Prelude. Cycle 1. Introduction. Cycle 2. Structure defines function. Cycle 3. Diversity of cortical functions is provided by inhibition. Cycle 4. Windows on the brain. Cycle 5. A system of rhythms: from simple to complex dynamics. Cycle 6. Synchronization by oscillation. Cycle 7. The brain's default state: self-organized oscillations in rest and sleep. Cycle 8. Perturbation of the default patterns by experience. Cycle 9. The gamma buzz: gluing by oscillations in the waking brain. Cycle 10. Perceptions and actions are brain state-dependent. Cycle 11. Oscillations in the "other cortex:" navigation in real and memory space. Cycle 12. Coupling of systems by oscillations. Cycle 13. The tough problem. References.

Rhythms of the brain

Naturally occurring variations in maternal care alter the expression of genes that regulate behavioral and endocrine responses to stress, as well as hippocampal synaptic development. These effects form the basis for the development of stable, individual differences in stress reactivity and certain forms of cognition. Maternal care also influences the maternal behavior of female offspring, an effect that appears to be related to oxytocin receptor gene expression, and which forms the basis for the intergenerational transmission of individual differences in stress reactivity. Patterns of maternal care that increase stress reactivity in offspring are enhanced by stressors imposed on the mother. These findings provide evidence for the importance of parental care as a mediator of the effects of environmental adversity on neural development.

Maternal care, gene expression, and the transmission of individual differences in stress reactivity across generations.

Synaptic plasticity in adult neural circuits may involve the strengthening or weakening of existing synapses as well as structural plasticity, including synapse formation and elimination. Indeed, long-term in vivo imaging studies are beginning to reveal the structural dynamics of neocortical neurons in the normal and injured adult brain. Although the overall cell-specific morphology of axons and dendrites, as well as of a subpopulation of small synaptic structures, are remarkably stable, there is increasing evidence that experience-dependent plasticity of specific circuits in the somatosensory and visual cortex involves cell type-specific structural plasticity: some boutons and dendritic spines appear and disappear, accompanied by synapse formation and elimination, respectively. This Review focuses on recent evidence for such structural forms of synaptic plasticity in the mammalian cortex and outlines open questions.

Experience-dependent structural synaptic plasticity in the mammalian brain.

Reductions in blood flow to the brain of sufficient duration and extent lead to stroke, which results in damage to neuronal networks and the impairment of sensation, movement or cognition. Evidence from animal models suggests that a time-limited window of neuroplasticity opens following a stroke, during which the greatest gains in recovery occur. Plasticity mechanisms include activity-dependent rewiring and synapse strengthening. The challenge for improving stroke recovery is to understand how to optimally engage and modify surviving neuronal networks, to provide new response strategies that compensate for tissue lost to injury.

Plasticity during stroke recovery: from synapse to behaviour.

Behavioural, cellular and molecular studies have revealed significant effects of enriched environments on rodents and other species, and provided new insights into mechanisms of experience-dependent plasticity, including adult neurogenesis and synaptic plasticity The demonstration that the onset and progression of Huntington's disease in transgenic mice is delayed by environmental enrichment has emphasized the importance of understanding both genetic and environmental factors in nervous system disorders, including those with Mendelian inheritance patterns A range of rodent models of other brain disorders, including Alzheimer's disease and Parkinson's disease, fragile X and Down syndrome, as well as various forms of brain injury, have now been compared under enriched and standard housing conditions Here, we review these findings on the environmental modulators of pathogenesis and gene-environment interactions in CNS disorders, and discuss their therapeutic implications

Enriched environments, experience-dependent plasticity and disorders of the nervous system.

1. A quantitative 2-[14C]deoxy-D-glucose (2DG) autoradiographic study was undertaken to determine the functional (metabolic) organization of an individual column in the first somatosensory cortex (SI) of the awake restrained rat. Manual or mechanically controlled brush stroking of a single vibrissa (typically C3) was used in order to evoke neural activity and increase glucose utilization in a single cortical barrel in lamina IV and in adjacent supra- and infragranular layers in register with the single cortical barrel labeling in lamina IV. 2. The single activated vibrissal column was found to extend from layer I to the superficial half of layer VI of the contralateral SI cortex and was fusiform in shape, being of largest diameter (650-micron) in layer IV and smallest diameter (200 micron) in layer VI. 3. This single metabolic column was not uniform in its density of labeling. The greatest local cerebral metabolic rate of glucose (LCMRG) was found in layer IV (170 mumol.100 g-1.min-1), layers II-III, and V had, on the average, similar LCMRG values (115 mumol.100 g-1.min-1), which decreased with distance from layer IV. 4. The functional (metabolic) columnar activity center situated in layer IV corresponded in size to the appropriate anatomical barrel as determined from thionin-stained sections. Increased metabolic activity was not strictly confined to the candle-pin-shaped column but extended tangentially as radiating fingerlike projections toward the neighboring barrels. 5. In cortical layers other than IV, the metabolic column was less prominently labeled, and the metabolic activity also branched in the tangential plane. The labeling pattern profile in upper layers was characterized by numerous lateral spreading fingerlike projections of increased glucose metabolism. 6. Neonatal follicle lesions sparing only C3 vibrissa caused a great increase (125%) in cortical territory driven by the spared whisker with a concomitant loss of columnar shape and decrease in intensity of metabolic activity in response to its stimulation. 7. Similar lesions in adult rats produced a significant increase (40%) in dimensions of the spared C3 cortical column, which was, however, smaller than that produced after neonatal lesions. The metabolic activation of layer Vb in the spared C3 column was increased (17%) compared with that of the control column.(ABSTRACT TRUNCATED AT 400 WORDS)

Single vibrissal cortical column in SI cortex of rat and its alterations in neonatal and adult vibrissa-deafferented animals: a quantitative 2DG study.

Huntington's disease (HD) is one of a group of neurodegenerative diseases caused by an expanded trinucleotide (CAG) repeat coding for an extended polyglutamine tract. The disease is inherited in an autosomal dominant manner, with onset of motor, cognitive, and psychiatric symptoms typically occurring in midlife, followed by unremitting progression and eventual death. We report here that motor presymptomatic R6/1 HD mice show a severe impairment of somatosensory-discrimination learning ability in a behavioral task that depends heavily on the barrel cortex. In parallel, there are deficits in barrel-cortex plasticity after a somatosensory whisker-deprivation paradigm. The present study demonstrates deficits in neocortical plasticity correlated with a specific learning impairment involving the same neocortical area, a finding that provides new insight into the cellular basis of early cognitive deficits in HD.

https://www.jneurosci.org/content/jneuro/25/12/3059.full.pdf

Deficits in Experience-Dependent Cortical Plasticity and Sensory-Discrimination Learning in Presymptomatic Huntington's Disease Mice

It has been known for several years that receptive field properties of sensory cortical neurons can be altered by learning experiences. We attempted to visualize a global change of the cortical body map induced by learning. In order to do this a short-duration classical conditioning involving stimulation of a row of mystacial vibrissae in mice was followed with 2-deoxyglucose (2DG) mapping of functional activity. Three conditioning sessions that paired stimulation of a row of whiskers with a tail shock produced an increase of the functional representation in somatosensory cortex (SI) of a row of the whiskers stimulated during the training. This plastic change of vibrissal representation in SI was visualized with 2DG autoradiography a day after completion of training. The expansion of representation was the most pronounced in cortical layer IV, and to a lesser extent in layer Illb. The expansion was observed in conditioned but not in pseudoconditioned mice or in animals that received only the conditioned stimulus. If training was discontinued, the enlargement of vibrissal representation progressively faded. The reversal could be accelerated by a behavioral extinction procedure. This study gives the pictorial demonstration of rapid, transient, and extinguishable learning-dependent changes in SI cortical maps.

/pdf/short-lasting-classical-conditioning-induces-reversible-qd13bpuied.pdf

Short-Lasting Classical Conditioning Induces Reversible Changes of Representational Maps of Vibrissae in Mouse SI Cortex—A 2DG Study

Glutamate receptors (GluRs) provide the major excitatory input to cortical neurons. Four main subtypes of GluRs are distinguished, namely, N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, kainate, and metabotropic receptors. All of them have been implicated in neuronal plasticity, and this paper reviews data that may be pertinent to the role played by GluRs in neocortical plasticity both in adult animals as well as during postnatal development. Emphasis is given to receptor distribution analyzed by various means, such as physiological responses, ligand binding as revealed by receptor autoradiography, and expression of receptor subunits at both mRNA and protein (immunoreactivity) levels. Possible mechanisms of involvement of GluRs in plastic changes on cortical neuron response are reviewed, and data on up- and downregulation of GluRs in neocortical plasticity are summarized. Functional studies involving either activation or blocking, and effects of such manipulation on cortical plasticity are discussed.

Malgorzata Kossut

Papers

Single vibrissal cortical column in SI cortex of rat and its alterations in neonatal and adult vibrissa-deafferented animals: a quantitative 2DG study.

Deficits in Experience-Dependent Cortical Plasticity and Sensory-Discrimination Learning in Presymptomatic Huntington's Disease Mice

Short-Lasting Classical Conditioning Induces Reversible Changes of Representational Maps of Vibrissae in Mouse SI Cortex—A 2DG Study

Glutamate receptors in cortical plasticity: molecular and cellular biology

Plasticity of the barrel cortex neurons