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Biomedical subjects

A Peppe

Publications and source records attributed to A Peppe.

34 records · Page 2Linked to original sources
PubMed1998

D1 agonist CY208-243 attenuates the pattern electroretinogram to low spatial frequency stimuli in the monkey.

We investigated whether or not the D1 agonist, CY 208-243, affects the spatial tuning function of pattern electroretinogram (PERG). Two lightly anaesthetised monkeys were studied before and after CY 208-243 or placebo administration. The results show that the PERG response to 0.5 cycles/degree (c/d; coarse), but not to 2.3 c/d (medium) spatial frequency stimuli disappears following systemic administration of this drug. Since previous results show that D2 blockers attenuate the PERG only above 2.3 c/d, foremost the peak of the normal spatial frequency response function, the current results suggest that dopamine itself, via D1 receptors, may be responsible for the low spatial frequency decline of normal spatial PERG tuning function. We infer that the synergistic activation of D1 and D2 receptors is needed to shape the spatially tuned primate ERG.

Animals↗
PubMed1998

Does pattern electroretinogram spatial tuning alteration in Parkinson's disease depend on motor disturbances or retinal dopaminergic loss?

Systemic decrease of dopaminergic cells, such as in Parkinson's disease may produce visual alterations in humans. In order to show possible pattern electroretinogram (PERG) spatial tuning function (STF) alterations due to impaired dopaminergic transmission in humans, we studied a group of Parkinson's disease patients before and during treatment with the dopamine precursor, levodopa, and compared their performances with those of an age-matched control group. Moreover, in order to exclude the possible involvement of motor disabilities to produce PERG alterations, we also investigated PERG responses in post-traumatic parkinsonian patients who exhibited motor abnormalities as a consequence of focal lesions of basal ganglia, in the absence of systemic dopaminergic degeneration. Our results showed a clear decrease of PERG responses in Parkinson's disease patients particularly at medium spatial frequency range (2.7-4.0 cycles/degree) with a substantial preservation of responses at low frequencies. Levodopa therapy reversed these alterations in Parkinson's disease patients, resulting in the recovery of a normal tuning function shape. In contrast to Parkinson's disease, the tuning function appeared to be preserved in post-traumatic parkinsonian patients. Our results clearly establish a relationship between retinal alteration in PD patients and dopaminergic retinal function.

Adult↗
PubMed1998

Age and stage dependency of P300 latency alterations in non-demented Parkinson's disease patients without therapy.

Acoustic P300 was recorded from Fz, Cz and Pz by means of an 'odd-ball' paradigm in 44 non-demented de novo Parkinson's disease patients (PD) or PD patients under treatment withdrawal, and in 31 age-matched normal subjects, to evaluate whether a P300 latency increase was present in PD patients. The influence of age and disease stage on latency was successively verified by subgrouping PD patients according to different age ('young' and 'old') and disease stage ('early' or 'advanced'). PD patient data were compared to data of normal subjects subgrouped into 'young' and 'old' or, to eliminate the age-dependent shift of latency, this latter was adjusted to 60 years in all the examined subjects. A significant increase of latency has been found in Fz and Cz in the 'old' group of PD patients (n = 23) but not in the 'young' group (n = 21) utilising both methods. Moreover, a significant latency increase was also present in Fz and Cz in the group of 'advanced' PD patients (n = 8), but not in the group of 'early' PD patients (n = 36) utilising age-adjusted measurements. When the 'early' PD patient group was divided into 'young' (n = 20) and 'old' (n = 16), the 'early old' group displayed significantly increased latencies in Fz compared with normal subjects. Abnormal P300 latencies were observed, at least in one electrode, by analysing the raw data, in 5.0% of the 'early young', 43.7% of the 'early old' and up to 62.7% of the 'advanced' patients. Fz represented the site in which abnormal P300 latencies were most often observed. Moreover, in the total group of PD patients, the P300 delay was significant only on the frontal (Fz) site when compared with normal subjects. The reported findings were interpreted as if PD produces a sort of 'accelerated effect of age' on the cognitive functions, presumably produced by a mechanism different from that producing motor impairment since no clear correlation could be detected between P300 latency and motor score. The frontal impairment of P300 is in line with previous neuropsychological findings obtained in these patients. Considering that about 30% of PD patients develop dementia during their disease progression, a border-line or abnormal P300 latency observed at disease onset may represent a predictive marker of this evolution.

Adult↗
PubMed1996

Effects of kappa receptor agonists on D1 and D2 dopamine agonist and antagonist-induced behaviors.

Striatal dynorphin-containing neurons receive dopaminergic inputs from the substantia nigra pars compacta and project primarily to the substantia nigra pars reticulata and entopeduncular nucleus. These neurons mainly express dopamine (DA) D1 receptors and thus dynorphin system stimulation might be expected largely to influence D1 receptor agonist or antagonist effects on motor function. It is well known the interaction existing between DA D1 and D2 drugs in the induction of behavioral effects. However, the effects of dynorphin on selective D1 and D2 DA agonist and antagonist-induced behaviors have not yet been investigated. Administration of the kappa agonists spiradoline (0.5, 1 and 5 mg/kg) or U50,488H (1, 10 and 25 mg/kg) decreased non-stereotyped grooming induced by the selective D1 agonist SKF38393. This effect was inhibited by the non-selective opioid receptor antagonist naloxone (20 mg/kg) and by the selective kappa antagonist nor-binaltorphimine (nor-BNI, 20 mg/kg). Stereotypies induced by the selective D2 agonist quinpirole were decreased by spiradoline (1 and 5 mg/kg) and by U50,488H (1, 10 and 25 mg/kg), while jerking movements of a type associated with increased D2 receptor and decreased D1 receptor stimulation emerged. Kappa agonist effects were inhibited by the prior administration of SKF38393 (10 mg/kg); these inhibitory effects were blocked by prior administration of the D1 antagonist SCH23390 (5 mg/kg). Naloxone reversed the effects of both kappa agonists on quinpirole-induced stereotypies. Kappa agonists increased D1 antagonist-induced catalepsy, but had no effect on D2 antagonist-induced catalepsy. Naloxone and nor-BNI inhibited this effect. These results suggest that the motoric effects of D1 receptor antagonists in part reflect stimulation of striatal dynorphin containing efferents.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

Increasing doses of l-sulpiride reveal dose- and spatial frequency-dependent effects of D2 selective blockade in the human electroretinogram.

The amplitude and phase of the second harmonic (15 Hz) of the electroretinographic responses to three different spatial frequency grating stimuli (0.25, 1 and 4 c/deg), reversed at 7.5 Hz, were studied i normal human subjects, before and 30 min after the systemic administration of three doses (0.071, 0.357 or 1.428 mg/kg) of a selective D2 blocker, l-sulpiride, to three populations of 18, 19, or 20 subjects. The effect of the drug on the pattern electroretinogram (PERG) was clearly dose-dependent, being greatest on the responses to 4 c/deg. The mean decrease in second harmonic amplitude was -13.8% after 0.071 mg/kg of l-sulpiride, -23.5% after 0.357 mg/kg and -28.5% after 1.428 mg/kg. The last two variations were significant at P < 0.01 and P < 0.01 respectively. These data suggest that a dose-dependent effect on the human retinal response to 4 c/deg stimuli exists, probably mediated by a coupling between l-sulpiride and D2 receptors. Lastly, our data suggest that D2 receptors may play an important role in the pathophysiology of visual dysfunction in Parkinson's disease, that has been described to be more significant at medium spatial frequency (2-5 c/deg).

Adult↗
PubMed1995

Visual alterations in de novo Parkinson's disease: pattern electroretinogram latencies are more delayed and more reversible by levodopa than are visual evoked potentials.

There are increased latencies of pattern-reversal visual evoked potentials (VEPs) and electroretinograms (PERGs) in Parkinson's disease (PD) patients who have not received therapy. This study aimed to evaluate whether these delays are present in the early stage of PD and whether they are dopamine-sensitive. The results show that both PERG P50 and VEP P100 latencies are increased (p < 0.0001) in a group of patients with de novo PD (13 subjects; 13.3 +/- 5.6 months' mean disease duration) before therapy in comparison with an age-matched control group (eight subjects). A larger latency increase (9.9% at the 47% contrast level and 7.8% at the 96% contrast level) was present in PERG recordings than in VEPs (6.2% at the 47% contrast level and 3.9% at the 96% contrast level). Levodopa therapy produced recovery of both PERG and VEP latency increases at both contrast levels, but only the PERG recovery at 47% of contrast was statistically significant. Before therapy, five eyes from PD patients showed no reproducible PERG at the 47% contrast level although the simultaneously recorded VEP was present. Both potentials were recordable in the same eyes at the 96% contrast level. During therapy, four of those five eyes showed a clear PERG even at the 47% contrast level. We conclude that, using an adequate midspatial frequency, both VEPs and PERGs are delayed even in the early stage of PD, and that PERGs are more sensitive if low contrast (47%) is used. The larger alterations, as well as the larger recovery during levodopa therapy, seem to correlate the PERG response more than the VEP response to dopaminergic transmission.

Aged↗
PubMed1993

D1 and D2 dopamine receptor-mediated mechanisms and behavioral supersensitivity.

The contribution of D1 and D2 dopamine (DA) receptor mechanisms to the behavioral supersensitivity and receptor upregulation induced by chronic DA antagonist administration were compared. Rats received either the selective D1 DA receptor antagonist SCH23390, the selective D2 DA receptor antagonist raclopride, their combination, or haloperidol, a predominantly D2 antagonist, for 21 days. Equivalent cataleptogenic doses of all drugs and drug combinations were employed. Tolerance to the cataleptic response was observed only in the haloperidol-treated group. Apomorphine-induced stereotypies were significantly enhanced in SCH23390-, raclopride-, and haloperidol-treated rats. In contrast, coadministration of both SCH23390 and raclopride had no effect on apomorphine-induced stereotypy. These findings suggest that neuroleptics blocking in equal proportion D1 and D2 receptor sites might be less likely to induce tardive dyskinesia and drug tolerance than those acting selectively on one or the other of these receptor subtypes.

Animals↗
PubMed1993

Visual and visual perceptual disorders in neurodegenerative diseases.

Optic neuropathy is reported to occur in 10-30% of patients, while retinopathy is characteristic of type III OPCA. The use of visual and visual electrophysiological tests in early diagnosis and classification is promising. The relationship between visual impairment and other manifestations of these diseases has not been explored.

Brain Diseases↗
PubMed1992

Low contrast stimuli enhance PERG sensitivity to the visual dysfunction in Parkinson's disease.

The pattern electroretinogram (PERG) was recorded at different contrast levels (96%, 71%, 47%) in 10 Parkinson's disease patients before and during dopaminergic monotherapy. The data were compared to a control group of 8 normal subjects recorded with the same procedure. PERG P50 latency progressively increased as contrast was decreased both in normal subjects and patients; however, this trend was much more pronounced in PD patients without therapy; consequently in this group the difference between P50 latency obtained with 96% and 47% contrast was statistically significant (P = 0.01, analysis of variance corrected by post-hoc Tukey test). By contrast this was not seen in the control group. Statistical analysis (Bonferroni's t test) showed at the 47% contrast level a significant P50 latency increase (P less than 0.01) in PD patients without therapy if compared with the control group. Dopaminergic monotherapy induced a P50 latency recovery in PD patients. We conclude that low contrast stimuli enhance PERG sensitivity to the visual dysfunction of PD patients. Moreover, the effects observed after therapy confirm that abnormal contrast response functions in PD patients are linked to dopaminergic deficiency.

Aged↗
PubMedDate not supplied

Antiepileptic effects of a calcium antagonist (nimodipine) on cefazolin-induced epileptogenic foci in rabbits.

The epileptogenic properties of cefazolin (CFZ) were utilized to induce an electrophysiological pattern of epilepsy in the rabbit. CFZ, cortically applied in different concentrations (2 or 4%), produced epileptic activity in a degree proportional to the concentration of the substance. In this experimental epilepsy model, we evaluated the effects of increasing doses (0.025, 0.05, and 0.1 mg/kg i.v.) of the calcium antagonist nimodipine (Bay e 9736). In the evaluation of nimodipine effects, the spike-and-wave burst frequency per minute was taken into account. These data were compared with those of placebo-treated (Bay e 9736 control test) control groups and statistically evaluated by two-tailed t test. In 2% CFZ-induced epilepsy, nimodipine at the 0.025- and 0.05-mg/kg doses did not produce significant changes in the EEG pattern. A statistically significant reduction (p less than 0.001) in epileptic activity was observed at the 0.1-mg/kg nimodipine dose. This reduction was seen first in the contralateral focus leads and persisted for the entire time of observation. In the more intense epileptic form (4% CFZ), nimodipine at the doses employed did not induce noteworthy EEG modifications. These data indicate that nimodipine exerts an antiepileptic effect. The possible mechanisms involved in this activity of a calcium antagonist are discussed.

Animals↗
PubMedDate not supplied

[Miller Fisher syndrome: review of the literature and presentation of 2 cases].

Miller Fisher Syndrome (MFS), which is characterized by ophthalmoplegia, ataxia and tendon areflexia, is generally considered as a clinical variant of Guillain-Barré Syndrome. However some features of the disease are still debated, particularly regarding possible central nervous system involvement. After presenting two new cases of MFS, the authors provide a critical review of the literature and discuss the nosographical position of the disease. The main conclusions can be summarized as follows: MFS is a predominantly axonal inflammatory neuropathy with prevailing involvement of oculomotor nerves. It is associated to spinal multi or polyneuropathy, which in mildly affected cases is manifested by areflexia, while in severe ones it can be responsible of sense and/or motor impairment. In addition to peripheral neuropathy CNS involvement, exclusive or more marked in posterior fossa, occurs not infrequently. The prognosis of the disease is often benign, but disabling or even fatal outcome is possible. Corticosteroid treatment, possibly because of antiinflammatory and/or immunosuppressive action, could be effective in some patients. Finally, in spite of some similarities with GBS, MFS should be considered as a separate entity with its own nosographical position.

Adult↗
PubMedDate not supplied

[Intravenous infusion of L-dopa: current prospective therapies].

Most of Parkinson's disease patients treated with Levodopa develop the Long Treatment Levodopa Syndrome. Many authors showed a correlation between clinical features and plasma level of Levodopa. In our study, five parkinsonian patients with severe clinical response fluctuations, oral levodopa treatment was replaced by repeated continuous infusions of Levodopa (with oral carbidopa). Our results confirm that repeated intravenous infusion are very effective in PD patients with LTS.

Adult↗