Common sunflower is a competitive annual native dicot found in disturbed areas, on roadsides, dry prairies, and in row crops. Common sunflower is a competitive weed, but little data exist on interference, economic impacts, and competition in field corn. Field studies were conducted in 2006 and 2007 to 1) define the density-dependent effects of common sunflower competition with corn; 2) define the necessary weed-free periods of common sunflower in corn; 3) evaluate common sunflower control with herbicides; 4) and define the economic impact of common sunflower interference with corn. Corn grain yield was significantly reduced when common sunflower densities reached 1 plant/m of row and potentitially damaging common sunflower densities occurred if allowed to compete for more than 2 to 4 wk after planting for maximum corn yield. No significant corn yield reduction occurred if common sunflowers emerged 8 wk after planting. Growing degree day (GDD) heat units for corn showed that the critical point for control of common sunflower was approximately 300 GDD. Atrazine applied PRE, atrazine followed by (fb) glyphosate or halosulfuron POST, glyphosate POST, halosulfuron POST, and halosulfuron plus nicosulfuron POST controlled >87% of common sunflower. Atrazine applied PRE in a 30-cm band, nicosulfuron POST, and atrazine broadcast plus S-metolachlor PRE showed significantly lower common sunflower control and corn grain yield, when compared to atrazine PRE fb glyphosate POST. Economic impact of one sunflower/6 m of crop row caused a yield loss of 293 kg/ha. Various corn planting densities showed that corn yield can be reduced 1990 kg/ha with common sunflower competition. Corn planting densities of 49400 and 59300 plants/ha provided the greatest net returns with or without the presence of common sunflower competition. The highest net returns occurred with no common sunflower competition in 2006 and 2007, at $3,046/ha and $2,687/ha, respectively, when net corn prices were $0.24/kg ($6.00/bu). Potential control costs of various herbicide treatments revealed net returns of $1,156 to $1,910/ha in 2006 and $1,158 to $1,943/ha in 2007. Determining the economic impact of common sunflower interference in field corn allows producers to estimate the overall net return based upon density and duration of common sunflower interference, while considering varying net corn prices, crop planting density, and herbicide application costs.

Oestrogen decline during the menopause leads to decline in cognitive performance because oestrogen receptor sites are found in the prefrontal cortex and hippocampus of the female brain, areas associated with memory and attention functions. Extensive research over the past two decades has tested the effects of administering Hormone Replacement Therapy (HRT) to maintain oestrogen levels. MRI studies have shown improvements in hippocampal volume and frontal functions with HRT, but evidence for associated improvements in verbal memory performance has been mixed. Some studies have even found detrimental effects of HRT, leading to the suggestion of a critical period for HRT administration relative to menopause. Oestrogen receptor sites are found in frontal brain regions associated with working memory (WM) functions including attention. These functions have been researched less than verbal memory, but with similarly mixed findings. The research reported in this thesis tested the critical period hypothesis in relation to WM. Study one tested the prediction that HRT will benefit WM if the therapy is initiated during the peri-menopause, and will harm it if initiated post-menopause. A naturalistic sample of 121 women were recruited, comprising women who varied in the time they had begun taking HRT, and menopausal status-matched controls who had never taken HRT. Participants completed three tests of WM span and the Sustained Attention to Response Task (SART) on two occasions 12 months apart. WM performance supported the critical period hypothesis, with women who had begun the therapy after the menopause displayed worsened WM capacity when compared to peri-menopausal initiators and post-menopausal women with no history of HRT use. At one year follow up, postmenopausal HRT users were still underperforming compared to peri-HRT initiators and those in the post-menopausal stage with no history of HRT use. No significant differences were identified between groups on the SART. The effects of natural supplements on physical symptoms of the menopause have been researched, but there is little research on their effects on cognitive symptoms and none specifically testing the critical period hypothesis. Study two tested the effects of soya isoflavones on WM during peri- and post-menopausal stages. One hundred and twelve peri- and post-menopausal women were randomly allocated to receive either placebo or 100mg soya supplement in capsules daily for three months. Participants and researcher were blind to this allocation. Participants completed two tests of WM span and two Sustained Attention (SA) tasks at baseline, after three months of soya/placebo, and after a further three months without supplement. There was no effect of isoflavones on cognition, regardless of time of initiation of the supplement. This thesis offers a unique contribution to the literature, by establishing empirically that HRT may have long-lasting benefits for WM if administered in the peri-menopause period, and detriments if taken post-menopause. There was no evidence that administration of soya-based phytoestrogens for three months peri- or post-menopause replicated these effects of HRT on cognition.

Primary visual cortex is a classic model to study experience-dependent brain plasticity. In early life, if one eye is deprived of normal vision, there can be a dramatic change in the ocular dominance of the striate cortex such that the large majority of neurons lose responsiveness to the deprived eye and, consequently, the ocular dominance distribution shifts in favor of the open eye. Interestingly, the visual experience dependent plasticity following monocular deprivation (MD) occurs during a transient developmental period, which is called the critical period. MD hardly induces ocular dominance plasticity beyond critical period. The mechanisms underlying ocular dominance plasticity during the critical period are not fully understood. It has been proposed that long-term depression (LTD) may underlie the loss of cortical neuronal responsiveness to the deprived eye. However, discordant results have been reported in terms of the role of LTD and LTP in visual plasticity due to the lack of specific blockers. Here we report the prevention of the normally-occurring ocular dominance (OD) shift to the open eye following MD by using a specific long-term depression (LTD) blocking peptide derived from the GluR2 subunit of the a-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR). We were able to prevent the shift of OD to the open eye with systemic or local administration of the GluR2 peptide. Both electrophysiological and anatomical approaches were taken to demonstrate the peptide effect. Moreover, enhancing LTD with D-serine, a NMDA receptor co-agonist, brought back the ocular dominance plasticity in adult mice subject to four-day MD and, therefore, reopened the critical period. Our data indicate that LTD plays an essential role in visual plasticity during the critical period and the developmental regulation of LTD may account for the closure of critical period in adult. In an additional study, we have found anisomycin, a protein synthesis inhibitor, produces a time-dependent decline in the magnitude of the field EPSP (fEPSP) in mouse primary visual cortex and that this anisomycin-mediated fEPSP depression occludes NMDA receptor dependent LTD. In contrast, another two protein synthesis inhibitors, emetine and cycloheximide, have no effect either on baseline synaptic transmission and or on LTD. We propose that anisomycin-LTD might be mediated by p38 MAP kinase since anisomycin is also a potent activator of the P38/JNK MAPK pathway. In agreement with notion, the decline of the fEPSP caused by anisomycin can be rescued by the application of the P38 inhibitor SB203580, but not by the JNK inhibitor SP600125. The occlusion of LFS-LTD by anisomycin-induced fEPSP decline suggests that common mechanisms may be shared between the two forms of synaptic depression. Consistent with this view, bath application of the membrane permeant peptide discussed above, which specifically blocks regulated AMPA receptor endocytosis, thereby preventing the expression of LFS-LTD, prior to anisomycin treatment significantly reduced the anisomycin-induced decline of the fEPSP. In conclusion, this study indicates that anisomycin produces long-lasting depression of AMPA receptor-mediated synaptic transmission by activating P38 MAPK-mediated endocytosis of AMPA receptors in neonatal mouse visual cortex.

Unlike principal excitatory neurons, cortical interneurons comprise a diverse group of distinct subtypes. They can be classified by their morphology, molecular content, developmental origins, electrophysiological properties and specific connectivity patterns. The parvalbumin-positive \((PV^+)\), large basket interneuron has been implicated in two cortical functions: 1) the control and shaping of the excitatory response, and 2) the initiation of critical periods for plasticity. Disruptions in both phenomena have been implicated in the etiology of cognitive developmental disorders. Careful characterization of \(PV^+\) cell function and plasticity in response to their primary afferent, the thalamocortical synapse, is needed to directly relate their vital contribution at a synapse-specific or network level to whole animal behavior. Here, I used electrophysiological, anatomical and molecular genetic techniques in a novel slice preparation to elucidate \(PV^+\) circuit development and plasticity in mouse visual cortex. I found that GFP-positive \(PV^+\) cells in layer 4 undergo a rapid maturation after eye opening just prior to onset of the critical period. This development occurs across a number of intrinsic physiological properties that shape their precise, fast spiking. I further optimized and characterized a visual thalamocortical slice to examine the primary afferent input onto both pyramidal and \(PV^+\) cells. Thalamic input onto \(PV^+\) cells is larger, faster and again matures ahead of the critical period. Both the intrinsic and synaptic properties of \(PV^+\) cells are then maintained by a secreted homeoprotein, Otx2 (Sugiyama et al, 2008), which is mediated by an extracellular glycosaminoglycan recognition. Since the plasticity of fast-spiking, inhibitory neurons is dramatically distinct from their neighboring pyramidal neurons in vivo (Yazaki-Sugiyama et al. 2009), I directly examined the plasticity of thalamocortical synapses in vitro. After brief monocular deprivation, thalamic input specifically onto \(PV^+\) cells is reduced while remaining unaltered in pyramidal cells. Deprivations prior to critical period onset or in GAD65 knockout mice neither produce a shift of visual responsiveness in vivo (Hensch et al, 1998) nor reduce thalamocortical input onto \(PV^+\) cells. These results directly confirm that \(PV^+\) cells are uniquely sensitive to visual experience, which may drive further rewiring of the surrounding excitatory cortical network.

Extensive experience-dependent refinement of cortical circuits is restricted to critical periods of plasticity early in life. The timing of these critical periods is tightly regulated by the relative levels of excitatory and inhibitory (E/I) neurotransmission during development. Genetic disruption of synaptic proteins that normally maintain E/I balance can result in severe behavioral dysfunction in neurodevelopmental disorders like autism, but the mechanisms are unclear. We propose that abnormal critical periods of sensory circuit refinement could represent a key link between E/I imbalance and the cognitive and behavioral problems in autism.

Primary visual cortex is a classic model to study experience-dependent brain plasticity. In early life, if one eye is deprived of normal vision, there can be a dramatic change in the ocular dominance of the striate cortex such that the large majority of neurons lose responsiveness to the deprived eye and, consequently, the ocular dominance distribution shifts in favor of the open eye. Interestingly, the visual experience dependent plasticity following monocular deprivation (MD) occurs during a transient developmental period, which is called the critical period. MD hardly induces ocular dominance plasticity beyond critical period. The mechanisms underlying ocular dominance plasticity during the critical period are not fully understood. It has been proposed that long-term depression (LTD) may underlie the loss of cortical neuronal responsiveness to the deprived eye. However, discordant results have been reported in terms of the role of LTD and LTP in visual plasticity due to the lack of specific blockers. Here we report the prevention of the normally-occurring ocular dominance (OD) shift to the open eye following MD by using a specific long-term depression (LTD) blocking peptide derived from the GluR2 subunit of the a-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR). We were able to prevent the shift of OD to the open eye with systemic or local administration of the GluR2 peptide. Both electrophysiological and anatomical approaches were taken to demonstrate the peptide effect. Moreover, enhancing LTD with D-serine, a NMDA receptor co-agonist, brought back the ocular dominance plasticity in adult mice subject to four-day MD and, therefore, reopened the critical period. Our data indicate that LTD plays an essential role in visual plasticity during the critical period and the developmental regulation of LTD may account for the closure of critical period in adult. In an additional study, we have found anisomycin, a protein synthesis inhibitor, produces a time-dependent decline in the magnitude of the field EPSP (fEPSP) in mouse primary visual cortex and that this anisomycin-mediated fEPSP depression occludes NMDA receptor dependent LTD. In contrast, another two protein synthesis inhibitors, emetine and cycloheximide, have no effect either on baseline synaptic transmission and or on LTD. We propose that anisomycin-LTD might be mediated by p38 MAP kinase since anisomycin is also a potent activator of the P38/JNK MAPK pathway. In agreement with notion, the decline of the fEPSP caused by anisomycin can be rescued by the application of the P38 inhibitor SB203580, but not by the JNK inhibitor SP600125. The occlusion of LFS-LTD by anisomycin-induced fEPSP decline suggests that common mechanisms may be shared between the two forms of synaptic depression. Consistent with this view, bath application of the membrane permeant peptide discussed above, which specifically blocks regulated AMPA receptor endocytosis, thereby preventing the expression of LFS-LTD, prior to anisomycin treatment significantly reduced the anisomycin-induced decline of the fEPSP. In conclusion, this study indicates that anisomycin produces long-lasting depression of AMPA receptor-mediated synaptic transmission by activating P38 MAPK-mediated endocytosis of AMPA receptors in neonatal mouse visual cortex.

Primary visual cortex is a classic model to study experience-dependent brain plasticity. In early life, if one eye is deprived of normal vision, there can be a dramatic change in the ocular dominance of the striate cortex such that the large majority of neurons lose responsiveness to the deprived eye and, consequently, the ocular dominance distribution shifts in favor of the open eye. Interestingly, the visual experience dependent plasticity following monocular deprivation (MD) occurs during a transient developmental period, which is called the critical period. MD hardly induces ocular dominance plasticity beyond critical period. The mechanisms underlying ocular dominance plasticity during the critical period are not fully understood. It has been proposed that long-term depression (LTD) may underlie the loss of cortical neuronal responsiveness to the deprived eye. However, discordant results have been reported in terms of the role of LTD and LTP in visual plasticity due to the lack of specific blockers. Here we report the prevention of the normally-occurring ocular dominance (OD) shift to the open eye following MD by using a specific long-term depression (LTD) blocking peptide derived from the GluR2 subunit of the a-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR). We were able to prevent the shift of OD to the open eye with systemic or local administration of the GluR2 peptide. Both electrophysiological and anatomical approaches were taken to demonstrate the peptide effect. Moreover, enhancing LTD with D-serine, a NMDA receptor co-agonist, brought back the ocular dominance plasticity in adult mice subject to four-day MD and, therefore, reopened the critical period. Our data indicate that LTD plays an essential role in visual plasticity during the critical period and the developmental regulation of LTD may account for the closure of critical period in adult. In an additional study, we have found anisomycin, a protein synthesis inhibitor, produces a time-dependent decline in the magnitude of the field EPSP (fEPSP) in mouse primary visual cortex and that this anisomycin-mediated fEPSP depression occludes NMDA receptor dependent LTD. In contrast, another two protein synthesis inhibitors, emetine and cycloheximide, have no effect either on baseline synaptic transmission and or on LTD. We propose that anisomycin-LTD might be mediated by p38 MAP kinase since anisomycin is also a potent activator of the P38/JNK MAPK pathway. In agreement with notion, the decline of the fEPSP caused by anisomycin can be rescued by the application of the P38 inhibitor SB203580, but not by the JNK inhibitor SP600125. The occlusion of LFS-LTD by anisomycin-induced fEPSP decline suggests that common mechanisms may be shared between the two forms of synaptic depression. Consistent with this view, bath application of the membrane permeant peptide discussed above, which specifically blocks regulated AMPA receptor endocytosis, thereby preventing the expression of LFS-LTD, prior to anisomycin treatment significantly reduced the anisomycin-induced decline of the fEPSP. In conclusion, this study indicates that anisomycin produces long-lasting depression of AMPA receptor-mediated synaptic transmission by activating P38 MAPK-mediated endocytosis of AMPA receptors in neonatal mouse visual cortex. / Medicine, Faculty of / Graduate

Master of Science / Department of Agronomy / Johanna A. Dille / An opportunity for postemergence (POST) grass weed control has recently been approved with ALS-resistant grain sorghum, however, grass weed emergence timing and crop tolerance to grass competition are not well understood. To address the importance of POST application timing, a critical period of weed control (CPWC) for grass competition in grain sorghum was developed. Field experiments were established near Manhattan and Hays, KS in 2016 and 2017, and near Hutchinson, KS in 2017 to determine the CPWC. Each site provided a different grass species community. A total of ten treatments were included, with four treatments maintained weed-free until 2, 3, 5, or 7 weeks after crop emergence, four treatments receiving no weed control until 2, 3, 5, or 7 weeks after crop emergence, and two treatments were maintained weed-free or weedy all season. Treatments did not influence grain yield at Hutchinson because of a lack of season-long weed emergence. At Hays the CPWC began at crop emergence and ended 28 days later. At Manhattan the CPWC began 27 days after emergence and continued through grain harvest. The CPWC in grain sorghum depends on rainfall and competitive ability of the weed species. The start of the CPWC began when weeds emerged, thus a POST application should be targeted 14 to 21 days after emergence of grain sorghum. Emergence and development of large crabgrass, barnyardgrass, shattercane, and giant, green, and yellow foxtails were studied near Manhattan, KS after seeding on April 11, 2017. Barnyardgrass had the longest duration of emergence, beginning at 180 GDD after seeding and continuing through July. Large crabgrass had the shortest duration of emergence from 325 to 630 GDD after seeding. In general, all grasses began to emerge in late April and most species completed 90% emergence by early June. Grain sorghum is typically planted at this time, so grass weed control prior to planting is critical. Palmer amaranth is a troublesome weed in double-crop grain sorghum production fields in Kansas. The presence of herbicide-resistant populations limits options for weed management. Field experiments were conducted to evaluate 14 different herbicide programs for the management of atrazine-resistant Palmer amaranth in double-crop grain sorghum at Manhattan and Hutchinson, KS in 2016 and 2017. Programs included eight PRE only and six PRE followed by POST treatments. Programs that had very long chain fatty acid-inhibiting herbicides provided greater control of atrazine-resistant Palmer amaranth by three weeks after planting sorghum. Programs of PRE followed by POST provided greater control of both atrazine-resistant and -susceptible Palmer amaranth by eight WAP compared to PRE alone. These results illustrate the value of residual herbicides, as well as an effective postemergence application, in double-crop grain sorghum. Early season grass and Palmer amaranth control with the use of residual herbicides such as very long chain fatty acid-inhibitors provide a competitive advantage to grain sorghum. Utilizing weed emergence patterns to time effective POST applications, in unison with residual herbicides, will provide season-long weed control in Kansas grain sorghum fields.

<p>Trafficking of the glutamatergic AMPA receptors (AMPARs) has been implicated in synaptic plasticity regulation, including long-term potentiation, long-term depression, and synaptic scaling. Two proteins, GRIP for stabilization at the synapse and PICK for internalization, are involved in trafficking GluR2-containing AMPARs in and out of the synapse. In this thesis, I addressed the changes in the mechanisms of AMPAR trafficking by characterizing the developmental trajectories of GluR2, the phosphorylated form pGluR2, GRIP, and PICK and comparing expression in visual vs. frontal cortex. I found significant differences between cortical areas in the developmental trajectories of GluR2 and pGluR2. In visual cortex, expression levels exhibited smooth developmental increases. In frontal cortex, GluR2 and pGluR2 rose to an exuberant expression between P18 and P35. Developmental trajectories for GRIP and PICK showed smooth increases that were consistent across cortical areas. Furthermore, looking at the correlation between the surface components (GluR2 and GRIP) and internalized components (pGluR2 and PICK), I found that the development of AMPAR trafficking components is tightly regulated across the cortex.</p> <p>In this thesis, I also looked at AMPAR expression in adult cortex. Fluoxetine has previously been reported to induce a juvenile like state of plasticity in visual cortex and this plasticity was assessed through monocular deprivation. My results indicated that fluoxetine administration was not associated with significant changes in AMPAR expression levels. However, monocular deprivation induced significant upregulation in expression levels of all four proteins. These results imply the presence of AMPAR-mediated plasticity in the adult brain.</p> / Master of Science (MSc)

Doctor of Philosophy / Department of Agronomy / J. Anita Dille / Integrated weed management (IWM) is an ecological approach to weed control that reduces dependence on herbicides through understanding of weed biology and involves using multiple weed control measures including cultural, chemical, mechanical and biological methods. The critical period of weed control is the duration of the crop life cycle in which it must be kept weed-free to prevent yield loss from weed interference. Eight experiments were conducted throughout Kansas between October 2010 and June 2012 to identify this period in winter wheat grown under dryland and irrigated conditions. Impact of henbit and downy brome density on winter wheat yields were evaluated on four farmer’s fields with natural populations and on a research station with overseeded populations. Henbit density up to 156 plants m-2 did not affect winter wheat yield, while downy brome at a density of 40 plants m-2 reduced yield by 33 and 13% in 2011 and 2012, respectively. In the presence of downy brome, winter wheat should be kept weed-free approximately 30 to 45 days after planting to prevent yield loss; otherwise, weeds need to be removed immediately following release from winter dormancy to prevent yield loss due to existing weed populations. Flumioxazin and pyroxasulfone are herbicides registered for use in winter wheat, soybean and corn for control of broadleaf and grass weeds. Flumioxazin and pyroxasulfone were evaluated for plant response to localized herbicide exposure to roots, shoots, or both roots and shoots utilizing a novel technique. Two weed species, ivyleaf morningglory and shattercane, as well as two crops, wheat and soybean, were evaluated for injury after localized exposures. The location and expression of symptoms from the flumioxazin and pyroxasulfone herbicides were determined to be the shoot of seedling plants. The utilization of preemergence herbicides in winter wheat is not a common practice, although application may protect winter wheat from early season yield losses as determined by the critical weed-free period. Kansas wheat growers should evaluate the presence and density of weed species to determine which weed management strategy is most advantageous to preserving winter wheat yield.