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No / This paper begins by recalling that advances in neuroscience were used for hostile purposes, for example, in the development of lethal nerve gasses, in the last century, and it is argued that in the kinds of asymmetric warfare likely to characterize coming decades, such advances could again be utilized to develop novel weapons. The paper then suggests that the idea that the problem is that bioterrorists will immediately be able to design and use advanced biological and chemical weapons is misguided and that the real question is how the wholesale militarization of the life sciences can be prevented. It is in that context that the paper examines the dangers of misuse that could arise from some current developments in neuroscience. It is argued, for example, that benignly intended civil work on transcranial magnetic stimulation (TMS) and brain-computer interfaces (BCIs) has to be understood in the context of modern military interests in data collection and analysis from drones and the probable development of autonomously acting systems. The difficulties that such novel weapon-related developments will cause for our present understanding of morality and international law are reviewed, and finally, it is suggested that neuroscientists trying to adjust their concepts of responsible conduct in these circumstances will need the help of neuroethicists.

Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / While memory function in primates depends on the integrity of the medial temporal lobe, the contribution of the hippocampal formation (HF) independent of the overlying ventromedial temporal cortices, particularly the entorhinal (ENT) and parahippocampal (PHG) cortices, remains unclear. To address this issue we have prepared groups of rhesus monkeys with ibotenic acid lesions of the HF or aspiration lesions of the ENT or PHG cortices. We then administered behavioral tasks to assess the effects of these lesions relative to normal controls. To test recognition memory, the Delayed Non-Matching to Sample (DNMS) task and the Delayed Recognition Span Task (DRST) were administered. On DNMS, all groups were impaired on both acquisition and 2 and 10 minute delays. The DRST, administered in Spatial, Color and Object conditions, yielded slightly different results. On the Spatial condition, all groups were impaired on both unique and repeated trials of the task. On the Color condition, all groups were impaired on unique trials while only the HF group was impaired on repeated trials. On the Object condition, ENT and PHG groups were only impaired on unique trials, while the HF group was unimpaired. To assess associative memory, two choice reversals were administered in Spatial (SR) and Object (OR) modalities. On the SR task, The HF group was impaired on acquisition and the first of three reversal phases. The ENT group was impaired on all three reversals, and the PHG group was impaired on only the last. On the OR task, HF animals were impaired on all reversals, while ENT animals were impaired on the initial reversal and PHG animals on the last two. These results indicate that damage to the HF alone causes impairments in recognition, spatial processing and object reversal learning. They also indicate that ENT and PHG regions make unique contributions to memory processes as seen in additional impairments on DRST and the inability to perform spatial reversals. Thus impairments previously attributed to hippocampal damage in studies where the ENT and PHG cortices were removed in conjunction with the HF need to be reevaluated in view of additional contributions provided by these cortical regions. / 2999-01-01

Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / Neuroanatomical work has shown that the auditory system is different in different mammals, with primates and bats representing two extremes in this regard. It has been suggested that these differences are related to auditory localization. The present work examined auditory localization in several representative mammalian speciesa squirrel monkey, bat {Phyllostomus hastatus), albino rat and cat. A semi-naturalistic localization situation was used. The animal was placed in a wire cage located in a sound-deadened room. Two loudspeakers were located one on either side of the cage. Two response lavers were located in the front wall of the cage, flanking a liquid food dispenser. When tone bursts were presented from one of the loudspeakers, a response on the "correct" lever resulted in the delivery of a small amount of food to the animal. The left-hand lever was correct when the tone bursts were from the left-hand loudspeaker, the right-hand lever was correct when the tone bursts were from the right-hand loudspeaker. The percentage of correct responses on both levers was the measure of performance on the discrimination under a given set of conditions. [TRUNCATED] / 2999-01-01

A mathematical model for goal oriented learning in a network of neuron-like elements was developed. Using a mouse/goal box analogy, a simulation of a network with four elements was programmed in Turbo Pascal, Version 4.0 (Borland International) to test the model. Each location in the network corresponded to a particular network input. The output of the network consisted of one of four behaviors: forward, backward, left or right. The network successfully learned sequences of up to six movements in increasingly complex mazes. / Master of Science

Reversible hyperosmotic blood-brain barrier disruption (BBBD) has been used in pharmaceutical research as well as human medicine to enhance drug delivery across the blood-brain barrier. However a technique for repeatable BBBD in the canine has not been described. This study describes a repeatable technique for BBBD in the dog and evaluates the clinical and morphological effects of BBBD. Using fluoroscopic guidance, an arterial catheter was directed into the internal carotid artery via the femoral artery in ten dogs. BBBD was achieved in 5 dogs using 25% mannitol while 5 control dogs received only saline. Following recovery, dogs were monitored for clinical signs before a second, non-survival procedure was performed 2-3 weeks later. BBBD was estimated using CT densitometry as well as Evan's blue staining on post-mortem exam. Histopathological evaluation of the brain was performed on all dogs. Seven dogs completed the study. Two treatment dogs were lost after the first infusion with deteriorating neurologic function attributed to CNS edema and increased intracranial pressure. One control dog was lost due to vessel wall damage during catheterization. The remaining dogs exhibited only transient neurologic, ocular, and vasculature injury. Successful BBBD was demonstrated in all treatment dogs as evidenced by CT and Evan's blue staining. Histopathological evaluation revealed multifocal areas of infarction in all dogs indicating refinement of the technique is needed. This study shows that repeatable disruption the BBB in the dog is possible and opens the way for further investigations of BBBD using the dog as a model. / Master of Science

To test whether SKF 38393 could ontogenetically sensitize dopamine (DA) D$\sb1$ receptors and whether this sensitization would be associated with biochemical changes, intact and neonatal 6-hydroxydopamine (6-OHDA)-lesioned rats (200 $\mu$g i.c.v.) were treated daily from birth with SKF 38393 (3.0 mg/kg i.p. x 28 days) or its vehicle. In DA D$\sb1$ neonatally sensitized 6-OHDA rats, enhanced locomotor responses were observed with the first SKF 38393 challenge dose (3.0 mg/kg i.p.) at 6 weeks. This response increased further with weekly SKF 38393 treatments. Enhanced stereotyped behaviors were seen in both lesioned and sensitized rats at 8 weeks. There was no change in the percentage of high affinity D$\sb1$ sites in these groups of rats. Striatal mRNA levels for D$\sb1$ receptors were reduced in the lesioned rats, but restored to control level after treatments with SKF 38393 in adulthood. Basal, DA-, NaF- and forskolin-stimulated adenylate cyclase activities were similar among treatment groups. Striatal DA content was reduced ($>$99%), whereas serotonin (5-HT) content was elevated ($>$50%) in the 6-OHDA groups. To study possible interaction between DA and 5-HT systems, the effects of a series of 5-HT agents on the induction of oral activity were determined. The 5-HT$\sb{\rm 1C}$ receptor agonist, m-chlorophenylpiperazine (m-CPP), produced a marked increase in oral activity in 6-OHDA-lesioned rats. The respective 5-HT$\sb{\rm 1A}$ and 5-HT$\sb{\rm 1B}$ agonists, 8-OH-DPAT and CGS-12066B did not increase oral activity. The m-CPP-induced oral response in the lesioned rats was attenuated by mianserin, a 5-HT$\sb{\rm 1C}$ antagonist, but not by ketanserin or MDL-72222, 5-HT$\sb2$ and 5-HT$\sb3$ antagonists, respectively. Although the supersensitized oral response of lesioned rats to m-CPP was not attenuated by SCH 23390, the enhanced response of SKF 38393 was attenuated by mianserin. Additionally, mRNA levels for 5-HT$\sb{\rm 1C}$ receptor were not altered in both intact and lesioned rats. These findings demonstrate that ontogenetic treatments of neonatal 6-OHDA-lesioned rats with a D$\sb1$ agonist produce partial sensitization of DA D$\sb1$ receptors in adulthood without altered biochemical markers, and that this neonatal lesion is associated with both supersensitized DA D$\sb1$ and 5-HT$\sb{\rm 1C}$ receptors. Moreover, induction of oral activity by DA agonists is mediated via a serotonergic system.