Randy W. Cohen

Diet Balancing in the Cockroach Rhyparobia madera: Does Serotonin Regulate this Behavior?

Animals, including insects, have the ability to self-select an optimal diet from a choice of two or more incomplete diets that lack an essential nutrient. This paper demonstrates that nymphs of the cockroach Rhyparobia madera also have this ability. The nymphs chose a protein:carbohydrate (P:C) ratio of approximately 25:75 when faced with a choice between one cube of protein (casein) and another of carbohydrate (sucrose). This self-selected ratio was shown to promote growth as well or better than other diets tested. When given a wide range of P:C choices, the R. madera nymphs consistently selected a P:C ratio of approximately 25:75, suggesting that they have the ability to diet-balance. Finally, injections of various serotonergic drugs into self-selecting nymphs influenced their choice of diets. Serotonin promoted a decrease in carbohydrate feeding, while injection of the antagonist α-methyltryptophan caused the nymphs to overfeed on carbohydrate. The results suggest that serotonin may help alter the carbohydrate feeding response in cockroaches.

Phototactic Responses to Ultraviolet and White Light in Various Species of Collembola, Including the Eyeless Species, Folsomia candida

Abstract Previous observations have indicated homology in the cellular components between collembolan eyes and the compound eyes of insects. However, behavioral or physiological studies indicating similarities in function are lacking. Collembolan eyes were examined from three species in the Family Isotomidae using scanning electron microscopy. Collembolan eyes are arranged dorsally and laterally on each side of the head in two species, Proisotoma minuta with eight eyes on each side of the head and Folsomia similis with one eye on each side of the head. In both of these species the eyes were located just posterior to the postantennal organ. In Folsomia candida, no external eye structures were detected. These three species were assayed for a series of behavioral preferences using ultraviolet (UV), white light and dark, and temperature conditions. The tests demonstrated that over 76% of all three species, including the eyeless F. Candida, chose white over UV light, over 69% preferred dark over UV, and over 77% favored dark over white light. The results demonstrated that all three species detect both UV and white light and avoid it, preferring cool, dark habitats. From the results of this study, it is hypothesized that F. candida may, in fact, be only “lensless” and may be able to detect light by having internal, non-ocular photoreceptors. Further histological studies are needed to investigate this possibility.

Possible Regulation of Feeding Behavior in Cockroach Nymphs by the Neurotransmitter Octopamine

Insects, including cockroaches, have the ability to select a proper diet from different nutrient choices. We have showed previously that various neurotransmitters and neuromodulators appear to regulate certain aspects of feeding in the cockroach, Rhyparobia madera. In the current study, we examined the role of octopamine in feeding behavior of cockroach nymphs. By either injection or direct incorporation into the diet blocks, an octopamine agonist (octopamine or synephrine) or antagonist (phentolamine) was effective in altering feeding in R. madera nymphs. Both octopamine and synephrine increased feeding slightly, while phentolamine decreased feeding dramatically. Phentolamine was able to decrease feeding, but not motor activity, when injected directly into the nymphs. Octopamine appears to cause increased feeding in the cockroach.

The Neuroprotective Effects of Non-NMDA Antagonists in the Cerebellum of the spastic Han Wistar Mutant

Excitotoxicity resulting from the dysfunction of glutamate receptors has been attributed to neurodegeneration seen in many brain disorders. In our laboratory, the spastic Han Wistar mutant is currently utilized as a potential model of excitotoxicity. The mutant is characterized by progressive neuronal degeneration, hindlimb paresis and ataxia which culminates in the animal’s death at approximately 65 days of age. In this study, neuroprotection derived from acute administration of the non-NMDA antagonist GYKI 52466, and chronic administration of the non-NMDA antagonist CNQX was examined in order to determine the potential roles of non-NMDA receptors in the observed neurodegeneration. Mutants injected with GYKI 52466 (15 mg/kg), twice a week for 3 weeks, exhibited increased life spans (14%) and extended motor activity than their vehicle-treated mutant siblings. In a separate group of mutants, CNQX (either 50 or 500 μM) was infused directly into the third ventricle of the mutant’s brain utilizing osmotic pumps. A statistically significant increase in motor activity (22%) was detected for mutants treated with a dose of 50 μM CNQX compared to their vehicle-treated siblings. Finally, cerebellar histological evaluations of mutants treated with both 50 and 500 μM CNQX showed dose-dependent higher cerebellar Purkinje cell counts. These findings suggest that non-NMDA receptors play a significant role in neurodegeneration in this animal.

Exercise-Induced Neuroprotection in the Spastic Han Wistar Rat: The Possible Role of Brain-Derived Neurotrophic Factor

Moderate aerobic exercise has been shown to enhance motor skills and protect the nervous system from neurodegenerative diseases, like ataxia. Our lab uses the spastic Han Wistar rat as a model of ataxia. Mutant rats develop forelimb tremor and hind limb rigidity and have a decreased lifespan. Our lab has shown that exercise reduced Purkinje cell degeneration and delayed motor dysfunction, significantly increasing lifespan. Our study investigated how moderate exercise may mediate neuroprotection by analyzing brain-derived neurotrophic factor (BDNF) and its receptor TrkB. To link BDNF to exercise-induced neuroprotection, mutant and normal rats were infused with the TrkB antagonist K252a or vehicle into the third ventricle. During infusion, rats were subjected to moderate exercise regimens on a treadmill. Exercised mutants receiving K252a exhibited a 21.4% loss in Purkinje cells compared to their controls. Cerebellar TrkB expression was evaluated using non-drug-treated mutants subjected to various treadmill running regimens. Running animals expressed three times more TrkB than sedentary animals. BDNF was quantified via Sandwich ELISA, and cerebellar expression was found to be 26.6% greater in mutant rats on 7-day treadmill exercise regimen compared to 30 days of treadmill exercise. These results suggest that BDNF is involved in mediating exercise-induced neuroprotection.

Muscle-specific changes in length-force characteristics of the calf muscles in the spastic Han-Wistar rat

The purpose of the present study was to investigate muscle mechanical properties and mechanical interaction between muscles in the lower hindlimb of the spastic mutant rat. Length-force characteristics of gastrocnemius (GA), soleus (SO), and plantaris (PL) were assessed in anesthetized spastic and normally developed Han-Wistar rats. In addition, the extent of epimuscular myofascial force transmission between synergistic GA, SO, and PL, as well as between the calf muscles and antagonistic tibialis anterior (TA), was investigated. Active length-force curves of spastic GA and PL were narrower with a reduced maximal active force. In contrast, active length-force characteristics of spastic SO were similar to those of controls. In reference position (90° ankle and knee angle), higher resistance to ankle dorsiflexion and increased passive stiffness was found for the spastic calf muscle group. At optimum length, passive stiffness and passive force of spastic GA were decreased, whereas those of spastic SO were increased. No mechanical interaction between the calf muscles and TA was found. As GA was lengthened, force from SO and PL declined despite a constant muscle-tendon unit length of SO and PL. However, the extent of this interaction was not different in spastic rats. In conclusion, the effects of spasticity on length-force characteristics were muscle specific. The changes observed for GA and PL muscles are consistent with the changes in limb mechanics reported for human patients. Our results indicate that altered mechanics in spastic rats cannot be attributed to differences in mechanical interaction, but originate from individual muscular structures.

Dopamine as an anorectic neuromodulator in the cockroach Rhyparobia maderae

SUMMARY Insects, including cockroaches, self-select a balanced diet when faced with different nutrient choices. For self-selection to be carried out effectively, insects possess neuroregulatory systems to control their food intake. In the present study, we examined the role of the neurotransmitter dopamine (DA) in the feeding regulation of the Madeira cockroach (Rhyparobia maderae). When R. maderae nymphs were injected with 20 μl of 100 mmol l–1 DA, they showed an 83.3% reduction in sucrose intake and a 78.9% reduction in total intake compared with saline-injected controls. The DA agonist, 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene (6,7-ADTN) (100 mmol l–1 in 1 μl), caused a significant reduction in sucrose feeding, reducing feeding by 47.3% compared with saline-injected controls. Protein feeding was also significantly reduced by 6,7-ADTN to 62%. Rhyparobia maderae nymphs injected with the DA antagonist chlorpromazine (100 mmol l–1 in 1 μl) did not differ significantly from control nymphs in their feeding behavior. Interestingly, R. maderae nymphs injected with 2 μl or 5 μl chlorpromazine (100 mmol l–1) showed significantly increased mortality rates of 47.5% or 66.7%, respectively. The DA antagonist, spiperone (100 mmol l–1 in 1 μl), caused a significant feeding response, showing an increase in feeding in both sucrose (310.6%) and total intake (236.3%). Casein feeding in R. maderae nymphs was also elevated (70.8%) but this was not statistically significant. The experiments with DA, the DA agonist 6,7-ADTN and the DA antagonist spiperone strongly suggest that the neurotransmitter DA is involved in regulating feeding in the cockroach R. maderae.

Modeling capsule tissue growth around disk-shaped implants: a numerical and in vivo study

We propose a new mathematical model that describes the growth of fibrous tissue around rigid, disk-shaped implants. A solution methodology based on an efficient regularized iterative method is presented to calibrate the model from some measurements of the capsule tissue concentration. Numerical results obtained with synthetic data are presented to demonstrate the ability of the proposed solution methodology to determine the model parameters corresponding to a given implant. In addition, numerical results obtained with experimental data are presented to illustrate the validity of the proposed model.

Enhanced epileptogenic susceptibility in a genetic model of reactive synaptogenesis: The Spastic han-wistar rat

Our laboratory has been studying the spastic Han-Wistar (sHW) rat as a model of neuronal degeneration. Mutant sHW rats display a number of developmental abnormalities that eventually lead to hippocampal pyramidal cell death and synaptic reorganization starting around 30 days of age. The present study examined the contribution of hippocampal reorganization to the expression of seizures induced by systemic injections of kainic acid. Behavioral observations, EEG recordings and hippocampal Fos protein expression in these animals indicated that mutants develop paroxysmal discharges and seizures earlier than controls and the intensity of epileptic manifestations is greater. Kainate injections were lethal in 50% of mutants compared to only 5% of controls. Fos expression was increased approximately twofold in the mutant hippocampus, implicating abnormal excitation in this region. Additional studies in untreated animals indicated that GluR2 mRNA expression was significantly increased throughout the hippocampus in mutant animals, possibly contributing to the enhanced susceptibility to kainate treatment. These results confirm the role of synaptic reorganization in the increased propensity to develop epileptic discharges. Our data also underscore the usefulness of this natural model of cell degeneration and reactive synaptogenesis for understanding the mechanisms of neuronal hyperexcitability.

Validation of Acoustic Wave Induced Traumatic Brain Injury in Rats

Background: This study looked to validate the acoustic wave technology of the Storz-D-Actor that inflicted a consistent closed-head, traumatic brain injury (TBI) in rats. We studied a range of single pulse pressures administered to the rats and observed the resulting decline in motor skills and memory. Histology was observed to measure and confirm the injury insult. Methods: Four different acoustic wave pressures were studied using a single pulse: 0, 3.4, 4.2 and 5.0 bar (n = 10 rats per treatment group). The pulse was administered to the left frontal cortex. Rotarod tests were used to monitor the rats’ motor skills while the water maze test was used to monitor memory deficits. The rats were then sacrificed ten days post-treatment for histological analysis of TBI infarct size. Results: The behavioral tests showed that acoustic wave technology administered an effective insult causing significant decreases in motor abilities and memory. Histology showed dose-dependent damage to the cortex infarct areas only. Conclusions: This study illustrates that the Storz D-Actor effectively induces a repeatable TBI infarct, avoiding the invasive procedure of a craniotomy often used in TBI research.