on.

Parallel to his well-known work on the microarchitecture of the CNS, Santiago Ramón y Cajal conducted various investigations of its de- and regenerative capacities. However, Ramón y Cajal's theoretical stance on the issue remains rather ambiguous and can even be assumed to reflect modern views on the potential of structural plasticity in the CNS.

History, 19th Century↗
PubMed2004

Neuronal plasticity after spinal cord injury: identification of a gene cluster driving neurite outgrowth.

Functional recovery after spinal cord injury (SCI) may result in part from axon outgrowth and related plasticity through coordinated changes at the molecular level. We employed microarray analysis to identify a subset of genes the expression patterns of which were temporally coregulated and correlated to functional recovery after SCI. Steady-state mRNA levels of this synchronously regulated gene cluster were depressed in both ventral and dorsal horn neurons within 24 h after injury, followed by strong re-induction during the following 2 wk, which paralleled functional recovery. The identified cluster includes neuritin, attractin, microtubule-associated protein 1a, and myelin oligodendrocyte protein genes. Transcriptional and protein regulation of this novel gene cluster was also evaluated in spinal cord tissue and in single neurons and was shown to play a role in axonal plasticity. Finally, in vitro transfection experiments in primary dorsal root ganglion cells showed that cluster members act synergistically to drive neurite outgrowth.

Animals↗