A Histochemical Method for Localizing Cholinesterase Activity.

Koelle, George B.; Friedenwald, Jonas S.

doi:10.3181/00379727-70-17013

Cited by 1,059 publications

(269 citation statements)

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“…Using a freezing microtome, the hippocampus was sectioned at 40 m within 12 h of fixing while the rest of the brain was kept in 18% sucrose in phosphate-buffered saline for at least 72 h at 4 • C. For the AChE staining, hippocampal sections were mounted on chrome-alum gelatin coated slides. AChE staining protocol was modified from the Koelle copper thiocholine method [48], using acetylthiocholine iodide as a false substrate to tag the AChE enzyme and ethopropazine as an inhibitor of non-specific cholinesterases.…”

Section: Histologymentioning

confidence: 99%

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Tai

Leung

2012

Behavioural Brain Research

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Section: Histologymentioning

confidence: 99%

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Tai

Leung

2012

Behavioural Brain Research

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“…The degree of preservation of cholinergic fibers in the neocortex and hippocampus was assessed by acetylcholinesterase (AChE) histochemistry (Leung, 1987). AChE staining protocol was modified from the Koelle copper thiocholine method (Koelle and Friedenwald, 1949), using acetylthiocholine iodide as a false substrate to tag the AChE enzyme and ethopropazine as an inhibitor of non-specific cholinesterases Digital photographs were taken using the same parameters (microscope lighting, digital camera aperture and shutter speed settings) at FC (~A2), VC (~P7.3), parietal cortex (~P3) and dorsal hippocampus (~P3). A computer software program (ImageJ, National Institutes of Health, U.S.A.) was used to quantify AChE staining by means of an average optical density (OD) measure on one side.…”

Section: Histological and Immunocytochemical Stainingmentioning

confidence: 99%

Lesion of cholinergic neurons in nucleus basalis enhances response to general anesthetics

Leung

Petropoulos

Shen

et al. 2011

Experimental Neurology

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"Lesion of cholinergic neurons in nucleus basalis enhances response to general anesthetics" (2011). Physiology and Pharmacology Publications. 72. https://ir.lib.uwo.ca/physpharmpub/72 This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. Acetylcholine in the brain has been associated with consciousness and general anesthesia effects. We tested the hypothesis that the integrity of the nucleus basalis magnocellularis (NBM) affects the response to general anesthetics. Cholinergic neurons in NBM were selectively lesioned by bilateral infusion of 192IgG-saporin in adult, male Long-Evans rats, and control rats were infused with saline. Depletion of choline-acetyltransferase (ChAT)-immunoreactive cells in the NBM and decrease in optical density of acetylcholinesterase (AChE) staining in the frontal and visual cortices confirmed a significant decrease in NBM cholinergic neurons in lesioned as compared to control rats. AChE staining in the hippocampus and ChAT-positive neurons in the medial septum-vertical limb of the diagonal band were not different between lesioned and control rats. When a general anesthetic was administered, lesioned compared to control rats showed significantly longer duration of loss of righting reflex (LORR) after propofol (5 or 10 mg/kg i.v.), pentobarbital (20 or 40 mg/kg i.p.) but not halothane (2%). However, the behavioral excitation, as indicated by horizontal movements, induced by halothane was reduced in lesioned as compared to control rats. Reversible inactivation of NBM with GABA A receptor agonist muscimol increased slow waves in the neocortex during awake immobility, and prolonged the duration of LORR and loss of tail-pinch response after propofol, pentobarbital and halothane. In summary, lesion of NBM cholinergic neurons or inactivation of the NBM prolonged the LORR response to general anesthetic drugs.

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“…(b) Cholinacetyl transferase reaction (Kassa & Morris, 1972). (c) Acetylcholinesterase reaction (Koelle & Friedenwald, 1949 Control: The characteristic yellow and/or green fluorescence of the biogenic amines was visible throughout the length of the spinal cord. This was seen in the form of small terminals (0·5U-2/l).…”

Section: Methodsmentioning

confidence: 99%

Morphological and histochemical correlation of recovery after spinal transection in rat

Sahgal

Subramani

1981

Spinal Cord

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A Histochemical Method for Localizing Cholinesterase Activity.

Cited by 1,059 publications

References 0 publications

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

Lesion of cholinergic neurons in nucleus basalis enhances response to general anesthetics

Morphological and histochemical correlation of recovery after spinal transection in rat

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