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Biomedical subjects

S R Snider

Publications and source records attributed to S R Snider.

At least 37 records · Page 2Linked to original sources
PubMed1979

Kainic acid: enduring alterations in cerebellar morphology and in cerebral catecholamine and GABA concentrations after cerebellar injection in the rat.

Kainic acid injected locally in the vermian cortex produces a focal lesion with severe cellular loss. Microscopic changes in 3-week-old preparations are given for both central and peripheral segments. Biochemical studies indicate that norepinephrine, dopamine and gamma-aminobutyric acid (gaba) concentrations in the forebrain are consistently higher on the side of the lesion and remain elevated for at least 3 weeks. It is postulated that disinhibition of cerebellar activity traversing the uncrossed pathway from cerebellar nuclei to catecholamine cell bodies was a major mechanism causing increased catecholamine metabolism in the ipsilateral forebrain.

Animals↗
PubMed1979

The role of bromocriptine in the treatment of parkinsonism.

Fifty-three patients with parkinsonism, either with intractable symptoms despite optimum-dosage levodopa therapy or with adverse effects from levodopa limiting its usefulness, were treated with bromocriptine, with gradually increasing doses until benefit or adverse effect was encountered. All were initially maintained on optimal levodopa therapy. Improvement was seen in 26 patients, of whom 19 (36 percent of the total 53 patients) had sustained improvement. Effective doses of bromocriptine ranged from 5 to 90 mg per day. Improvement occurred in all categories of clinical problems, including patients who lost some benefit from chronic levodopa therapy as well as those with adverse effects from levodopa. A high incidence (70 percent) of adverse effects of bromocriptine limited the usefulness of this drug. Since one cannot predict which patients might benefit from bromocriptine, this drug is worth a trial in patients not doing well on levodopa therapy if other means to improve their condition are not successful.

Aged↗
PubMed1979

Analysis of the clinical problems in parkinsonism and the complications of long-term levodopa therapy.

We evaluated the current status of 131 patients with idiopathic parkinsonism who were receiving levodopa therapy. The residual parkinsonian symptoms and signs were tabulated, as were the adverse effects from medication. Response to therapy was correlated with duration of the disease and with duration of treatment. Patients with on-off or wearing-off effects were likely to have been treated for 4 years or longer. Patients treated with levodopa for 4 to 8 years were significantly more impaired with parkinsonism than patients treated for 0 to 3 years, even when patients were matched for total duration of disease. These data suggest that the deterioration of responsiveness after several years of levodopa therapy may be due to the therapy itself. Our findings support the concept that utilization of levodopa therapy should be delayed until a patient becomes significantly impaired in occupational or social situations.

Adolescent↗
PubMed1978

Focal brain hyperthermia. I. The cerebellar cortex.

Focal brain hyperthermic methodology has been described and data presented on the cerebellum which show that enhancement of electrical activity of cerebellar cortex occurs when this method is used with careful monitoring of temperature. The duration of electrically induced cerebral after-discharges is shortened when cerebellar warming reaches 39.5--42.0 degrees C,. Since these effects are repeatable over many hours, there appears to be little, if any, resultant damage. Such induced changes in the cerebrum resemble those previously reported in which electrical stimuli were applied to the cerebellar cortex.

Animals↗
PubMed1977

Phenytoin and cerebellar lesions. Similar effects on cerebral catecholamine metabolism.

Phenytoin has been shown to inhibit catecholamine (CA) metabolism in vitro. The present investigation examined its longer-term in vivo effects in rats. Phenytoin 100 mg/kg/day for two weeks, caused an increase in hindbrain norepinephrine (NE) concentration, a slight decrease in forebrain NE concentration, and little change in dopamine (DA) levels. The turnover rates of forebrain DA and NE estimated by synthesis inhibition, were increased by 70% and 100%, respectively. Surgical lesions of the anterior cerebellar vermis produced similar (but not additive) increases in turnover. It is concluded that long-term phenytoin use stimulates CA metabolism in the forebrain and that this effect may be mediated indirectly by the cerebellar vermis.

Animals↗
PubMed1977

Is dopamine a neurohormone of the adrenal medulla? Studies with morphine stimulation.

Dopamine (da) concentrations in rat adrenals, plasma and brain were variably elevated 1 h after a large parenteral dose of morphine. In adrenals, unlabelled DA increased 2-fold and labelled DA, synthesized from 3H-tyrosine, increased more than 4-fold. The increases could be prevented by inhibition of DA-synthesizing enzymes and spinal cord transection, respectively. Labelled DA in plasma increased 2.7-fold after morphine in intact rats but did not increase in those with spinal cord transection. It is concluded that: (1) morphine stimulates the adrenal by increasing nerve impulse flow, (2) increased nerve impulse flow increases DA synthesis and levels, and (3) the increased DA levels result in increased release of DA into the bloodstream.

Adrenal Medulla↗
PubMed1977

Alterations in forebrain catecholamine metabolism produced by cerebellar lesions in the rat.

Projections from the midline cerebellar nuclei to norepinephrine (NE) and dopamine (DA) cell groups in the brain stem have been demonstrated histologically. To determine if these connections are significant biochemically, unilateral electrolytic lesions were placed in either vermis or paravermis and levels of DA, NE and gamma-aminobutyric acid (GABA) were measured in each half of the forebrain at 1 1/2, 3 or 6 weeks. In the cerebral hemisphere ipsilateral to a vermis lesion, there was a decrease in NE levels at 3 and 6 weeks. Relative to the opposite side DA was also reduced at 3 and 6 weeks. Paravermal lesions caused a contralateral reduction in DA at 3 weeks but no change in NE. GABA was only slightly altered. These results suggest that the cerebellum can modify levels and turnover of catecholamines in the brain, possibly via direct anatomic connections as well as by functional interaction with catecholaminergic pathways.

Animals↗
PubMed1977

Detection of presymptomatic carriers of Huntington's chorea.

Laterality of thumb opposition and handedness were determined in three groups of subjects: patients with Huntington's chorea (n = 18), asymptomatic offspring of patients (n = 40), and asymptomatic siblings of patients over 50 years of age termed 'escapees' (n = 17). 100% of patients and 55% of young at-risk offspring had crossed laterality of thumb opposition and handedness. Only 2 (11.8%) of the 'escapees' had crossed laterality. Crossed laterality may be associated with symptomatic presymptomatic Huntington's chorea.

Adolescent↗
PubMed1977

Interaction between bromocriptine and levodopa. Biochemical basis for an improved treatment for parkinsonism.

The present investigation examined the biochemical interaction of bromocriptine and levodopa with respect to monoamine and gamma-aminobutyric acid metabolism in the brain. Rats were treated with levodopa, 250 mg per kilogram of body weight intraperitoneally, with or without carbidopa, 25 mg per kilogram, 1 or 2 hours before sacrifice. Some were also given bromocriptine, 5.0 mg per kilogram, 4 hours before sacrifice. Rats were killed 1 and 2 hours after levodopa and brain levels of gamma-aminobutyric acid and monoamines, and their metabolites were measured. Dopamine levels and metabolism were not markedly altered when bromocriptine was added to levodopa treatment. The level of serotonin, which was reduced 25 to 40 percent by levodopa alone, was close to normal with the combination treatment. Serotonin metabolism was also enhanced by the addition of bromocriptine as shown by increased levels of 5-hydroxyindoleacetic acid. The results suggest that bromocriptine not only may improve the motor disorder of parkinsonism but also may reduce some side effects of levodopa therapy, such as depression, which could be due to serotonin depletion.

Animals↗
PubMed1976

Recovery of dopamine in peripheral adrenergic nerves after reserpine treatment.

The endogenous levels of dopamine (DA) in the rat heart and submaxillary gland after a single, large dose of reserpine (10 mg/kg i.p.) were reduced to near zero within 1 h and were restored to normal within 48 h, while the noradrenaline (NA) levels reacted much more slowly. The data suggest that newly formed DA is rapidly taken up by the reserpinesensitive mechanism of the amine storage granules. The more rapid restoration of DA than of NA levels may be due to preferential release of newly formed NA by the nerve impulse. Electrical stimulation of the cervical sympathetic with 5 Hz for 30 min 4 h after the administration of reserpine increased the DA level of the submaxillary gland of the stimulated side, suggesting an increased tyrosine hydroxylase activity during stimulation, also in nerve terminals affected by reserpine. The use of an inhibitor of monoamine oxidase (pargyline) and/or an inhibitor of dopamine beta-hydroxylase (FLA-63) did not significantly alter the increase of DA following nerve stimulation, suggesting DA was protected by granular uptake. The stimulation-induced increase in DA was, however, much less in reserpine-treated than in normal animals, demonstrating the importance of the reserpine-sensitive uptake mechanisms for preserving newly formed DA.

Animals↗