Critical Period of Mungbean (Phaseolus Radiatus L.) to Weed Competition

A field experiment was conducted to study the critical period of weed control on the crop of mungbean (Phaseolus radiatus L.). The studies were done in the field of BIOTROP Experimental Station with the natural existing weed population. It was found that the critical period of mungbean to weed competition was from 3-6 weeks after planting

Neural correlates without reduction: the case of the critical period

Researchers in the cognitive sciences often seek neural correlates of psychological constructs. In this paper, I argue that even when these correlates are discovered, they do not always lead to reductive outcomes. To this end, I examine the psychological construct of a critical period and briefly describe research identifying its neural correlates. Although the critical period is correlated with certain neural mechanisms, this does not imply that there is a reductionist relationship between this psychological construct and its neural correlates. Instead, this case study suggests that there may be many-to-many psychological-neural mappings, not just one-to-one or even one-to-many relations between psychological kinds and types of neural mechanisms

Neuromodulatory control of localized dendritic spiking in critical period cortex.

Sensory experience in early postnatal life, during so-called critical periods, restructures neural circuitry to enhance information processing1. Why the cortex is susceptible to sensory instruction in early life and why this susceptibility wanes with age are unclear. Here we define a developmentally restricted engagement of inhibitory circuitry that shapes localized dendritic activity and is needed for vision to drive the emergence of binocular visual responses in the mouse primary visual cortex. We find that at the peak of the critical period for binocular plasticity, acetylcholine released from the basal forebrain during periods of heightened arousal directly excites somatostatin (SST)-expressing interneurons. Their inhibition of pyramidal cell dendrites and of fast-spiking, parvalbumin-expressing interneurons enhances branch-specific dendritic responses and somatic spike rates within pyramidal cells. By adulthood, this cholinergic sensitivity is lost, and compartmentalized dendritic responses are absent but can be re-instated by optogenetic activation of SST cells. Conversely, suppressing SST cell activity during the critical period prevents the normal development of binocular receptive fields by impairing the maturation of ipsilateral eye inputs. This transient cholinergic modulation of SST cells, therefore, seems to orchestrate two features of neural plasticity-somatic disinhibition and compartmentalized dendritic spiking. Loss of this modulation may contribute to critical period closure

The effect of static incubation on the yolk sac vasculature of the Japanese quail (Coturnix c. japonica)

Static incubation affects early embryonic development with, notably, a reduction area vasculosa expansion and diminished sub-embryonic fluid (SEF) volume, effects produced during a ‘critical’ period (3-7 days in the chick) (Baggott et al., 2002). Also, as noted by Babiker & Baggott (1992), SEF is produced in bulk only after the appearance of the yolk sac vasculature (YSV), which undergoes extensive proliferation before and during the critical period. Quantification of such changes in YSV requires estimates of both the quantity of vessels and the degree of branching. In the chick, total vessel length increased linearly up to 160h of incubation, whereas branching was maximal by about 96 h (Vico et al., 1998); so, by the critical period branching is complete yet vessel growth continues. It would seem likely, therefore, that a lack of turning would reduce both measures of YSV proliferation during the critical period. In quail the effect of static incubation seems not to be simply due to retardation of YSV proliferation, as vascular density index was reduced in unturned eggs in the middle of the critical period, only to increase again by 168 h. Also early in the critical period fractal dimension was 1.70 (as in the chick, Vico et al., 1998), yet then decreased in unturned eggs, although not significantly, and subsequently an increase occurred. Thus during the critical period static incubation specifically affects the structuring of the YSV but whether this is because of, or independent of, retardation of area vasculosa expansion is not known

Pulsation-triggered mass loss from AGB stars: the 60-day critical period

Low- and intermediate-mass stars eject much of their mass during the late, red giant branch (RGB) phase of evolution. The physics of their strong stellar winds is still poorly understood. In the standard model, stellar pulsations extend the atmosphere, allowing a wind to be driven through radiation pressure on condensing dust particles. Here we investigate the onset of the wind, using nearby RGB stars drawn from the Hipparcos catalogue. We find a sharp onset of dust production when the star first reaches a pulsation period of 60 days. This approximately co-incides with the point where the star transitions to the first overtone pulsation mode. Models of the spectral energy distributions show stellar mass-loss rate suddenly increases at this point, by a factor of ~10 over the existing (chromospherically driven) wind. The dust emission is strongly correlated with both pulsation period and amplitude, indicating stellar pulsation is the main trigger for the strong mass loss, and determines the mass-loss rate. Dust emission does not strongly correlate with stellar luminosity, indicating radiation pressure on dust has little effect on the mass-loss rate. RGB stars do not normally appear to produce dust, whereas dust production by asymptotic giant branch stars appears commonplace, and is probably ubiquitous above the RGB-tip luminosity. We conclude that the strong wind begins with a step change in mass-loss rate, and is triggered by stellar pulsations. A second rapid mass-loss-rate enhancement is suggested when the star transitions to the fundamental pulsation mode, at a period of ~300 days.Comment: Accepted ApJ Letters, 5 pages, 2 figure

Autism: A “Critical Period” Disorder?

Cortical circuits in the brain are refined by experience during critical periods early in postnatal life. Critical periods are regulated by the balance of excitatory and inhibitory (E/I) neurotransmission in the brain during development. There is now increasing evidence of E/I imbalance in autism, a complex genetic neurodevelopmental disorder diagnosed by abnormal socialization, impaired communication, and repetitive behaviors or restricted interests. The underlying cause is still largely unknown and there is no fully effective treatment or cure. We propose that alteration of the expression and/or timing of critical period circuit refinement in primary sensory brain areas may significantly contribute to autistic phenotypes, including cognitive and behavioral impairments. Dissection of the cellular and molecular mechanisms governing well-established critical periods represents a powerful tool to identify new potential therapeutic targets to restore normal plasticity and function in affected neuronal circuits

Inter-areal coordination of columnar architectures during visual cortical development

The occurrence of a critical period of plasticity in the visual cortex has long been established, yet its function in normal development is not fully understood. Here we show that as the late phase of the critical period unfolds, different areas of cat visual cortex develop in a coordinated manner. Orientation columns in areas V1 and V2 become matched in size in regions that are mutually connected. The same age trend is found for such regions in the left and right brain hemisphere. Our results indicate that a function of critical period plasticity is to progressively coordinate the functional architectures of different cortical areas - even across hemispheres.Comment: 30 pages, 1 table, 6 figure

Beyond Critical Period Learning: Striatal FoxP2 Affects the Active Maintenance of Learned Vocalizations in Adulthood.

In humans, mutations in the transcription factor forkhead box P2 (FOXP2) result in language disorders associated with altered striatal structure. Like speech, birdsong is learned through social interactions during maturational critical periods, and it relies on auditory feedback during initial learning and on-going maintenance. Hearing loss causes learned vocalizations to deteriorate in adult humans and songbirds. In the adult songbird brain, most FoxP2-enriched regions (e.g., cortex, thalamus) show a static expression level, but in the striatal song control nucleus, area X, FoxP2 is regulated by singing and social context: when juveniles and adults sing alone, its levels drop, and songs are more variable. When males sing to females, FoxP2 levels remain high, and songs are relatively stable: this "on-line" regulation implicates FoxP2 in ongoing vocal processes, but its role in the auditory-based maintenance of learned vocalization has not been examined. To test this, we overexpressed FoxP2 in both hearing and deafened adult zebra finches and assessed effects on song sung alone versus songs directed to females. In intact birds singing alone, no changes were detected between songs of males expressing FoxP2 or a GFP construct in area X, consistent with the marked stability of mature song in this species. In contrast, songs of males overexpressing FoxP2 became more variable and were less preferable to females, unlike responses to songs of GFP-expressing control males. In deafened birds, song deteriorated more rapidly following FoxP2 overexpression relative to GFP controls. Together, these experiments suggest that behavior-driven FoxP2 expression and auditory feedback interact to precisely maintain learned vocalizations

Thalamocortical Inputs Show Post-Critical-Period Plasticity

SummaryExperience-dependent plasticity in the adult brain has clinical potential for functional rehabilitation following central and peripheral nerve injuries. Here, plasticity induced by unilateral infraorbital (IO) nerve resection in 4-week-old rats was mapped using MRI and synaptic mechanisms were elucidated by slice electrophysiology. Functional MRI demonstrates a cortical potentiation compared to thalamus 2 weeks after IO nerve resection. Tracing thalamocortical (TC) projections with manganese-enhanced MRI revealed circuit changes in the spared layer 4 (L4) barrel cortex. Brain slice electrophysiology revealed TC input strengthening onto L4 stellate cells due to an increase in postsynaptic strength and the number of functional synapses. This work shows that the TC input is a site for robust plasticity after the end of the previously defined critical period for this input. Thus, TC inputs may represent a major site for adult plasticity in contrast to the consensus that adult plasticity mainly occurs at cortico-cortical connections