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T J Parry

Publications and source records attributed to T J Parry.

6 recordsLinked to original sources
PubMed1995

Subthalamic nucleus lesions: widespread effects on changes in gene expression induced by nigrostriatal dopamine depletion in rats.

Lesions of the subthalamic nucleus block behavioral effects of nigrostriatal dopamine depletion in rats and primates, but the contribution of this region to the molecular effects of dopaminergic lesions is unknown. The effects of subthalamic nucleus lesions alone or in combination with a 6-hydroxydopamine-induced lesion of the substantia nigra were examined in adult rats. Unilateral subthalamic nucleus lesions caused ipsiversive rotation after peripheral administration of apomorphine and a small decrease in glutamic acid decarboxylase (GAD) mRNA in the ipsilateral globus pallidus (external pallidum). Confirming previous results, nigrostriatal dopaminergic lesions caused contraversive rotation after apomorphine injection, and increased enkephalin mRNA in the striatum, GAD mRNA in the globus pallidus, and somatostatin mRNA in the entopeduncular nucleus (internal pallidum) ipsilateral to the lesion. In addition, the lesion decreased substance P mRNA in the ipsilateral striatum compared to the contralateral side, and GAD mRNA in the contralateral entopeduncular nucleus. These effects were abolished in rats with lesions of the subthalamic nucleus and substantia nigra on the same side. Thus, the subthalamic lesions prevented changes in gene expression induced by dopamine depletion, not only in regions receiving a direct input from the subthalamic nucleus (ipsilateral pallidum), but also in regions which do not (striatum and contralateral pallidum). This suggests that polysynaptic pathways regulated by the subthalamic nucleus contribute to the effects of dopaminergic lesions in many regions of the basal ganglia. This pivotal role of the subthalamic nucleus may account for the beneficial effects of subthalamic nucleus lesions on motor symptoms resulting from dopamine depletion.

Animals↗
PubMed1994

Kainic acid administration in the fastigial nucleus produces differential cardiovascular effects in awake and anesthetized rats.

Kainic acid was microinjected or microdialyzed into the rostral medial aspect of the fastigial nucleus to determine its effect on mean arterial pressure and heart rate. This was carried out in both the awake and the anesthetized (alpha-chloralose) rat. In awake animals, kainic acid elicited an initial phasic pressor response which was followed by a long-term elevation of mean arterial pressure that lasted for the duration of the experiment (2 h). Rats anesthetized with alpha-chloralose exhibited only a tonic depressor response. This converted to a pressor response as the rats began to emerge from anesthesia after 2 h. Both the awake and the anesthetized rats exhibited regular phasic changes in mean arterial pressure that was superimposed on the longer term changes in the mean arterial pressure. Similar results were obtained in both the microinjected and the microdialyzed animals. Thus, stimulation of the intrinsic fastigial neurons by kainic acid evokes an elevation of the mean arterial pressure in the awake rat. This is manifested as a decrease in pressure in the anesthetized animal. Thus, stimulation of the cardiovascular region of the fastigial nucleus can increase or decrease mean arterial pressure. It is possible that the direction of the change in mean arterial pressure is dependent on the level of afferent or intrinsic fastigial neural activity.

Animals↗
PubMed1994

Dopaminergic stimulation of subthalamic nucleus elicits oral dyskinesia in rats.

The effects of dopaminergic stimulation of the subthalamic nucleus (STh) on motor behavior were examined in conscious rats. Unilateral infusion of apomorphine (0.1 to 3.2 micrograms) into the STh induced a dose-dependent increase in abnormal, nondirected orofacial movements without altering turning, sniffing, grooming, or rearing behaviors. Orofacial movements elicited by local infusion of apomorphine (1.0 microgram) into the STh were blocked by peripheral administration of the D1 antagonist, SCH 23390 (0.1 mg/kg, sc), but not by the D2 antagonists haloperidol (1.0 mg/kg, sc) or sulpiride (50 mg/kg, sc). Furthermore, coinfusion of SCH 23390 (1.0 microgram), but not sulpiride (5.0 micrograms), with apomorphine (1.0 microgram) into the STh blocked oral dyskinesia. Oral movements could not be reelicited by an infusion of apomorphine into the STh after a kainic acid lesion of the STh. In addition, infusion of apomorphine (1.0 microgram) into sites proximal to but deliberately outside of the STh failed to elicit nondirected oral movements above baseline levels. The results indicate that stimulation of D1 dopaminergic receptors within the STh induces abnormal orofacial movements. This highlights the importance of the dopaminergic input to the STh in the regulation of motor function and suggests that D1 receptor antagonists could prove useful in the treatment of orofacial dyskinesia in humans.

Animals↗
PubMed1993

A method for restraining awake rats using head immobilization.

A method for restraining awake rats using head implant immobilization is described. In order to reduce stress to the individual animal, rats were restrained side by side in pairs during the adaptation and experimental periods. This technique was used in studies of central regulation of cardiovascular function. In particular, microdialysis probes were placed stereotaxically in deep nuclei of the cerebellum while mean arterial pressure and heart rate were monitored in the awake rat. After initial habituation, normal levels of heart rate and blood pressure obtained during restraint indicated that this is essentially a nonstressful procedure. This technique could also be used for a variety of other experimental conditions where head movement is not desirable, such as during oculomotor or vestibular experiments.

Animals↗
PubMed1990

Physical and chemical considerations in the in vitro calibration of microdialysis probes for biogenic amine neurotransmitters and metabolites.

The object of the present study was to examine the effects of temperature, oxidation, and pH on in vitro relative recovery of catecholamine and indoleamine neurotransmitters and their metabolites using microdialysis probes. Relative recovery of norepinephrine (NE), dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic acid (5HIAA), dopamine (DA), homovanillic acid (HVA), and 5-hydroxytryptamine (5HT) increased with temperature from 0 to 46 degrees C. For each compound, the increase in the amount recovered with increasing temperature was different. The stability of norepinephrine and dopamine was not affected at any temperature using deoxygenated calibration standard solutions containing ascorbic acid but was greatly reduced when exposed to ambient air without antioxidant treatment; catecholamine metabolites and the indole compounds were less affected. No change for in vitro relative recovery was observed by varying the pH of the perfusing solution from 6 to 8. Thus, temperature control in probe calibration as well as analyte stability using antioxidant treatment are important in reducing the error when estimating extracellular concentrations of neurotransmitter and metabolites.

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