Analysis of the tremor induced by injection of cholinergic agents into the caudate nucleus

Connor, John D.; Rossi, G; Baker, Walter W.

doi:10.1016/0028-3908(66)90025-6

Cited by 63 publications

(8 citation statements)

References 15 publications

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“…On the basis of previous experiments in which cholinomimetic agonists were injected directly into cerebral tissue, Myers (1971aMyers ( , 1974 (Connor, Rossi & Baker, 1966). Thirdly, in the present experiments, the magnitude of hyperthermia produced by a push-pull perfusion of RX72601 at diencephalic sites never equalled the intensity of the response produced by an intraventricular injection implying, perhaps, that there is more than one site of action in the latter case.…”

Section: Discussionsupporting

confidence: 59%

Temperature and Behavioural Responses Induced in the Unanaesthetized Cat by the Central Administration of Rx72601, a New Anticholinesterase

Metcalf

Myers

Redgrave

1975

British J Pharmacology

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The central effects produced by a new anticholinesterase RX72601 injected into the cerebral ventricles or perfused within circumscribed forebrain structures have been investigated in the unanaesthetized cat. When injected into the cerebral ventricles in doses of 1–10 μg, RX72601 produced a dose‐related hyperthermia together with behavioural and autonomic responses. Experiments designed to localize the site or sites of these actions demonstrated that hyperthermia could be produced from several diencephalic sites but that the other effects were not normally produced from these same sites.

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Section: Discussionsupporting

confidence: 59%

Temperature and Behavioural Responses Induced in the Unanaesthetized Cat by the Central Administration of Rx72601, a New Anticholinesterase

Metcalf

Myers

Redgrave

1975

British J Pharmacology

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“…Moreover, intracerebroventricular injection of either dopamine or serotonin has no significant effect on tremorine tremor. 131 Stimulation of central muscarinergic receptors is responsible for tremorine-induced tremor, because muscarinergic, but not nicotinergic cholinergic antagonists, suppress tremorine tremor, 115,132 and the tremor remains unchanged with peripheral application of quaternary cholinergic antagonists, which are unable to cross the blood-brain barrier and therefore stimulate only peripheral receptors. The absence of oxotremorine tremor in newborn dogs is probably the result of the immaturity of the central cholinergic system at that time.…”

Section: Neurotransmitters Involved In Tremorgenesismodulation Of Trementioning

confidence: 99%

Animal models of tremor

1999

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“…Several lines of evidence indicate that an imbalance in the striatum between dopamine and acetylcholine results in tremors (Connor et al, 1966; Lalley et al, 1973). For example, microinjection of carbachol (cholinergic agonist) or acetylcholinesterase inhibitors into the striatum caused resting tremors in animals (Lalley et al, 1973).…”

Section: Discussionmentioning

confidence: 99%

Increased diisopropylfluorophosphate‐induced toxicity in μ‐opioid receptor knockout mice

Tien

Fan

et al. 2004

J of Neuroscience Research

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The potential involvement of mu-opioid receptors in mediating the changes of toxic signs and muscarinic receptor bindings after acute administration of irreversible antiacetylcholinesterase diisopropylfluorophosphate (DFP) was investigated. DFP-induced chewing movement and tremors were monitored for a period of 180 min in mu-opioid receptor knockout and wild-type mice. The autoradiographic studies of total, M1, and M2 muscarinic receptors were conducted using [(3)H]quinuclidinyl benzilate, [(3)H]pirenzepine, and [(3)H]AF-DX384 as ligands, respectively. Saline-treated mu-opioid receptor knockout and wild-type mice did not show chewing movement or tremors. Although DFP (1, 2, or 3 mg/kg, subcutaneous injection, s.c.)-induced chewing movement and tremors were shown in a dose-dependent manner, there were no significant differences in tremors induced by 1 or 2 mg/kg of DFP between mu-opioid receptor knockout and wild-type mice. There were also no significant differences in chewing movement induced by all doses of DFP between mu-opioid receptor knockout and wild-type mice. However, DFP (3 mg/kg)-induced tremors in mu-opioid receptor knockout mice were significantly increased over those in wild-type controls. Acetylcholinesterase activity in the striatum of saline-treated mu-opioid receptor knockout mice was significantly higher than that of the wild-type controls. After administration of DFP, acetylcholinesterase activity in the striatum of both mu-opioid receptor knockout and wild-type mice was significantly decreased (more than 36%, 58%, and 94% reduced at the doses of 1, 2, and 3 mg/kg, respectively) than that of their respective saline controls. M2 muscarinic receptor binding in saline-treated mu-opioid receptor knockout mice was significantly lower than that of the wild-type controls in the striatum. However, there were no significant differences in total, M1, or M2 muscarinic receptor binding in the cortex, striatum, or hippocampus of mu-opioid receptor knockout and wild-type mice after DFP administration. Our data show increased DFP-induced tremors, compensatory up-regulation of acetylcholinesterase activity, and compensatory down-regulation of M2 muscarinic receptors in the striatum of mice lacking mu-opioid receptor gene. These results suggest that the enhancement of DFP-induced tremors may be associated with the compensatory up-regulation of acetylcholinesterase activity and compensatory down-regulation of M2 muscarinic receptors in the striatum of mu-opioid receptor knockout mice.

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Analysis of the tremor induced by injection of cholinergic agents into the caudate nucleus

Cited by 63 publications

References 15 publications

Temperature and Behavioural Responses Induced in the Unanaesthetized Cat by the Central Administration of Rx72601, a New Anticholinesterase

Temperature and Behavioural Responses Induced in the Unanaesthetized Cat by the Central Administration of Rx72601, a New Anticholinesterase

Animal models of tremor

Increased diisopropylfluorophosphate‐induced toxicity in μ‐opioid receptor knockout mice

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