Selective acetylcholine and dopamine lesions in neonatal rats produce distinct patterns of cortical dendritic atrophy in adulthood

Sherren, Nicole; Pappas, Bruce A.

doi:10.1016/j.neuroscience.2005.08.053

Cited by 31 publications

(38 citation statements)

References 66 publications

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“…A recent study (Solis et al, 2007) reported that 6-OHDA injections of the substantia nigra resulted in a decrease in spine density but not dendritic length in layer V PCs of what appears to be the medial precentral (shoulder) cortex, dorsal to the prelimbic cortex that we analyzed. A recent study of neonatal rats that received intraventricular injections of 6-OHDA, which caused a significant decline in PFC dopamine but not norepinephrine concentrations, did not observe any changes in the dendrites of layer V PCs (Sherren and Pappas, 2005). It will be interesting to determine if compensatory mechanisms that prevent spine loss in the face of cortical dopamine depletion are present in neonatal animals.…”

Section: Dopamine-dependent Remodeling Of Dendritic Morphologymentioning

confidence: 99%

Dopamine Depletion of the Prefrontal Cortex Induces Dendritic Spine Loss: Reversal by Atypical Antipsychotic Drug Treatment

Wang

Deutch

2007

Neuropsychopharmacol

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Dystrophic changes in dendrites of cortical neurons are present in several neuro-psychiatric disorders, including schizophrenia. The mechanisms that account for dendritic changes in the prefrontal cortex (PFC) in schizophrenia are unclear. Cognitive deficits in schizophrenia have been linked to compromised cortical dopamine function, and the density of the PFC dopamine innervation is decreased in schizophrenia. We determined if 6-hydroxydopamine lesions of the ventral tegmental area that disrupt the PFC dopamine innervation cause dystrophic changes in cortical neurons. Three weeks post-operatively we observed a marked decrease in basal dendritic length and spine density of layer V pyramidal cells in the prelimbic cortex; no change was seen in neurons of the motor cortex. We then examined rats in which the PFC dopamine innervation was lesioned and 3 weeks later were started on chronic treatment with an atypical (olanzapine) or typical (haloperidol) antipsychotic drug. Olanzapine but not haloperidol reversed lesion-induced changes in PFC pyramidal cell dendrites. These data suggest that dopamine regulates dendritic structure in PFC neurons. Moreover, the findings are consistent with a decrease in cortical dopaminergic tone contributing to the pathological changes in the cortex of schizophrenia, and suggest that the progressive cortical loss in schizophrenia may be slowed or reversed by treatment with atypical antipsychotic drugs.

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Section: Dopamine-dependent Remodeling Of Dendritic Morphologymentioning

confidence: 99%

Dopamine Depletion of the Prefrontal Cortex Induces Dendritic Spine Loss: Reversal by Atypical Antipsychotic Drug Treatment

Wang

Deutch

2007

Neuropsychopharmacol

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“…Damaging the nucleus basalis has been found to reduce branching of pyramidal neurons in the frontal cortex a finding that could explain the reduced plasticity in cortical neurons (Harmon and Wellman, 2003;Works et al, 2004). Moreover, neonatal depletions have been shown to decrease dendritic branching in cortical neurons examined in adulthood (Robertson et al, 1998;Sherren and Pappas, 2005). …”

Section: Impaired Experience-dependent Plasticity In Cholinergic Deplmentioning

confidence: 99%

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

Craig

Hong

McDonald

2011

Neuroscience & Biobehavioral Reviews

411

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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“…This technique presents the advantage of localizing discrete dopamine stores, which because of its limits of detection, likely do not correspond to the catecholamine pools that are part of the noradrenaline synthetic pathways. Membrane (DAT) and vesicular (VMAT -1 and -2) transport system for monoamines (dopamine, noradrenaline, and serotonin) are involved in the regulation of synaptic communication and neuronal plasticity (17,27). Increasing evidence indicates that DAT and VMAT-2 transporters are probably the most specific markers of dopaminergic neurons (18).…”

Section: Discussionmentioning

confidence: 99%

Dopamine, vesicular transporters, and dopamine receptor expression in rat major salivary glands

Tomassoni

Traini

Mancini

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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The localization of dopamine stores and the expression and localization of dopamine (DAT) and vesicular monoamine transporters (VMAT) type-1 and -2 and of dopamine D1-like and D2-like receptor subtypes were investigated in rat submandibular, sublingual, and parotid salivary glands by HPLC with electrochemical detection, as well as immunochemical and immunohistochemical techniques. Male Wistar rats of 2 mo of age were used. The highest dopamine levels were measured in the parotid gland, followed by the submandibular and sublingual glands. Western blot analysis revealed DAT, VMAT-1, VMAT-2, and dopamine receptors immunoreactivity in membrane preparations obtained from the three glands investigated. Immunostaining for dopamine and transporters was developed within striated ducts. Salivary glands processed for dopamine receptors immunohistochemistry developed an immunoreaction primarily in striated and excretory ducts. In the submandibular gland, acinar cells displayed strong immunoreactivity for the D2 receptor, while cells of the convoluted granular tubules were negative for both D1-like and D2-like receptors. Parotid glands acinar cells displayed the highest immunoreactivity for both D1 and D2 receptors compared with other salivary glands. The above localization of dopamine and dopaminergic markers investigated did not correspond closely with neuron-specific enolase (NSE) localization. This indicates that at least in part, catecholamine stores and dopaminergic markers are independent from glandular innervation. These findings suggest that rat major salivary glands express a dopaminergic system probably involved in salivary secretion. The stronger immunoreactivity for dopamine transporters and receptors in striated duct cells suggests that the dopaminergic system could regulate not only quality, but also volume and ionic concentration of saliva.

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Selective acetylcholine and dopamine lesions in neonatal rats produce distinct patterns of cortical dendritic atrophy in adulthood

Cited by 31 publications

References 66 publications

Dopamine Depletion of the Prefrontal Cortex Induces Dendritic Spine Loss: Reversal by Atypical Antipsychotic Drug Treatment

Dopamine Depletion of the Prefrontal Cortex Induces Dendritic Spine Loss: Reversal by Atypical Antipsychotic Drug Treatment

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

Dopamine, vesicular transporters, and dopamine receptor expression in rat major salivary glands

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