huntington disease/scopolamine

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Acute effects of scopolamine in Huntington's disease.

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Scopolamine induces impairments in the recognition of human facial expressions of anger and disgust.

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BACKGROUND Recent psychopharmacological studies lend support to the notion of partially dissociable neuronal systems dedicated to processing specific emotions. For example, GABA-ergic enhancement after an acute dose of the benzodiazepine, diazepam, produces specific impairments in anger and fear

Effect of cholinergic agents in Huntington's disease: a reappraisal.

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The effects of centrally and peripherally active anti-cholinergic agents were investigated in four patients with Huntington's disease. Scopolamine reduced chorea, increased incoordination, induced sedation, and produced confusion. Benztropine produced similar but milder effects. A peripheral

Plastic and behavioral abnormalities in experimental Huntington's disease: a crucial role for cholinergic interneurons.

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Huntington's disease (HD) is a fatal hereditary neurodegenerative disease causing degeneration of striatal spiny neurons, whereas cholinergic interneurons are spared. This cell-type specific pathology produces an array of abnormalities including involuntary movements, cognitive impairments, and

Patterns of memory failure after scopolamine treatment: implications for cholinergic hypotheses of dementia.

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To test the idea that scopolamine provides a suitable pharmacological model of the memory defects associated with cortical or subcortical dementias, we assessed memory on a battery of tasks in healthy young normal subjects who received 0.5 mg scopolamine, 0.1-0.2 mg glycopyrrolate or physiological

Tetrahydrocannabinol potentiates reserpine-induced hypokinesia.

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Delta-9-tetrahydrocannabinol (THC), a substance in marihuana, was found to produce a profound potentiation of reserpine-induced hypokinesia in rats as measured with a bar test. In these experiments, THC had no hypokinetic effect by itself but produced a more than 20-fold increase in the hypokinesia

Quinolinic acid-induced lesions of the rat striatum: quantitative autoradiographic binding assessment.

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Injection of the excitatory amino-acid analog quinolinic acid into the striatum of rats produces neuropathological and neurochemical alterations that are reminiscent of those observed in Huntington's disease. In the present study, we evaluated quinolinic acid-induced striatal changes using

Bifunctional drug derivatives of MAO-B inhibitor rasagiline and iron chelator VK-28 as a more effective approach to treatment of brain ageing and ageing neurodegenerative diseases.

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Degeneration of nigrostriatal dopamine neurons and cholinergic cortical neurones are the main pathological features of Parkinson's disease (PD) and for the cognitive deficit in dementia of the Alzheimer' type (AD) and in dementia with Lewy bodies (DLB), respectively. Many PD and DLB subjects have

Galantamine and donepezil attenuate pharmacologically induced deficits in prepulse inhibition in rats.

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Acetylcholinesterase inhibitors (AChEIs) are currently being evaluated as adjunctive therapy for the cognitive dysfunction of schizophrenia. This core symptom of schizophrenia has often been attributed to impaired attention and abnormal sensory motor gating, features that are also found in

Kainic acid injections in the striatum alter the cataleptic and locomotor effects of drugs influencing dopaminergic and cholinergic systems.

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Rats with bilateral injections of kainic acid into the striatum were tested for their motor responsiveness to drugs influencing dopaminergic and cholinergic systems. The kainic acid-induced lesions potentiated the locomotor response to both the dopaminergic agonist, d-amphetamine, and the

Quantitative assessment of quinolinic acid-induced striatal toxicity in rats using radioligand binding assays.

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To validate specific, sensitive and quantitative markers of the rat model of Huntington's disease produced by the intrastriatal injection of quinolinic acid, we used striatal homogenate binding assays for [3H]MK-801-labelled N-methyl-D-aspartate receptors, [3H]SCH 23390-labelled D1 and

Effects of sulforaphane in the central nervous system.

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Sulforaphane (SFN) is an active component extracted from vegetables like cauliflower and broccoli. Activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling is a common mechanism for the anti-oxidative and anti-inflammatory activity of some herb-derived compounds, such as

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