

Tremulous jaw movements also are induced by muscarinic agonists such as arecoline and pilocarpine, ,, ,, and anticholinesterases such as physostigmine or tacrine, ,,. These movements can be induced by a number of conditions that parallel the neurochemistry of the pathology of Parkinsonism, including DA depletions in the ventrolateral neostriatum, , acute or sub-chronic injections of DA antagonists, , and reserpine. Tremulous jaw movements are defined as rapid and repetitive vertical deflections of the lower jaw that are not directed at any particular stimulus. Nevertheless, one of the rodent behavioral procedures that has emerged within the last few years as a potential model of Parkinsonian resting tremor is drug-induced tremulous jaw movements. In general, there have been few reports of Parkinsonian tremor in rodents.

For these reasons, it is important to focus additional research on the pharmacology and neurochemistry of tremor, and studies employing animal models are an important part of this research. As noted in several recent articles, ,, there still is considerable uncertainty about the central mechanisms through which Parkinsonian tremor is generated. Although resting tremor is one of the cardinal symptoms of Parkinsonism, much of the clinical pharmacology research in this area has focused upon akinesia, or general indices of Parkinsonism, and relatively few clinical pharmacology studies have specifically emphasized tremor. Considerable research in this area has focused upon the pharmacological and neurochemical interactions between ACh and DA,. Current models of basal ganglia function suggest that Parkinsonian symptoms are produced by a cascade of neurochemical and physiological events involving several transmitters in various parts of basal ganglia circuitry, ,. Idiopathic and drug-induced Parkinsonism typically is treated by drugs that stimulate DA tone or block muscarinic acetylcholine (ACh) receptors,. In addition, Parkinsonian symptoms can be produced or exacerbated by various drugs, including DA antagonists and cholinomimetics. Idiopathic Parkinson’s disease results from the degeneration of nigrostriatal dopamine (DA) neurons. Parkinsonism is a family of movement disorders, with symptoms that include rigidity, bradykinesia, akinesia, and tremor. Together with previous studies, the present results suggest that cholinomimetic-induced jaw movements in rats can be used to characterize dopaminergic antiparkinsonian agents and to investigate the basal ganglia circuits involved in the generation of tremulous movements.

Across several studies, the rank order of potency for suppressing cholinomimetic-induced jaw movements in rats is related to the potency for producing antiparkinsonian effects in humans. The D1 agonist CY 208–243, which has been reported to suppress tremor, also reduced jaw movement activity (4.0 mg/kg). The selective D2 agonist ropinirole, which also is used clinically as an antiparkinsonian drug, suppressed jaw movements in the dose range of 2.5–20.0 mg/kg. The non-selective dopamine agonist pergolide, a widely used antiparkinsonian drug, was highly potent at suppressing tacrine-induced jaw movements (e.g. The present study investigated three different types of dopamine agonists, which have known antiparkinsonian characteristics, for their ability to suppress the tremulous jaw movements induced by tacrine (5.0 mg/kg). Caffeine, unlike aminophylline, was not associated with irritable behaviour at standard dose.Considerable evidence indicates that cholinomimetic-induced tremulous jaw movements in rats share many characteristics with human Parkinsonian tremor, and several antiparkinsonian drugs suppress cholinomimetic-induced tremulous jaw movements. We assessed tremulous movement (a sub-score of General Movements Optimality Score) in 18 caffeine-treated subjects and 18 aminophylline-treated subjects. N2 - This paper is an examination of irritable behaviour in very low-birth-weight infants in relation to caffeine or aminophylline. T1 - Caffeine not associated with irritable behaviour in very low-birth-weight infants.
