Hippocampal kindled seizures impair spatial cognition in the Morris water maze

Gilbert, Trevor H.; Hannesson, Darren K.; Corcoran, Michael E.

doi:10.1016/s0920-1211(99)00064-9

Cited by 41 publications

(18 citation statements)

References 15 publications

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“…Gilbert et al (1996) reported no effect on water maze performance in rats that had been kindled to non-convulsive seizures 24 hours prior to training, but in a later paper reported impairment in partially kindled rats that were trained and tested 25 -45 minutes after kindling (Gilbert et al, 2000). Sutherland et al (1997) reported no impairment on the standard version of the Morris water maze, following repeated afterdischarges that did not lead to seizures.…”

Section: Discussionmentioning

confidence: 99%

Revisiting the cholinergic hypothesis in the development of Alzheimer's disease

Craig

Hong

McDonald

2011

Neuroscience & Biobehavioral Reviews

410

263

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Alzheimer's disease (AD) is the most common form of dementia affecting the elderly population today; however, there is currently no accurate description of the etiology of this devastating disorder. No single factor theory has been demonstrated as being causative; however, an alternative theory suggests that the interaction of multiple risk factors is responsible for AD. In this thesis I present data suggesting a neuroprotective role for acetylcholine during aging. Using a rat model of cholinergic depletion of the medial septum, I explored the effects of four common risk factors for AD (stress, seizures, stroke and circadian dysfunction) targeted at the hippocampus and examined the effects on measures of hippocampal dependent (water maze) and hippocampal independent (fear conditioning) memory. Here, I propose a role for acetylcholinemediated compensatory mechanisms in the functional recovery observed following sub threshold insults similar to those commonly observed in the elderly. m First and foremost I would like to thank my supervisor, Dr. Robert McDonald. Thank you for your support and encouragement, and for allowing me the independence to pursue my own projects and to learn from my experiences. I would also like to thank Nhung Hong for doing the majority of the cholinergic depletion and stroke surgeries used in this thesis and for teaching me the techniques. I would like to give a huge thank you to Joelle Kopp who was an invaluable asset who assisted in histology and spent many hours on the microscope counting cholinergic neurons. I would also like to thank Dr. Christine Werk for patiently reading and re-reading early drafts of my papers and this thesis and Dr.Hugo Lehmann for all his help in running statistics and interpreting my data. In addition, many thanks go out to Courtney Lamb, Robert Court and Arthur Verhoef for helping me with histology and behavioural testing, to Keri Colwell for running the corticosterone assays, the Metz lab for kindly allowing me the use of their microscope and to Karen Dow-Cazel and the rest of the animal care staff for taking care of my rats and helping me set up the circadian experiements. The cholinergic hypothesis of Alzheimer's disease 6 Acknowledgements IVThe basal forebrain cholinergic system 8The role of the basal forebrain cholinergic system in learning and memory 10The current state of the cholinergic hypothesis of Alzhimer's disease 15Risk factors for Alzheimer's disease 16Multiple combinations of co-factors theory of Alzheimer's disease 22The role of the hippocampus in learning and memory 24Objective of the present thesis 25Chapter 2: A series of pilot studies to determine the threshold for behaviourally sub threshold stroke, seizures and stress 28Abstract 29Experiment la: The effect of a chronic variable stress schedule on performance of the water maze task 32 Materials and Methods 33Results 36Experiment lb: The effects of a variable restraint stress procedure on levels of blood borne CORT 39 Materials and Methods 39Results 40Discussion 41Experiment 2: T...

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Section: Discussionmentioning

confidence: 99%

Revisiting the cholinergic hypothesis in the development of Alzheimer's disease

Craig

Hong

McDonald

2011

Neuroscience & Biobehavioral Reviews

410

263

View full text Add to dashboard Cite

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“…Previous studies have stimulated, either electrically or chemically, different areas of the Ent–Hip network to induce seizures including the CA1 (Gilbert et al, 2000), CA3 (Bragin et al, 2005) dentate gyrus (Zhang et al, 2001), angular bundle (Sardo et al, 2008), and entorhinal cortex (Heidarianpour et al, 2006). However, to our knowledge this is the first investigation that pharmacologically manipulated GS in several locations within the Ent–Hip network in the same study, thus allowing for direct comparisons of the site-specific effects of MSO treatment on the frequency, severity, and the temporal progression of seizures.…”

Section: Discussionmentioning

confidence: 99%

Effects of site-specific infusions of methionine sulfoximine on the temporal progression of seizures in a rat model of mesial temporal lobe epilepsy

et al. 2015

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SUMMARY Glutamine synthetase (GS) in astrocytes is critical for metabolism of glutamate and ammonia in the brain, and perturbations in the anatomical distribution and activity of the enzyme are likely to adversely affect synaptic transmission. GS is deficient in discrete regions of the hippocampal formation in patients with mesial temporal lobe epilepsy (MTLE), a disorder characterized by brain glutamate excess and recurrent seizures. To investigate the role of site-specific inhibition of GS in MTLE, we chronically infused the GS inhibitor methionine sulfoximine (MSO) into one of the following areas of adult laboratory rats: (1) the angular bundle, n = 6; (2) the deep entorhinal cortex (EC), n = 7; (3) the stratum lacunosum-moleculare of CA1, n = 7; (4) the molecular layer of the subiculum, n = 10; (5) the hilus of the dentate gyrus, n = 6; and (6) the lateral ventricle, n = 6. Twelve animals were infused with phosphate buffered saline (PBS) into the same areas to serve as controls. All infusions were unilateral, and animals were monitored by continuous video-intracranial EEG recordings for 3 weeks to capture seizure activity. All animals infused with MSO into the entorhinal–hippocampal area exhibited recurrent seizures that were particularly frequent during the first 3 days of infusion and that continued to recur for the entire 3 week recording period. Only a fraction of animals infused with MSO into the lateral ventricle had recurrent seizures, which occurred at a lower frequency compared with the other MSO infused group. Infusion of MSO into the hilus of the dentate gyrus resulted in the highest total number of seizures over the 3-week recording period. Infusion of MSO into all brain regions studied, with the exception of the lateral ventricle, led to a change in the composition of seizure severity over time. Low-grade (stages 1–3) seizures were more prevalent early during infusion, while severe (stages 4–5) seizures were more prevalent later. Thus, the site of GS inhibition within the brain determines the pattern and temporal evolution of recurrent seizures in the MSO model of MTLE.

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“…Extensive evidence indicates that the hippocampal formation is a critical brain area for spatial learning and memory (Morris et al, 1982). For example, rats with hippocampal damage show deficits in spatial learning and memory in the water maze (Block et al, 1997;Gilbert et al, 2000). The dentate gyrus is a particularly important part of the hippocampal formation for spatial learning (Nakao et al, 2001;Schuster et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Age-Specific Impairment of Morris Water Maze Performance Following Neonatal Exposure to Magnetic Resonance Image in Rats

Yang

Guo²,

Han³

et al. 2007

CNR

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To investigate the effects of magnetic resonance image (MRI) exposure on CNS development, we examined the effects of neonatal exposure of rats to a MRI magnetic field on their performance in the Morris water maze. After birth, all litters were randomly divided into an MRI-scanning group (experimental group) comprised of 7 mother rats and their offspring, and a control group, which consisted of the other 7 mothers and their pups. Newborn rat pups of MRI-scanning group were exposed to a 1.5 T magnetic resonance image (MRI) magnetic field for 7 days (postnatal day 1-day 7, 10 min/day). And behavioral tests were taken at 1st-, 2nd- and 5th-month after birth. At the age of 2 months postnatal, both male and female rats of the experimental groups made fewer crossings over the target area in the probe trial than did the control group. This result showed that the exposed animals represented a "reference memory" deficit, that is to say, these rats had a deficit ability to use environmental cues to locate the former position in space. No deficits were evident in the 1st- and 5th-month groups. These results demonstrate an age-specific cognitive/behavioral deficit induced by neonatal exposure to an MRI magnetic field. These findings indicate that the safety of MRI exposure must be considered with care and appropriate cautions should be taken.

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Hippocampal kindled seizures impair spatial cognition in the Morris water maze

Cited by 41 publications

References 15 publications

Revisiting the cholinergic hypothesis in the development of Alzheimer's disease

Revisiting the cholinergic hypothesis in the development of Alzheimer's disease

Effects of site-specific infusions of methionine sulfoximine on the temporal progression of seizures in a rat model of mesial temporal lobe epilepsy

Age-Specific Impairment of Morris Water Maze Performance Following Neonatal Exposure to Magnetic Resonance Image in Rats

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