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1
Khanna, Sanjay. "The hippocampus in nociception". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30685.
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Limbic structures, including the hippocampus, are thought to be involved in pain though not much is known of their neuronal responses to noxious stimuli. Experiments were therefore performed in lightly anaesthetized rats to determine the effect of noxious heat stimuli on the excitability of dorsal hippocampal field CA1 pyramidal neurones. A prolonged and substantial depression of the CA1 population spike was produced by a brief but intense noxious stimulus applied to the tail. This depression was temperature-dependent and habituated to subsequent noxious stimuli applied more than 1 hr later. In other animals, a similar depression and habituation was also obtained with noxious heat stimuli applied to the left hind paw. However, following this habituation of the hind paw, a persistent depression of the CA1 population spike was seen if the tail was exposed to a noxious heat stimulus.
The persistent depression was absent when noxious heat was applied in the presence of hippocampal theta rhythm. If, however, the hippocampal electroencephalographic ( EEG ) activity was in an irregular pattern at the time noxious heat was applied, a 4-6 Hz theta rhythm was produced along with the depression of the population spike. The latency and intensity of the reflex response was combined into a reflex-reaction score. There appeared to be a relationship between the reflex-reaction score and the duration of theta rhythm induced by different intensities of noxious heat stimuli but there was no habituation to these responses.
The CA1 population spike evoked either by ipsilateral or contralateral CA3 stimulation was similarly depressed following a noxious stimulus. Concomitantly, the persistent depression and habituation of the commissural CA1 population spike was also accompanied by similar changes in the corresponding dendritic field excitatory postsynaptic
potential ( EPSP ). However, the amplitude of the CA1 antidromic spike was increased in the majority of cases. These findings suggest that a presynaptically mediated decrease in synaptic transmission may account for the depression of the population spike and dendritic field EPSP.
There is evidence to suggest that the noxious stimulus-induced persistent depression of CA1 pyramidal cell synaptic excitability is due to a cholinergic projection from the medial septal-vertical limb of the diagonal band of Broca complex ( MS-VLDBB ). Thus, atropine sulphate ( 40 mg/kg, i.p. ) prevented the persistent depression of the CA1 population spike to a noxious stimulus. It also antagonized the septal tetanus-evoked, cholinergic mediated facilitation of the CA1 commissural population spike but had no effect on the corresponding paired-pulse facilitation. Atropine, applied iontophoretically to the cell body region antagonized the iontophoretic acetylcholine-induced facilitation of the CA1 population spike but not its depression to a noxious stimulus. On the other hand, apical dendritic application of atropine antagonized iontophoretic acetylcholine and noxious stimulus-induced depression of the CA1 dendritic field EPSP. However, such iontophoretic application of atropine had no effect on dendritically applied gamma aminobutyric acid ( GABA )-induced depression of the CA1 dendritic field EPSP. These results support the notion that acetylcholine release in the dendritic region of CA1 neurones is involved in the depression of synaptic excitability of these neurones evoked by a noxious stimulus.Pharmaceutical Sciences, Faculty of
Graduate
2
Cornish, S. "Hippocampal suspension grafts in the Kainic acid lesioned hippocampus of the rat". Thesis, University of Southampton, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384375.
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Armstrong, Beth Diane. "Hippocampus: seahorse; brain-structure; spatial map; concept". Thesis, Rhodes University, 2010. http://hdl.handle.net/10962/d1002224.
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Through an exploration of both sculptural and thought processes undertaken in making my Masters exhibition, ‘Hippocampus’, I unpack some possibilities, instabilities, and limitations inherent in representation and visual perception. This thesis explores the Hippocampus as image (seahorse) and concept (brain-structure involved in cognitive mapping of space). Looking at Gilles Deleuze’s writings on representation, I will expand on the notion of the map as being that which does not define and fix a structure or meaning, but rather is open, extendable and experimental. I explore the becoming, rather than the being, of image and concept. The emphasis here is on process, non-representation, and fluidity of meaning. This is supportive of my personal affirmation of the practice and process of art-making as research. I will refer to the graphic prints of Maurits Cornelis Escher as a means to elucidate a visual contextualization of my practical work, particularly with regard to the play with two- and three-dimensional space perception. Through precisely calculated ‘experiments’ that show up the partiality of our visual perception of space, Escher alludes to things that either cannot actually exist as spatial objects or do exist, but resist representation. Similarly I will explore how my own sculptures, although existing in space resist a fixed representation and suggest ideas of other spaces, non-spaces; an in-between space that does not pin itself down and become fixed to any particular image, idea, objector representation.
4
Wais, Peter Edward. "The roles of the hippocampus in recognition memory". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3315575.
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Thesis (Ph. D.)--University of California, San Diego, 2008.Title from first page of PDF file (viewed September 3, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 128-137).
5
Darling, Ryan Daniel. "HIPPOCAMPAL THETA-TRIGGERED CONDITIONING: ENHANCED RESPONSES IN HIPPOCAMPUS AND PREFRONTAL CORTEX". Connect to this document online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=miami1130446123.
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Thesis (M.A.)--Miami University, Dept. of Psychology, 2005.Title from first page of PDF document. Document formatted into pages; contains [1], v, 48 p. : ill. Includes bibliographical references (p. 16-20).
6
Weeden, Christy Samantha Star. "Neuroprotective Potential of Methamphetamine: Behavioral and Histological Analysis". Thesis, Montana State University, 2007. http://etd.lib.montana.edu/etd/2007/weeden/WeedenC0507.pdf.
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Stroke is a leading cause of death and ischemic stroke is the most common form. The deficits that follow ischemic stroke include memory and learning impairment. There are presently no treatments that can combat the effects of ischemia after the attack has occurred. Immediately following insult, locomotor activity increases in rodent models. The goal of the current research is to determine if methamphetamine administration following ischemic attack will have neuroprotective effects and prevent changes in locomotor behavior that are observed following insult. Ischemic insult was induced in gerbils by clamping the carotid arteries for 5 mins. Subjects in the sham surgical condition underwent similar surgical procedures, but the carotids were not clamped. Then, subjects were assigned randomly to saline or methamphetamine (5 mg/kg) injection groups. Drug treatment was administered within 2 mins of surgery. Measures of distance traveled, average speed, and number of line crossings were evaluated. Differences in levels of locomotion during the first and second halves of testing were also evaluated. Finally, sections containing the hippocampal CA1 region were rated on a 4-point scale for level of damage. Results show that subjects in the ischemic and saline condition traveled significantly further than those in the sham conditions and ischemic and methamphetamine condition. The speed of ischemic subjects treated with saline was significantly higher than ischemic subjects that received methamphetamine and sham conditions. Also, subjects in the ischemic and saline treatment group crossed more lines than sham and ischemic animals treated with methamphetamine. Analysis of cresyl violet-stained brain sections of ischemic animals treated with saline were rated as having less neuronal cell bodies in the CA 1 region. Ischemic and methamphetamine treated subjects' sections were similar to sham and saline treatment sections. These results suggest that methamphetamine, when injected after transient ischemic attack, may provide neuroprotection from damage that occurs to the CA1 region and prevent the impairments in locomotor behavior.
7
Gulbrandsen-MacDonald, Tine L., i University of Lethbridge Faculty of Arts and Science. "The role of the hippocampus and post-learning hippocampal activity in long-term consolidation of context memory". Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Neuroscience, c2011, 2011. http://hdl.handle.net/10133/2635.
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Sutherland, Sparks and Lehmann (2010) proposed a new theory of memory consolidation, termed Distributed Reinstatement Theory (DRT), where the hippocampus (HPC) is needed for initial encoding but some types of memories are established in non-HPC systems through post-learning HPC activity. An evaluation of the current methodology of temporary inactivation was conducted experimentally. By permanently implanting two bilateral guide cannulae in the HPC and infusing ropivacaine cellular activity could be reduced by 97%. Rats were trained in a context-fear paradigm. Six learning episodes distributed across three days made the memory resistant to HPC inactivation while three episodes did not. Blocking post-learning HPC activity following three of six training sessions failed to reduce the rat’s memory of the fearful context. These results fail to support DRT and indicate that one or more memory systems outside the HPC can acquire context memory without HPC post-event activity.x, 85 leaves : ill. ; 29 cm
8
May, Patrick B. Y. "Studies on the induction of short- and long-term synaptic potentiation in the hippocampus". Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26497.
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High frequency repetitive stimulation of an excitatory input in the hippocampus results in a post-tetanic potentiation (PTP) of short duration (about 3 min) that can be followed by a long-term synaptic potentiation (LTP) of the same excitatory input (Schwartzkroin and Wester, 1975; Andersen
et al., 1977). It has been reported that this tetanus-induced LTP cannot be
elicited in a Ca²⁺-free medium and is therefore a Ca²⁺-dependent process
(Dunwiddie et al., 1978; Dunwiddie and Lynch, 1979; Wigstrӧm et al., 1979).
Whether the induction of LTP is directly dependent upon Ca²⁺, or whether, Ca²⁺ is required because synaptic transmission is needed to initiate
certain postsynaptic process(es) (a postsynaptic depolarization, for
instance) leading to LTP, is unknown. Recent studies from this laboratory
showed that both short-term potentiation (STP; with a duration resembling
PTP) and LTP can be associatively induced if activation of a test input
co-occured with either a tetanic stimulation of separate excitatory inputs
or a sufficient depolarization of the postsynaptic neurone (Sastry et al.,
1985). In this study, experiments were performed to investigate (1) whether
associative STP could be induced when activation of the test input preceded
or followed the onset of the conditioning train and (2) whether LTP could be
induced in the absence of Ca²⁺ in the extracellular medium if sufficient depolarizations of the presynaptic terminals and postsynaptic neurones were provided.
All experiments were performed using the transversely sectioned hippocampal slice preparation. Test stimuli were delivered via an electrode located in the stratum radiatum while the conditioning tetani (100 Hz, 10 pulses per train) were delivered via another electrode located in the recorded from the apical dendritic area of CA₁ neurones. After the initial control stimulation period, 5 conditioning tetani were given at a frequency of 0.2 Hz. The test stimuli either preceded (-) or followed ( + ) the onset of each conditioning train by 0 to 100 ms. When the test stimulus followed the onset of each conditioning train, there was significant STP of the test EPSP up to a conditioning-test interval of +80 ms. When the test stimulus preceded the onset of each conditioning train, there was significant STP of the test EPSP up to a conditioning-test interval of -50 ms. Conditioning tetani that were given without co-activation of the test input resulted in a subsequent depression of the test EPSP. It is suggested that either the test or the conditioning input can initiate some postsynaptic process(es) which can in turn affect the activated presynaptic terminals to increase transmitter release or alter the subsynaptic dendritic properties.
For studying the possibility of the induction of LTP in the absence of
Ca²⁺ in the extracellular medium, population EPSPs were recorded from
apical dendritic area of CA₁ neurones in response to stratum radiatum
stimulation. After the control stimulation period, slices were exposed
either to Ca²⁺-containing or Ca²⁺-free (with Mn²⁺ and Mg²⁺ replacing
Ca²⁺) medium, with the concentration of KC1 at 10 to 80 mM. Long-term
potentiation of the population EPSPs was observed following the exposure to
high K⁺ in Ca²⁺-free media. Following a brief period of potentiation
initially, population EPSPs often exhibited a tendency toward depression
after exposure to high K⁺ in Ca²⁺-containing media. LTP induced by high
K⁺ in Ca²⁺-free medium could also be observed when a fixed number of axons were being activated, indicating that a recruitment of presynaptic fibres cannot entirely account for the potentiation. LTP of the depolarizing commands were paired with activation of the stratum radiatum
while the slices were exposed to Ca²⁺ -free medium (normal concentration of
KC1). These results suggest that extracellular Ca²⁺, synaptic transmission and thus subsynaptic receptor activation are not necessary for the induction of LTP as long as sufficient depolarizations of the presynaptic terminals and postsynaptic neurones are provided.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
9
Yim, Tonia Tan-Ling, i University of Lethbridge Faculty of Arts and Science. "Multiple-object memory requires the hippocampus". Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2007, 2007. http://hdl.handle.net/10133/678.
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This thesis investigates the role of the hippocampus in object memory. Currently,
the role of the hippocampus in object recognition is unclear, with some studies
demonstrating a delay-dependent impairment after hippocampal damage, others showing
no impairment. The present thesis used the novel object recognition task and its variants
to investigate various types of object memory in hippocampal lesion rats. In the first
study, impairments were observed in discriminating object order and associating objects
with contexts, while no impairment was observed in novel object recognition. In the
second study, it was found that encountering another object shortly prior to or after
encountering a target object impairs the recognition of the target object. In a control
procedure, encountering a novel context either shortly before or after encountering the
target object did not impair object recognition. In sum, in the absence of the hippocampus,
object memory becomes vulnerable to interference, rendering rats unable to discern
memories of multiple objects. The present thesis concludes that the hippocampus
discriminates multiple objects via pattern separation. A stimulus-response model relating
the role of the hippocampus to object memory is proposed.vii, 150 leaves : ill. ; 29 cm. --
10
Hochman, Daryl W. "Chloride-cotransport modulation of synchronous epileptiform discharge /". Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/10326.
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Thorne, Beverley Ann. "Nicotinic regulation of acetylcholine release from rat brain hippocampus". Thesis, University of Bath, 1990. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237086.
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Manns, Joseph Robert. "Episodic memory, semantic memory, and the human hippocampus /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC IP addresses, 2002. http://wwwlib.umi.com/cr/ucsd/fullcit?p3061654.
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Bellace, Matthew John Williams J. Michael. "Activation of the hippocampus during emotional learning /". Philadelphia, Pa. : Drexel University, 2005. http://dspace.library.drexel.edu/handle/1860/480.
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Tranberg, Mattias. "N-acetylaspartate in brain : studies on efflux and function /". Göteborg : Institute of Neuroscience and Physiology, Department of Physiology, The Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/718.
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Lubenov, Evgueniy V. "Phase-locking of neurons in the hippocampus and the medial prefrontal cortex of the rat to the hippocampal theta rhythm". Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/35700.
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Thesis (Ph. D. in Neuroscience)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2005.Includes bibliographical references (p. 53-59).
The interactions between cortical and hippocampal circuits are critical for memory formation, yet their basic organization at the neuronal network level is not well understood. Here we investigate the timing relationships between neuronal activity in the medial prefrontal cortex of freely behaving rats and the hippocampal theta rhythm. We demonstrate that a significant portion of prefrontal neurons are phase-locked to the hippocampal theta rhythm and we compare the phase-locking properties of prefrontal and hippocampal cells. We also show that prefrontal neurons phase-lock best to theta oscillations delayed by approximately 50 ms and confirm this hippocampo-prefrontal directionality and timing at the level of correlations between single cells. Finally we demonstrate that phase-locking of prefrontal cells is predicted by the presence of significant correlations with hippocampal cells at positive delays up to 150 ms, suggesting that direct hippocampal input has an important contribution to the observed prefrontal phase-locking. The theta entrained activity across cortico-hippocampal circuits described here may be important for gating information flow and guiding the plastic changes that are believed to underlie the storage of information across these networks.
by Evgueniy V. Lubenov.
Ph.D.in Neuroscience
16
Meighan, Peter Conklin. "The antithetical effects of matrix metalloproteinase inhibition on hippocampal plasticity between young-adult and aged-adult rodents". Online access for everyone, 2006. http://www.dissertations.wsu.edu/Dissertations/Fall2006/p_meighan_102406.pdf.
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McNeill, Damon Lee. "Hippocampal damage and novelty preference in the ischemic gerbil dissociating object and arrangement memory /". Thesis, Montana State University, 2007. http://etd.lib.montana.edu/etd/2007/mcneill/McNeillD0507.pdf.
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The most insidious consequences of transient ischemia are its effect on the hippocampus and the memory systems it serves. The novelty preference test is a direct measure of memory function and has been used in the rat and primate animal models. The gerbil animal model has been used extensively to study the mechanism of ischemic brain damage; however, the novelty preference paradigm has not been used to study memory impairment in this species. In addition, the novelty preference paradigm has not been tested with models of ischemia. In the present experiment, Mongolian gerbils were tested in two different types of novelty-preference tasks (Object and Arrangement) following either ischemic insult or a sham control surgery. There was no significant difference in preference for novel objects between ischemic and sham groups. However, ischemic gerbils showed a significant decrease in preference for novel arrangements relative to shams. These findings are consistent with previous studies that have demonstrated the dissociation between object and arrangement memory using rats and primates. The results of the present study indicate that the novelty preference paradigm can be successfully used with the gerbil model for ischemic brain damage to study memory impairment and neuroprotective agents.
18
Klempin, Friederike Claudia. "Adult brain plasticity". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15844.
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Der Hippocampus ist eine von zwei Gehirnregionen, in der zeitlebens kontinuierlich neue Nervenzellen gebildet werden. Er spielt eine wichtige Rolle bei der Gedächtniskonsolidierung und wird mit der funktionellen Entstehung neurodegenerativer Erkrankungen in Verbindung gebracht. Strukturveränderungen im erwachsenen Gehirn, die mit einer Depression einhergehen, sind laut Literatur auf einen geringen Serotoninspiegel und reduzierte hippocampale Neurogenese zurückzuführen. Selektive Serotonin-Wiederaufnahmehemmer (SSRI) erhöhen die Serotoninkonzentration im synaptischen Spalt und üben einen positiven Effekt auf die adulte Neurogenese aus. In der vorliegenden Arbeit wird untersucht, wie Veränderungen in der Serotonin (5-HT)-Neurotransmission durch einmalige oder chronische Gaben von Fluoxetin und speziellen Agonisten und Antagonisten für die Serotoninrezeptoren 5-HT1a und 5-HT2 in der erwachsenen Maus die Proliferation und Differenzierung von neugebildeten Nervenzellen im Gyrus dentatus beeinflussen. Die Ergebnisse zeigen, dass ein konträres Agieren beider Rezeptoren zu einem ausgewogenen Serotoninspiegel führt. 5-HT1a- und 5-HT2c-Rezeptoren haben einen Einfluss auf das Überleben neugebildeter Nervenzellen, wobei sie unterschiedliche Entwicklungsstadien innerhalb der adulten Neurogenese kontrollieren. Die vorliegende Arbeit bekräftigt außerdem, dass die chronische Gabe von Fluoxetin die adulte Neurogenese steigert.The hippocampus as one region with ongoing neurogenesis throughout life contributes to the formation of long-term memory and has also been implicated in the pathology of major depression. Studies suggest that depression might be due to decreased levels of serotonin and reduced neurogenesis in the adult brain and that the beneficial effects of selective serotonin reuptake inhibitors would require adult hippocampal neurogenesis. Here, I investigated how modulation of serotonergic neurotransmission by acute and chronic treatment with the antidepressant fluoxetine, and selective serotonin receptor agonists and antagonists in adult mice influences precursor cell activity during development. I focused on 5-HT1a and 5-HT2 receptors as major mediators of serotonin action. The present findings suggest that an opposed action of 5-HT1a and 5-HT2c receptor subtypes result in a balanced regulation of serotonin levels in the dentate gyrus. Both receptors differentially affect intermediate cell stages in adult hippocampal neurogenesis and play an important role in the survival of newly generated neurons. Furthermore, this study confirms that chronic fluoxetine treatment increases adult neurogenesis. In conclusion, the latency of onset of fluoxetine action can be explained by a balanced interplay of 5-HT1a and 5-HT2c receptor subtypes.
19
Hannay, Robert Timo. "Quantal analysis of synaptic plasticity in the rat hippocampus". Thesis, University of Oxford, 1994. http://ora.ox.ac.uk/objects/uuid:2c03ced6-548b-4798-93f1-71ba54818b73.
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Davidson, Thomas James Damon Cheakamus. "Replay of memories of extended behavior in the rat hippocampus". Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/54622.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2009.Cataloged from PDF version of thesis.
Includes bibliographical references.
The hippocampus is a highly conserved structure in the medial temporal lobe of the brain that is known to be critical for spatial learning in rodents, and spatial and episodic memory in humans. During pauses in exploration, ensembles of place cells in the rat hippocampus re-express firing sequences corresponding to recent spatial experience. Such 'replay' co-occurs with ripple events: short-lasting (~50-120 ms), high frequency (-200 Hz) oscillations that are associated with increased hippocampal-cortical communication. In previous studies, rats explored small environments, and replay was found to be anchored to the rat's current location, and compressed in time such that replay of the complete environment occurred during a single ripple event. In this thesis, we develop a probabilistic neural decoding approach that allows us to show that firing sequences corresponding to long runs through a large environment are replayed with high fidelity (in both forward and reverse order). We show that such replay can begin at remote locations on the track, and proceeds at a characteristic virtual speed of -8 m/s. Replay remains coherent across trains of sharp wave-ripple events. These results suggest that extended replay is composed of chains of shorter subsequences, which may reflect a strategy for the storage and flexible expression of memories of prolonged experience. We discuss the evidence for the operation of similar mechanisms in humans.
by Thomas James Davidson.
Ph.D.
21
Mody, Istvan. "Calcium regulation in long-term changes of neuronal excitability in the hippocampal formation". Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25929.
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The regulation of calcium (Ca²⁺) was examined during long-term changes of neuronal excitability in the mammalian CNS. The preparations under investigation included the kindling model of epilepsy, a genetic form of epilepsy and long-term potentiation (LTP) of neuronal activity. The study also includes a discussion of the possible roles of a neuron-specific calcium-binding protein (CaBP). The findings are summarized as follows:
1) The distribution of CaBP was determined in cortical areas of the rat using a specific radioimmunoassay. The protein was found to have an unequal distribution in various cortical areas with preponderence in ventral structures.
2) Extending previous studies on the role of CaBP in kindling-induced epilepsy, its decline was correlated to the number of evoked afterdischarges (AD's) during the process of kindling.
3) Marked changes in CaBP levels were also found in the brains of the epileptic strain of mice (El). The hippocampal formation and the dorsal occipital cortex contained significantly lower CaBP than the control (CF-1) strain. The induction of seizures further decreased the levels of CaBP in the El mice. These findings are indicative of a possible genetic impairment of neuronal Ca²⁺ homeostasis in the El strain. 4) The levels of total hippocampal Ca²⁺ and Zn²⁺ were measured by atomic absorption spectrophotometry in control and commissural-kindled animals. While no change was found in the total Ca²⁺ content of the region, hippocampal Zn²⁺ of kindled preparations was found to be significantly elevated.
5) To measure Ca²⁺ -homeostasis, the kinetic analysis of ⁴⁵Ca uptake curves was undertaken in the in vitro hippocampus. This technique was found to be a valid method for assessment of Ca²⁺-regulation in the CNS under both physiological and pathophysiological conditions. The effect of various extracellular Ca²⁺ concentrations, 2,3-dinitrophenol (DNP), calcitonin, nifedipine and 3-isobutyl-1-methylxanthine (IBMX) on ⁴⁵Ca uptake curves was examined in order to identify the two exchangeable Ca²⁺ pools derived through kinetic analysis.
6) The kinetic analysis of ⁴⁵Ca uptake curves revealed that Ca²⁺-regulation of the hippocampus is impaired following amygdala- and commissural kindling. The changes reflect an enhancement of a Ca²⁺ pool that includes free cytosolic Ca²⁺ and a concomitant decrease in the amount of buffered calcium probably as a result in the decrease of hippocampal CaBP levels.
7) A novel form of long-term potentiation (LTP) of neuronal activity in the CA1 region of the hippocampus is described. Perfusion of 100 uM of IBMX in the hippocampal slice preparation induced a long lasting increase in the amplitude of the stratum radiatum evoked population spike and EPSP responses with changes in synaptic efficacy as indicated by the altered input/output relationships. Intracellular correlates of IBMX-induced LTP included lowering of synaptic threshold and enhancement of the rate of rise of the EPSP with no alterations in the passive membrane characteristics of CA1 pyramidal neurons. The fact that IBMX was able to exert its effect even in the presence of the calcium-blocker cation Co²⁺, taken together with the drug's action on hippocampal exchangeable Ca²⁺, raises the possibility that the Ca²⁺ necessary for induction of LTP may be derived from an intraneuronal storage site.
These studies indicate the significance of intracellular Ca²⁺ -regulatory mechanisms in long-term changes of neuronal excitability which occur in experimental models of epilepsy and long-term potentiation.Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
22
Driscoll, Ira, i University of Lethbridge Faculty of Arts and Science. "The aging hippocampus : a multilevel analysis in the rat". Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2005, 2005. http://hdl.handle.net/10133/12.
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The purpose of the current thesis was twofold: (1) to examine various factors that might be contributing to age-related learning and memory deficits specifically related to the hippocampus, and (2) to validate our rat model of aging, employing a multilevel analysis. We found age-related deficits on both spatial and non-spatial hippocampus-dependent taks that were accompanied by structural alterations observed in vivo (volune, but not neuronal metabolic function) and post mortem (neuronal density and neurogenesis, but not synaptic or mitochondrial density). Furthermore, our results suggest that the observed hippocampal structural changes, named decreased volume and neurogenesis, predict learning and memory deficits, and both can be accounted for by neurogenic reduction. In addition, the above-mentioned pattern of age-related deficits closely resembles that seen in humans, suggesting the present rat version of aging to be a very useful model for investigating hippocampal aging in humans.iii, 236 leaves : ill. (some col.) ; 29 cm.
23
Krebs, Desiree L. "Glucose modulation of the septo-hippocampal system implications for memory /". unrestricted, 2006. http://etd.gsu.edu/theses/available/etd-09272006-142645/.
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Thesis (Ph. D.)--Georgia State University, 2006.Marise B. Parent, committee chair; Timothy J. Bartness, Kim L. Huhman, Kyle J. Frantz, committee members. Electronic text (352 p. : ill.)) : digital, PDF file. Description based on contents viewed July 12, 2007. Includes bibliographical references (p. 307-352).
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Adams, Beth Chick. "Kindling and activation induced hippocampal plasticity /". *McMaster only, 1998.
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Cham, Wai-chung, i 湛偉聰. "The role of heparanase in synaptic plasticity at the hippocampus". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B46089780.
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Yotter, Rachel A. "A network model of the hippocampus /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5887.
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Mahmoud, Ghada Saad Zaglool Ahmed. "Mechanisms of growth hormone enhancement of excitatory synaptic transmission in hippocampus /". Huntington, WV : [Marshall University Libraries], 2005. http://www.marshall.edu/etd/descript.asp?ref=532.
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Theses (Ph. D.)--Marshall University, 2005.Title from document title page. Includes abstract. Document formatted into pages: contains xiii, 156 pages including illustrations. Bibliography: p. 118-156.
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Koene, Randal A. "Functional requirements determine relevant ingredients to model for on-line acquisition of context dependent memory". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85561.
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Biophysical simulations of memory must choose which aspects of known neurophysiology and neuroanatomy to model. Relevant aspects were constrained by functional requirements determined for on-line acquisition in context dependent memory, memory that is retrieved by contextual cues. In an on-line task, the protocol of data presentation and the tunes at which encoding or retrieval in memory is needed are not predetermined. A sequence of neuronal spike patterns representing items may be presented only once. Yet, episodic memory of the sequence immediately encodes the temporal context of familiar items, a process known to depend on hippocampal function. For this, interference caused by overlapping spike patterns must be avoided, a requirement that suggested the relevance of coincidental spiking. Overlap in the input to the hippocampus was reduced by recruiting such spikes in a model of encoding in dentate gyrus. Durable encoding is required in the hippocampus, since hippocampal damage can cause retrograde amnesia in context dependent memory that spans years. Long-lasting synaptic changes involved modeling relevant neurophysiology concerning protein production elicited by the spaced reactivation of spike patterns. The likelihood of reactivation was increased by the well-known process of long-term potentiation of synaptic transmission. Such potentiation is elicited when a presynaptic spike precedes a postsynaptic spike within a specific time window repeatedly. The intervals in a sequence of spike patterns must be compressed and the sequence repeated, requirements that were achieved with a model of short-term memory based on persistent spiking. Retrieval may be concurrent with these encoding processes due to effects of different phases of a brain rhythm at theta frequency (3-12 Hz) that modulate transmission and plasticity. A model of short-term memory by Lisman and Idiart (Science 267:1512-15), extended by Jensen et al. (Learning and Memory 3:243
29
Stoney, Patrick Niall. "The roles of Pax6 in neural precursor migration and axon guidance". Thesis, University of Aberdeen, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=92509.
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The ability of migrating neurons and growth cones to navigate through their environment is crucial for the correct development of the brain. Cells and growth cones may be guided by electrical, chemical or topographical cues in their environment. Pax6 is a transcription factor vital for brain development. Pax6-/- mutant mice die perinatally with defects in neuronal proliferation and differentiation, cortical cell migration and axon guidance, yet it is not clear which guidance cues Pax6-/- mutant neurons fail to interpret. Dissociated cultured cells were used to study the cell-autonomous effects of Pax6 mutation on guidance of growth cones and migrating neural precursors by environmental cues. Neurites from mouse embryonic cortical neurons aligned perpendicular to 1 μm-wide, 130 nm-deep substratum grooves. Pax6-/- mutation abolished contact-mediated neurite guidance by these grooves. Laminin induced a switch from perpendicular to parallel alignment to grooves, via a β1 integrin-independent mechanism. Blocking cAMP signalling abolished perpendicular alignment to polylysine-coated grooves, but enhanced parallel alignment to laminin-coated grooves. Pax6 null mutation or overexpression also caused specific defects in contact-guided migration by cortical cells. An electric field applied to E16.5 cortical neurons increased the frequency of extension of neurites aligned perpendicular to the field axis. Pax6-/- mutant cells responded to an electric field with reduced anodal extension, but no significant increase in perpendicular neurite extension. Electrical cues were prioritised over topographical cues when presented in combination. Taken together, data suggest that Pax6 mutant cortical cells do not completely lack the ability to detect extracellular guidance cues, but they respond differently to wild-type cells. In combination with other defects identified in the cortex, this may contribute to the cell migration and axon guidance phenotypes in the brain of the Pax6-/- embryo. This study also identified novel Pax6 expression in the trigeminal ganglion, where it may regulate axon guidance and neurogenesis.
30
Foggetti, Angelica. "Anatomical and functional study of parvalbumin-positive interneurons in the hippocampal formation". Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=227103.
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It has long been acknowledged that inhibitory interneurons play a crucial role in regulating the input-output functions of principal cells in the hippocampus. The investigations we conducted focus on one specific population of interneurons, expressing the protein parvalbumin. The thesis describes three different studies, aimed to characterize anatomical and functional aspects of parvalbumin positive interneurons in the mouse hippocampal formation. The first study examines long-range projections of these neurons from CA1 and subiculum to distant regions of the brain, finding potential targets mainly in septal, thalamic and hypothalamic areas. The second study investigates the role of parvalbumin-positive interneurons of the dentate gyrus in spatial memory. Behavioural experiments with radial arm and Morris water maze have been carried out to understand how these GABAergic interneurons regulate information flow during reference and working memory. Finally, a third study describes basic anatomical features of parvalbuminpositive dendritic spines in the dentate gyrus. Their characteristics have been widely studied in principal neurons but little is known about spines in interneurons. Here I show a peculiar distribution of spines on apical dendrites of these cells, with a predominant localization within the inner third of the molecular layer. All studies utilized a combination of transgenic Cre-expressing mice and Creactivatable AAVs. For the first and third study AAV-based neuronal labeling was applied to visualize neurons, including their projections and their spines, respectively, through expression of fluorescent proteins. For the second study instead two genetic tools have been used in order to disrupt the neurotransmission from parvalbuminpositive interneurons and examine the effects on behavioral task performance.
31
Harrison, Elaine. "Morphological correlates of synaptic plasticity after long term potentiation in the rat hippocampus". n.p, 2000. http://library7.open.ac.uk/abstracts/page.php?thesisid=44.
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Murtha, Susan (Susan J. E. ). Carleton University Dissertation Psychology. "Neurotoxin induced lesions of acetylcholine and Serotonin afferents to the hippocampus; mnemonic, neurochemical, and histopathological effects". Ottawa, 1993.
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Kimonides, Victoria G. "The neuroprotective role of dehydroepiandrosterone (DHEA) on neurotoxicity in the hippocampus". Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265963.
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Siegle, Joshua H. (Joshua Hangman). "Causal evidence for the behavioral impact of oscillations in neocortex and hippocampus". Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/95857.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2014.Cataloged from PDF version of thesis.
Includes bibliographical references.
Neuroscientists hold widely divergent opinions on the behavioral relevance of oscillatory brain states. Some consider them to be a side effect of anatomical connectivity, with little or no role in guiding action. Others view them as a fundamental feature of the network states that underlie perception and cognition. In this thesis, I take a systematic approach to studying two of the most prominent types of oscillations,'gamma rhythms in the neocortex (30-80 Hz) and theta rhythms in the hippocampus (4-12 Hz). In both cases, I use light-gated ion channels to manipulate spike activity on a cycle-by-cycle basis in awake, behaving mice. By rhythmically stimulating fast-spiking interneurons in somatosensory cortex, I can emulate the activity patterns that define gamma oscillations under natural conditions. Emulating gamma enhances the detection of threshold-level vibrissae deflections, analogous to the behavioral effects of shifting attention. By triggering stimulation of fast-spiking interneurons in the hippocampus on peaks and troughs of endogenous rhythms, I can reduce spike activity at specific phases of theta. In the context of a spatial navigation task, I find that the ability of inhibition to enhance decision-making accuracy depends on both the theta phase and the task segment in which it occurs. Both of these experiments provide novel causal evidence for the behavioral impact of oscillations, which offers a much more compelling argument for their utility than traditional correlative measures. Finally, I present a new platform for extracellular electrophysiology. This platform, called Open Ephys, makes the closed-loop experiments that are ideal for studying oscillations accessible to a wider audience.
by Joshua H. Siegle.
Ph. D.
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MacPherson, Cameron Ross. "Transcriptional Regulatory Networks in the Mouse Hippocampus". Thesis, University of the Western Cape, 2007. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_1683_1259931126.
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This study utilized large-scale gene expression data to define the regulatory networks of genes expressing in the hippocampus to which multiple disease pathologies may be associated. Specific aims were: ident i fy key regulatory transcription factors (TFs) responsible for observed gene expression patterns, reconstruct transcription regulatory networks, and prioritize likely TFs responsible for anatomically restricted gene expression. Most of the analysis was restricted to the CA3 sub-region of Ammon&rsquo
s horn within the hippocampus. We identified 155 core genes expressing throughout the CA3 sub-region and predicted corresponding TF binding site (TFBS) distributions. Our analysis shows plausible transcription regulatory networks for twelve clusters of co-expressed genes. We demonstrate the validity of the predictions by re-clustering genes based on TFBS distributions and found that genes tend to be correctly assigned to groups of previously identified co-expressing genes with sensitivity of 67.74% and positive predictive value of 100%. Taken together, this study represents one of the first to merge anatomical architecture, expression profiles and transcription regulatory potential on such a large scale in hippocampal sub-anatomy.
36
Sparks, Fraser T. "Interactions of the hippocampus and non-hippocampal long-term memory systems during learning, remembering, and over time". Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Neuroscience, c2012, 2012. http://hdl.handle.net/10133/3116.
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The hippocampus and non-hippocampal long-term memory systems each have the capacity
to learn and express contextual fear memory. How these systems interact during learning
and remembering revolves around hippocampal mediated interference, where the hippocampus
dominates for both the acquisition and expression of long-term memory. Hippocampal
interference during learning can be overcome by modifying learning parameters
such that learning is distributed across multiple independent sessions. The standard view of
the role of the hippocampus in long-term memory retrieval is that it is temporally limited,
where recently acquired memory is dependent on hippocampal function though as a memory
ages, dependency is transferred to other memory systems by a process called systems
consolidation. Distributed training demonstrates that learning parameters create a memory
that is resistant to hippocampal damage. We find little evidence to support temporally based
systems consolidation, and present data that supports the view that if the hippocampus is
initially involved in learning a memory, it will always be necessary for accurate retrieval
of that memory. A critical assessment of the rat literature revealed that initial memory
strength, and/or lesion techniques might be responsible for the few studies that report temporally
graded retrograde amnesia using contextual fear conditioning. Our experiments
designed to directly test these possibilities resulted in flat gradients, providing further evidence
that the hippocampus plays a permanent role in long-term memory retrieval. We
propose and assess alternatives to the standard model and conclude that a dual store model
is most parsimonious within the presented experiments and related literature. Interactions
of the hippocampus and non-hippocampal systems take place at the time of learning and
remembering, and are persistent over time.xvi, 161 leaves : ill. (some col.) ; 29 cm
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Oliver, Michael W. "Electrophysiological properties of the hippocampal formation in rat : an in vitro study". Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/27503.
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The electrophysiological properties of dentate granule cells and hippocampal pyramidal neurons were examined with extracellular and intracellular recording techniques in the hippocampal slice.
Intracellular analysis revealed that there may exist two populations of granule cells distinguishable by the presence or absence of non-linear current-voltage (I-V) membrane properties (anomalous rectification, AR). The granule cells exhibiting AR also maintained greater resting membrane potentials and action potential (AP) amplitude values. The membrane input resistance (Rn) and time constant (Tc) measurements were similar between the populations in response to hyperpolarizing current injection, but granule cells displaying AR had significantly higher Rn and Tc values in response to depolarizing pulses. Both groups also responded to maintained depolarizing current injection with repetitive AP discharges; however, this response accommodated. Upon termination of the depolarizing current injection, an afterhyperpolarization (AHP) resulted, the amplitude of which appeared to depend on the duration of the depolarizing pulse and not on the number of APs generated during the pulse. Stimulation of either the lateral (LPP) or medial (MPP) perforant paths evoked a monosynaptic EPSP followed by a depolarizing afterpotential (DAP) and a long
afterhyperpolarization (LHP). In contrast, antidromic stimulation elicited a depolarizing-IPSP (D-IPSP) and a LHP. Both the DAP and D-IPSP were reversed by membrane depolarization, whereas, the LHP was inverted by membrane hyperpolarization. In all cases, however, the EPSP could not be inverted. Afterpotentials were associated with an increase in conductance, but the change accompanying the LHP was less than the DAP and D-IPSP. In addition, by reducing the [Ca]₀ and increasing the [Mg]₀, the DAP was attenuated and the LHP eliminated. Similar results were also obtained with the GABAB agonist, baclofen.
Paired pulse stimulation of either the LPP or MPP resulted in the potentiation of the intracellular EPSP at condition-test (C-T) intervals less than 100 ms; however, simultaneous extracellular records from the granule cell layer (GCL) illustrated depression of the EPSP. The discrepancy between the extra- and intracellular recordings was shown to be related to the presence of the DAP. In addition, the MPP evoked test EPSP at C-T intervals greater than 150 ms exhibited inhibition regardless of whether it was recorded inside or outside the granule cell and this EPSP depression was partially due to the granule cell LHP. The LPP evoked test EPSP potentiated at all C-T intervals less than 1s when recorded from the outer molecular layer (OML) but was inhibited at both the GCL and intracellular recording sites. These data confirmed that postsynaptic processes contribute to the short-term alterations observed with paired pulse stimulation.
The typical inhibition-potentiation-inhibition sequence of the perforant path (PP) evoked population spike (PS) was noted at C-T intervals of 20, 80 and 400 ms, respectively. The inhibition of the PS at 20 ms was abolished with perfusion of the GABA antagonist, bicuculline. In contrast, the PS inhibition at 400ms was unaffected by this treatment but was slightly attenuated by the gKca antagonist TEA. A number of factors appeared to contribute to the potentiation of the PS: 1) reduction in AP threshold; 2) the presence of the DAP; and 3) extrasynaptic events.
In addition to the PS data from normal tissue, hippocampal slices from chronically kindled rats exhibited depression of the PS at all C-T intervals tested. This augmentation of inhibition was dependent on the presence of hippocampal afterdischarges but not on motor seizures. Perfusing the kindled slices with either bicuculline or lowered [Cl]₀ did not markedly reverse the enhanced inhibition at C-T intervals which displayed dramatic facilitation in normal slices. Intracellular recordings of granule cells obtained from kindled slices also exhibited an increase in the Rn and Tc. Both the alterations in inhibition and membrane characteristics appear to be localized to.the granule cells, since these changes were not observed in CA1 pyramidal neurons.
These data indicate that short-term and long-term alterations in granule cell neuronal excitability are partially due to changes in the postsynaptic membrane.Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
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Chirwa, Sanika Samuel. "Studies on the asynchronous synaptic responses and endogenous potentiating substances of neurotransmission in the hippocampus". Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28641.
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In the hippocampus, transient tetanic stimulations of inputs, or brief simultaneous pairings of conditioning intracellular postsynaptic depolarizations
with activated presynaptic afferents at low stimulation frequencies, result in input specific long-term potentiation (LTP) of synaptic transmission.
LTP lasts for hours in vitro, or weeks in vivo, and it is thought to be involved in memory and learning. Experimental evidence in the literature suggests that postsynaptic mechanisms mediate LTP induction, whereas presynaptic
mechanisms are involved in its maintenance. Since LTP is thought to be generated by postsynaptic mechanisms and to be subsequently maintained by presynaptic processes, this suggests the presence of feedback interactions during LTP development, however, the experimental evidence for such interactions
is presently not available. Consequently, the present studies were conducted to examine possible feedback interactions between postsynaptic and presynaptic elements in the hippocampus. Furthermore, the experiments tested the hypothesis that substances released during tetanic stimulations caused the release of endogenous substances that interacted with activated afferents resulting in alterations in presynaptic functions and LTP production.
Experiments were conducted using transversely sectioned guinea pig hippocampal slices. Briefly, physiological medium containing 3.5 mNi Ba++ and 0.5 mM Ca (denoted as Ba medium) was used to induce the asynchronous
release of transmitters, observed as evoked miniature EPSPs (minEPSPs) in CA1b neurons after stimulation of the stratum radiatum. During transient Ba++ applications, short bursts of evoked minEPSPs were observed following stimulations of the stratum radiatum or conditioning depolarizing current injections into CA1b neurons. Moreover, the frequencies
of minEPSPs were significantly increased immediately after simultaneous stimulations of the stratum radiatum and conditioning depolarizing current injections into CA1b neurons. Significant increases in the frequencies of evoked minEPSPs were also observed during LTP induced by tetanic stimulations.
The above increases in the frequencies of evoked minEPSPs were attributed, in part, to presynaptic changes resulting in increases in transmitters
released. However, a thorough quanta! analysis is requirea to substantiate this conclusion.
In order to determine whether any substances released during tetanic stimulations were involved in the mooulation of presynaptic functions and induction of LTP, samples were collected from guinea pig hippocampus and rabbit neocortex. It was found that samples that were collected during tetanic stimulations of the guinea pig hippocampus in vivo or rabbit neocortex
in vivo produced LTP in the guinea pig hippocampal slice in vitro. Applications of these samples after heating and cooling failed to induce LTP. Subsequent studies demonstrated that PC-12 cells incubated in growth medium treated with samples collected during tetanic stimulations of the rabbit neocortex developed extensive neurite growths. In contrast, PC-12 cell cultures incubated in (1) heated and cooled samples, (2) samples collected in the absence of tetanic stimulations of the rabbit neocortex, or (3) plain growth medium, failed to develop neurite growths. In addition, PC-12 cell cultures that were incubatea in growth medium containing samples collected during tetanic stimulations plus saccharin (10 mM), a substance known to inhibit N6F-dependent neurite growth, failed to develop neurites. In separate experiments it was found that saccharin could block (1) the synaptic potentiating effects of the above collected and applied endogenous substances, and (2) LTP induced with tetanic stimulations, in the guinea pig hippocampus in vitro. The concentrations of saccharin used in these studies had insignificant effects on resting membrane potentials, input resistances, spontaneous or evoked responses of CA1b neurons. Furthermore, CA1b neuronal depolarizations induced by N-methyl-DL-aspartate (NMDA) or with tetanic stimulations of the stratum radiatum, were not altered by saccharin applications. In addition, saccharin had insignificant effects on paired-pulse facilitation, post-tetanic potentiations, minEPSP frequencies in CA1b neurons, and Schaffer collaterals terminal excitability. These results suggest that saccharin blocked LTP through mechanisms different from either non-specific alterations in CA1b cell properties or NMDA receptor activation. Perhaps the agent antagonized LTP at a step beyond NMDA receptor activation. That saccharin blocked LTP caused by the applied neocortical sample as well as by tetanic stimulation of the stratum radiatum,
and that saccharin also blocked neurite growth in PC-12 cells induced by the neocortical samples, raises the prospect that growth related substances are involved in LTP generation. In other control experiments, it was found that the potentiating effects of the collected endogenous substances were not antagonised by atropine or dihydro-e-erythroidine. Heated and then cooled solutions of glutamate (a putative transmitter at the Schaffer col laterals-CA1b synapses) still maintained their actions on the CA1b population spike. While brief applications of 2.5 μg/ml exogenous NGF (from Vipera lebetina) during low frequency stimulations of the stratum radiatum did not consistently induce LTP, this peptide significantly facilitated
the development of LTP when applied in association with tetanic stimulations
of weak inputs in the CA1b area. These weak inputs could not support LTP if tetanized in the absence of the exogenous NGF.
The results of the studies in this thesis suggested that postsynaptic depolarizations modulated presynaptic functions in the hippocampus. Tetanic stimulations in hippocampus and neocortex caused the release of diffusible substances, which were probably growth related macromolecules, that interacted
with activated presynaptic afferents and/or subsynaptic dendritic elements resulting in LTP development. The precise locus of actions of these agents awaits further investigations.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
39
Shende, Vishvesh H. "Long-term effects of prenatal and early postnatal environment on brain remodelling : focus on hippocampal volume and astroglia". Thesis, University of Roehampton, 2013. https://pure.roehampton.ac.uk/portal/en/studentthesis/“long-term-effects-of-prenatal-and-early-postnatal-environment-on-brain-remodelling(e6d0d93b-db49-4632-a3a9-9ff4e7b623da).html.
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The main aim of this thesis was to assess if early deprivation (ED) and glucocorticoid (GC) treatment exert long-term effects on the volume of the brain regions implicated in responses to stress, and if it associates with alterations in the distribution and structure of astroglia, which are known to support brain plasticity. This study also investigated the effects of prenatal dexamethasone (Dex) treatment on selected brain receptors, namely the oxytocin and 5-HT1A receptors, as they are implicated in the regulation of responses to stress. In addition, in vitro effects of Dex on neural stem cells were studied, in order to explore the drug effects on cell proliferation and differentiation, and on glial cell markers. Unbiased stereological estimation was employed to determine the regional brain volume, astroglial morphology and total cell count. Peripheral quantitative computed tomography (pQCT) technique was used to quantify total brain volume. Autoradiography technique was employed to visualise and analyse oxytocin and 5HT-1A serotonin receptor binding using selective radioactive ligands. The results of the present study demonstrate that both ED and prenatal Dex exposure leads to long-term effects on hippocampal remodelling with volume losses and impoverished astroglial morphology in the form of reduced primary process length. The observed deterioration in astroglial morphology adds further evidence that astrocytic changes contribute to hippocampal volume losses, a phenomenon that deserves more research in the context of effects of corticosteroid overload and stress-related pathologies. The present results also demonstrate that prenatal Dex induces long-term effects at the level of central neuroregulatory processes. Thus significant region- and sex-dependent reductions or increases in the oxytocin and 5-HT1A receptor binding were observed. The in vitro study has shown that Dex affects both proliferation and differentiation of GFAP positive NSCs with no toxic effects as such. Overall, both early postnatal or prenatal manipulations that increase levels of stress and/or glucocorticoids as the chemical mediators of stress, lead to a long-term maladaptive brain remodelling with losses in the hippocampal volume, impoverishment of hippocampal astroglial morphology and changes in the properties of central regulatory receptors in the brain areas involved in the reaction to stress.
40
Geddes, Donna Michelle. "Selective vulnerability of hippocampal vs cortical neurons to mechanically induced increases in plasma membrane permeability". Diss., Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/20289.
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Packard, Mark G. "The organization of memory in the brain : role of caudate nucleus and hippocampus". Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74684.
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The present experiments were designed to examine the hypothesis that the hippocampus and caudate nucleus are parts of independent memory systems which differ in the type of memory they mediate. In experiment 1, the mnemonic functions of the hippocampus and caudate were doubly dissociated; lesions of the caudate nucleus impaired acquisition of the "habit memory" component of the 4 x 4 radial maze task, but had no effect the "cognitive memory" component of the task. Lesions of the fimbria-fornix produced the opposite behavioral dissociation. In experiment 2, lesions of the caudate nucleus produced a transient deficit in cognitive win-shift radial maze behavior when rats were allowed to obtain food from maze arms on an unlimited basis prior to win-shift training. In contrast, lesions of the caudate had no effect on win-shift acquisition when rats were allowed to explore an empty maze prior to win-shift training. These results suggest that reinforcement contingencies may be important in determining the type of memory process initiated by a training experience. In experiments 3ab, systemic post-training injection of the dopamine (DA) agonist D-amphetamine (D-AMP) and the DA D2 receptor agonist LY 171555, but not the DA D1 receptor agonist SKF-38393, improved acquisition on both a habit memory win-stay radial maze task, and a cognitive memory win-shift radial maze task. In experiments 4ab, the mnemonic functions of the hippocampus and caudate nucleus were doubly dissociated using post-training intracerebral injections of these same DA agonists. Post-training intracaudate injection of D-AMP, LY 171555, and SKF-38393 improved acquisition of win-stay, but not win-shift radial maze behavior. Post-training intrahippocampal injection of these DA agonists produced the opposite behavioral dissociation. Taken together, the results are consistent with the hypothesis that the caudate nucleus mediates the acquisition of habit memory, while the hippocampus mediates the acquisition
42
Hulme, Sarah R., i n/a. "Heterosynaptic metaplasticity in area CA1 of the hippocampus". University of Otago. Department of Psychology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090818.161738.
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Long-term potentiation (LTP) is an activity-dependent increase in the efficacy of synaptic transmission. In concert with long-term depression (LTD), this synaptic plasticity likely underlies some types of learning and memory. It has been suggested that for LTP/LTD to act as effective memory storage mechanisms, homeostatic regulation is required. This need for plasticity regulation is incorporated into the Bienenstock, Cooper and Munro (BCM) theory by a threshold determining LTD/LTP induction, which is altered by the previous history of activity (Bienenstock et al., 1982). The present work aimed to test key predictions of the BCM model. This was done using field and intracellular recordings in area CA1 of hippocampal slices from young, adult male Sprague-Dawley rats. The first prediction tested was that following a strong, high-frequency priming stimulation all synapses on primed cells will show inhibition of subsequent LTP and facilitation of LTD induction (heterosynaptic metaplasticity). This was confirmed using two independent Schaffer collateral pathways to the same CA1 pyramidal cells. Following priming stimulation to one pathway, LTP induction was heterosynaptically inhibited and LTD facilitated. To more fully investigate whether all synapses show metaplastic changes, the priming stimulation was given in a different dendritic compartment, in stratum oriens, prior to LTP induction in stratum radiatum. This experiment supported the conclusion that all synapses show inhibited LTP following priming. A second prediction of the BCM model is that metaplasticity induction is determined by the history of cell firing. To investigate this, cells were hyperpolarized during priming to completely prevent somatic action potentials. Under these conditions inhibitory priming of LTP was still observed, and thus somatic action potentials are not critical for the induction of the effect. The next aim was to determine the mechanism underlying heterosynaptic metaplasticity. One way in which plasticity induction can be altered is through changes in gamma-aminobutyric acid (GABA)-mediated inhibition of pyramidal cells. For this reason, it was tested whether blocking all GABAergic inhibition, for the duration of the experiment, would prevent priming of LTP. However, priming inhibited subsequent LTP and it was concluded that GABAergic changes do not underlie either the induction, or expression, of the metaplastic state. Proposed revisions to the BCM model predict that postsynaptic elevations in intracellular Ca�⁺ determine the induction of metaplasticity. There are many potential sources for postsynaptic Ca�⁺ elevations, including entry through N-methyl-D-asparate receptors (NMDARs) or voltage-dependent calcium channels (VDCCs), or release from intracellular stores. Results of the present work demonstrate that the inhibition of LTP is dependent on the release of Ca�⁺ from intracellular stores during priming; however this release is not triggered by Ca�⁺ entry through NMDARs or VDCCs, or via activation of metabotropic glutamate receptors. Overall, the present results show that, in accordance with the BCM model, a high level of prior activity induces a cell-wide metaplastic state, such that LTD is facilitated and LTP is inhibited. In contrast to predictions of the BCM model, this is not mediated by cell-firing during priming. Instead the release of Ca�⁺ from intracellular stores is critical for induction of the metaplastic state.
43
Kennard, Jeremy Thomas Timothy, i n/a. "Glutamate receptor expression during the maintenance of long-term potentiation in the hippocampus". University of Otago. Department of Anatomy & Structural Biology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20081127.155142.
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Changes in the strength of connections between neurons underlie information storage in the mammalian brain. Long-term potentiation (LTP) is a long-lasting form of synaptic plasticity that has been described extensively in the hippocampus, a brain structure that plays a key role in memory formation. The molecular events that realise the persistence of LTP are not well understood, but it is known to require protein synthesis. The aim of this thesis was to investigate synaptic protein expression during the late-phase of hippocampal LTP in freely moving rats.
LTP was induced in the perforant path input to the dentate gyrus of Sprague-Dawley rats using high-frequency electrical stimulation paradigms known to produce LTP that persists for many days. To focus on late-occurring events, and complement existing data sets, rats were sacrificed 48 h after LTP induction. A broad survey of synaptic proteins was conducted by two-dimensional gel electrophoresis using postsynaptic density (PSD) fractions. Over 200 protein spots were resolved, from which 163 individual proteins were identified by mass spectrometry. These included cytoskeletal proteins, signalling molecules, molecular chaperones and mitochondrial components, but no transmembrane receptor proteins were detected.
Few of the identified proteins were found to undergo significant changes in expression, although proteomic comparison of PSDs prepared from LTP-stimulated and control dentate gyri showed reduced expression of the three component proteins of the mitochondrial voltage-dependent anion channel. While these data complement earlier studies suggesting that the late-phase of LTP is associated with mitochondrial restructuring, they cannot alone explain the persistence of LTP. To directly test whether LTP persistence is associated with increased expression of presynaptic marker proteins, suggesting increased neurotransmitter release; and/or increased postsynaptic receptor expression, implicating an increase in postsynaptic contact area, a targeted approach using Western Blot analysis of dentate gyrus subcellular fractions was undertaken.
44
Devan, Bryan David. "Functional organization of the dorsal striatum : comparison to the hippocampal system". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ44408.pdf.
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Coombs, Katie Marie. "Behavioral consequences following AAV mediated hippocampal EAAC1 knockdown". Thesis, Montana State University, 2007. http://etd.lib.montana.edu/etd/2007/coombs/CoombsK0507.pdf.
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El-Orabi, Naglaa Schwartz Dean D. "Heat stress induces downregulation of Hippocampal superoxide dismutase-1 a possible mechanism for heat-related neuronal cell death /". Auburn, Ala., 2006. http://repo.lib.auburn.edu/2006%20Fall/Dissertations/EL-ORABI_NAGLAA_43.pdf.
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Godman, Timothy Hugh. "The functional role of retinoic acid in the regulation of cell proliferation in the adult hippocampus". Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=167035.
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Levels of retinoic acid (RA), the active metabolite of vitamin A, are tightly regulated throughout vertebrate CNS development by RA synthesising and catabolising enzymes. However, increasing evidence suggests that similar regulatory mechanisms exist in the adult brain to maintain RA at the optimum level. The hippocampus is one of very few regions where neurons continue to be born. Furthermore, the hippocampus is one of the regions in which RA regulates function. RA is synthesised in the region of the hippocampus by the enzyme, retinaldehyde dehydrogenase 2 (RALDH2), expressed in the adjacent meninges. CYP26B1 has been previously shown to be present by in situ hybridisation in the CA4/3 region between the two blades of the dentate gyrus. We hypothesised that a gradient was set up between the source and sink of RA in the adult hippocampus. To test this, we disrupted the balance using exogenous RA and using inhibitors to its catabolising enzymes. A reporter mouse was used to detect RA signalling and significantly more lacZ expression was detected in the infrapyramidal blade (closest to the meninges) compared to the suprapyramidal blade. Furthermore, administration of RA equalised lacZ expression between the two blades. RA is a potent differentiation agent; however, its effects on cell proliferation are less clear. In order to examine the direct effects RA on cell proliferation, an organotypic hippocampal slice culture technique was optimised and it was found that RA inhibits cell proliferation specifically in the dentate gyrus in a dose dependent manner. Taken together, this thesis provides insight for the first time into a parallel regulatory mechanism in the adult hippocampus to the embryo where RA is tightly regulated by its synthesising and catabolising enzymes and this mechanism is involved in the regulation of cell proliferation in the adult dentate gyrus.
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O'Neill, Joseph. "Reactivation of waking firing patterns during sleep". Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670153.
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Gomes, Angelina. "Alterations in hippocampal neurogenesis and pain behavior in mice an experimental study /". Diss., Connect to the thesis, 2009. http://hdl.handle.net/10066/3726.
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Harp, Phillip Allan. "System to compress while electrically stimulating hippocampal brain slices (SCWESH) : design, development, and electromechanical validation". Thesis, Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/16828.
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