Matching Items (11)
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- All Subjects: Honey Bees
- All Subjects: Brain--Wounds and injuries.
- Creators: Smith, Brian
- Creators: Anderson, Trent
Description
Following a traumatic brain injury (TBI) 5-50% of patients will develop post traumatic epilepsy (PTE). Pediatric patients are most susceptible with the highest incidence of PTE. Currently, we cannot prevent the development of PTE and knowledge of basic mechanisms are unknown. This has led to several shortcomings to the treatment of PTE, one of which is the use of anticonvulsant medication to the population of TBI patients that are not likely to develop PTE. The complication of identifying the two populations has been hindered by the ability to find a marker to the pathogenesis of PTE. The central hypothesis of this dissertation is that following TBI, the cortex undergoes distinct cellular and synaptic reorganization that facilitates cortical excitability and promotes seizure development. Chapter 2 of this dissertation details excitatory and inhibitory changes in the rat cortex after severe TBI. This dissertation aims to identify cortical changes to a single cell level after severe TBI using whole cell patch clamp and electroencephalogram electrophysiology. The work of this dissertation concluded that excitatory and inhibitory synaptic activity in cortical controlled impact (CCI) animals showed the development of distinct burst discharges that were not present in control animals. The results suggest that CCI induces early "silent" seizures that are detectable on EEG and correlate with changes to the synaptic excitability in the cortex. The synaptic changes and development of burst discharges may play an important role in synchronizing the network and promoting the development of PTE.
ContributorsNichols, Joshua (Author) / Anderson, Trent (Thesis advisor) / Neisewander, Janet (Thesis advisor) / Newbern, Jason (Committee member) / Arizona State University (Publisher)
Created2014
Description
Selenium, a group 16 metalloid on the periodic table, is a necessary mineral for many organisms. Trace amounts of selenium are essential for normal development, antioxidant protein function, enzyme function, and hormone regulation (Burden et al., 2016). However, when selenium is found in toxic amounts in organisms, it has been found to substitute for sulfur in proteins, which can be toxic to these animals, and cause oxidative stress (Quinn et al., 2007). Using the previous research done with acute exposure to organic and inorganic selenium compounds, we hypothesized that the inorganic sodium selenate would significantly decrease learning and memory recall for both chronic and acute exposure. We also hypothesized that the consumption of organic methylseleno-L-cysteine by honey bees would decrease learning and memory recall for both the chronic and acute exposure. We further hypothesized that protein carbonyl content would be increased due to oxidative damage caused by selenium in both the sodium selenate and the methylseleno-L-cysteine treatment groups, but that the inorganic selenium compound would increase the carbonyl content more than the methylseleno-L-cysteine. To run the experiments, three tents outside had two colonies in each tent. One tent contained the sodium selenate group, another had the sucrose control, and one contained the methylseleno-L-cysteine group. The treatment groups were fed selenium in their sucrose feeders. The first part of the experiment was training the bees by using proboscis extension response (PER) to teach them to extend their proboscis to the rewarded odor and not to the unrewarded odor. This was done by pairing the rewarded odor with a sucrose reward and not pairing it with the unrewarded odor. Then their short-term and long-term memory recall was tested. The second part of the experiment was checking for oxidative damage by measuring the protein carbonyl content in the bees. Three boxes were set up with the same three treatment groups as used in the tents. The treatment group bees were exposed to selenium in the sucrose feeders and in the pollen patties. After one week, the living bees were removed and frozen. They were then homogenized to extract protein. The first assay run was the protein content assay to establish a standard protein concentration for samples. Then a protein carbonyl assay was run, to determine the protein carbonyl content. Overall, the experiment found that exposure to selenium negatively impacted honey bees learning and memory recall significantly. Chronic exposure to the inorganic selenate reduced the bees' long-term memory abilities to differentiate between odors. With methylseleno-L-cysteine, it had no significant effect for the chronic exposure, but for the acute exposure, it had a significant impairment on their abilities to distinguish between the rewarded and unrewarded odors during conditioning. Our results showed that from our experiment there appeared to be no significant effect of selenium exposure on the increase of carbonylation content in the different treatment groups. This is most likely due to the fact the carbonyl content was not detectable because the protein concentration was low in the samples (approximately 3.5 mg/mL).
ContributorsWinski, Alexandra (Co-author) / Winski, Brandon (Co-author) / Smith, Brian (Thesis director) / Harrison, Jon (Committee member) / Burden, Christina (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05
ContributorsLei, Harry (Author) / Smith, Brian (Thesis director) / Albin-Brooks, Christopher (Committee member) / Barrett, The Honors College (Contributor)
Created2023-05
ContributorsLei, Harry (Author) / Smith, Brian (Thesis director) / Albin-Brooks, Christopher (Committee member) / Barrett, The Honors College (Contributor)
Created2023-05
Description
In the face of widespread pollinator decline, research has increasingly focused on ways that pesticides could be harming bees. Fungicides are pesticides that are used in greater volumes than insecticides, yet significantly fewer studies have investigated the effects of these agrochemicals. The fungicide Pristine® is commonly used on bee-pollinated crops and has been shown to be detrimental to physiological processes that are key to honey bee foraging, such as digestion and learning. This study seeks to investigate how Pristine® exposure affects the amount of water, nectar, and pollen that honey bees collect. Colonies were fed either plain pollen patties or pollen patties containing 23 ppm Pristine®. Exposure to fungicide had no significant effect on corbicular pollen mass, the crop volumes of nectar or water foragers, or the proportions of foragers collecting different substances. There was a significantly higher sugar concentration in the crop of Pristine®-exposed nectar foragers (43.6%, 95% CI [38.8, 48.4]) compared to control nectar foragers (36.3%, 95% CI [31.9, 40.6]). The higher sugar concentration in the nectar of Pristine®-treated bees could indicate that the agrochemical decreases sucrose responsiveness or nutritional status in bees. Alternatively, fungicide exposure may increase the amount of sugar that bees need to make it back to the hive. Based on these results, it would appear that fungicides like Pristine® do not strongly affect the amounts of substances that honey bees collect, but it is still highly plausible that treated bees forage more slowly or with lower return rates.
ContributorsChester, Elise (Author) / Harrison, Jon (Thesis director) / DesJardins, Nicole (Committee member) / Smith, Brian (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2023-05
Description
In the face of widespread pollinator decline, research has increasingly focused on ways that pesticides could be harming bees. Fungicides are pesticides that are used in greater volumes than insecticides, yet significantly fewer studies have investigated the effects of these agrochemicals. The fungicide Pristine® is commonly used on bee-pollinated crops and has been shown to be detrimental to physiological processes that are key to honey bee foraging, such as digestion and learning. This study seeks to investigate how Pristine® exposure affects the amount of water, nectar, and pollen that honey bees collect. Colonies were fed either plain pollen patties or pollen patties containing 23 ppm Pristine®. Exposure to fungicide had no significant effect on corbicular pollen mass, the crop volumes of nectar or water foragers, or the proportions of foragers collecting different substances. There was a significantly higher sugar concentration in the crop of Pristine®-exposed nectar foragers (43.6%, 95% CI [38.8, 48.4]) compared to control nectar foragers (36.3%, 95% CI [31.9, 40.6]). The higher sugar concentration in the nectar of Pristine®-treated bees could indicate that the agrochemical decreases sucrose responsiveness or nutritional status in bees. Alternatively, fungicide exposure may increase the amount of sugar that bees need to make it back to the hive. Based on these results, it would appear that fungicides like Pristine® do not strongly affect the amounts of substances that honey bees collect, but it is still highly plausible that treated bees forage more slowly or with lower return rates.
ContributorsChester, Elise (Author) / Harrison, Jon (Thesis director) / DesJardins, Nicole (Committee member) / Smith, Brian (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2023-05
Description
In the face of widespread pollinator decline, research has increasingly focused on ways that pesticides could be harming bees. Fungicides are pesticides that are used in greater volumes than insecticides, yet significantly fewer studies have investigated the effects of these agrochemicals. The fungicide Pristine® is commonly used on bee-pollinated crops and has been shown to be detrimental to physiological processes that are key to honey bee foraging, such as digestion and learning. This study seeks to investigate how Pristine® exposure affects the amount of water, nectar, and pollen that honey bees collect. Colonies were fed either plain pollen patties or pollen patties containing 23 ppm Pristine®. Exposure to fungicide had no significant effect on corbicular pollen mass, the crop volumes of nectar or water foragers, or the proportions of foragers collecting different substances. There was a significantly higher sugar concentration in the crop of Pristine®-exposed nectar foragers (43.6%, 95% CI [38.8, 48.4]) compared to control nectar foragers (36.3%, 95% CI [31.9, 40.6]). The higher sugar concentration in the nectar of Pristine®-treated bees could indicate that the agrochemical decreases sucrose responsiveness or nutritional status in bees. Alternatively, fungicide exposure may increase the amount of sugar that bees need to make it back to the hive. Based on these results, it would appear that fungicides like Pristine® do not strongly affect the amounts of substances that honey bees collect, but it is still highly plausible that treated bees forage more slowly or with lower return rates.
ContributorsChester, Elise (Author) / Harrison, Jon (Thesis director) / DesJardins, Nicole (Committee member) / Smith, Brian (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2023-05
The Effect of Active Sensing on Electroantenneagram and Electrolobulargram Response in Honeybess.pdf
ContributorsLei, Harry (Author) / Smith, Brian (Thesis director) / Albin-Brooks, Christopher (Committee member) / Barrett, The Honors College (Contributor)
Created2023-05
Description
Active sensing is a sensory phenomenon in which organisms use self-generated energy to examine their surroundings. This experiment strives to better understand active sensing in honeybees, predicting that active sensing may display itself primarily through antennae movement and that preventing antennae movement may result in differences in electroantennogram dose-response curves and associative learning plasticity. This will be done by examining changes in amplitude in electroantennogram response in both fixed-antenna and free-antenna bees over the course of a differential training protocol that establishes learned behavior discrimination.
ContributorsLei, Harry (Author) / Smith, Brian (Thesis director) / Albin-Brooks, Christopher (Committee member) / Barrett, The Honors College (Contributor)
Created2023-05
Description
Pediatric traumatic brain injury (TBI) is a leading cause of death and disability in children. When TBI occurs in children it often results in severe cognitive and behavioral deficits. Post-injury, the pediatric brain may be sensitive to the effects of TBI while undergoing a number of age-dependent physiological and neurobiological changes. Due to the nature of the developing cortex, it is important to understand how a pediatric brain recovers from a severe TBI (sTBI) compared to an adult. Investigating major cortical and cellular changes after sTBI in a pediatric model can elucidate why pediatrics go on to suffer more neurological damage than an adult after head trauma. To model pediatric sTBI, I use controlled cortical impact (CCI) in juvenile mice (P22). First, I show that by 14 days after injury, animals begin to show recurrent, non-injury induced, electrographic seizures. Also, using whole-cell patch clamp, layer V pyramidal neurons in the peri-injury area show no changes except single-cell excitatory and inhibitory synaptic bursts. These results demonstrate that CCI induces epileptiform activity and distinct synaptic bursting within 14 days of injury without altering the intrinsic properties of layer V pyramidal neurons. Second, I characterized changes to the cortical inhibitory network and how fast-spiking (FS) interneurons in the peri-injury region function after CCI. I found that there is no loss of interneurons in the injury zone, but a 70% loss of parvalbumin immunoreactivity (PV-IR). FS neurons received less inhibitory input and greater excitatory input. Finally, I show that the cortical interneuron network is also affected in the contralateral motor cortex. The contralateral motor cortex shows a loss of interneurons and loss of PV-IR. Contralateral FS neurons in the motor cortex synaptically showed greater excitatory input and less inhibitory input 14 days after injury. In summary, this work demonstrates that by 14 days after injury, the pediatric cortex develops epileptiform activity likely due to cortical inhibitory network dysfunction. These findings provide novel insight into how pediatric cortical networks function in the injured brain and suggest potential circuit level mechanisms that may contribute to neurological disorders as a result of TBI.
ContributorsNichols, Joshua (Author) / Anderson, Trent (Thesis advisor) / Newbern, Jason (Thesis advisor) / Neisewander, Janet (Committee member) / Qiu, Shenfeng (Committee member) / Stabenfeldt, Sarah (Committee member) / Arizona State University (Publisher)
Created2015