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Biomedical subjects

M P Remler

Publications and source records attributed to M P Remler.

16 recordsLinked to original sources
PubMed1992

Altered postural reflexes in Parkinson's disease: a reverse hypothesis.

In subjects standing on a movable platform, sudden dorsiflexion of the ankle joint elicits a set of reflexes in leg muscles. These responses include a short latency (SL) and medium latency (ML) stretch reflex in the gastrocnemius muscle and a distal to proximal innervation sequence of long latency (LL) reflexes in the shortened tibialis anterior and vastus lateralis muscles. Because of their role in maintaining upright stance these responses have been termed postural reflexes. In patients with Parkinson's disease (PD), the following abnormalities have been described: 1) enhanced ML-amplitudes; 2) a reversed LL innervation sequence; and 3) delayed onset latencies. These abnormalities are thought to be due to defective motor programming and disturbed control of spinal and supraspinal reflex centers by basal ganglia circuits. The altered reflexes have been held responsible for some of the clinical features of PD, including balance impairment and rigidity. In this paper, we argue the reverse hypothesis that postural reflexes are essentially normal in PD, and that the observed alterations are at least in part consequence rather than cause of balance impairment, the stooped parkinsonian posture and rigidity of PD patients.

Humans↗
PubMed1991

Electrophysiological correlates of postural instability in Parkinson's disease.

Postural reflexes in response to sudden toe-up tilts of a supporting forceplate platform were studied in free-standing patients with stage III (N = 5) and stage IV (N = 5) Parkinson's disease and compared to 5 age- and sex-matched normals. Latencies of the short (SL), medium (ML) and long latency (LL) responses were normal in the patients. The normalized mean amplitudes of the ML responses were significantly increased only in the stage IV Parkinson patients (P less than 0.0005). The distal-proximal activation sequence of LL responses observed in all 5 controls was reversed in 1 of the stage III and 4 of the stage IV Parkinson patients. Both the enlargement of the ML response (P less than 0.01) and the inverted activation sequence of LL responses (P less than 0.01) were significantly correlated with severity of the disease. The data establish an association between abnormal modulation of postural reflexes in the lower extremity and clinically rated balance impairment in Parkinson's disease.

Aged↗
PubMed1991

Long latency postural responses are functionally modified by cognitive set.

We examined how cognitive set influences the long latency components of normal postural responses in the legs. We disturbed the postural stability of standing human subjects with sudden toe-up ankle rotations. To influence the subjects' cognitive set, we varied the rotation amplitude either predictably (serial 4 degrees versus serial 10 degrees) or unpredictably (random mixture of 4 degrees and 10 degrees). The subjects' responses to these ankle rotations were assessed from the EMG activity of the tibialis anterior, the medial gastrocnemius, and the vastus lateralis muscles of the left leg. The results indicate that, when the rotation amplitude is predictable, only the amplitude of the long latency (LL) response in tibialis anterior and vastus lateralis varied directly with perturbation size. Furthermore, when the rotation amplitude is unpredictable, the central nervous system selects a default amplitude for the LL response in the tibialis anterior. When normal subjects are exposed to 2 perturbation amplitudes which include the potential risk of falling, the default LL response in tibialis anterior appropriately anticipates the larger amplitude perturbation rather than the smaller or an intermediate one.

Adult↗
PubMed1991

Postural reflexes in patients on long-term neuroleptic medication.

It is not conclusively known whether the amplitude of medium latency postural reflexes is controlled by dopamine. To further assess the influence of supraspinal dopaminergic pathways on postural reflexes, we studied short (SL), medium (ML) and long latency (LL) reflexes in the lower extremity of 10 patients on long term (greater than 6 months) neuroleptic medication, 5 with and 5 without mild drug induced parkinsonism. A control group consisted of 10 age and sex matched healthy volunteers. In both patient groups, latencies and amplitudes of all 3 responses were identical to normal controls. These findings suggest that a moderate postsynaptic inhibition of central dopaminergic pathways is insufficient to cause enhanced amplitudes of ML responses.

Adult↗
PubMed1990

Forcing of coupled nonlinear oscillators: studies of intersegmental coordination in the lamprey locomotor central pattern generator.

1. This paper reports the results of an investigation of the basic mechanisms underlying intersegmental coordination in lamprey locomotion, by the use of a combined mathematical and biological approach. 2. Mathematically, the lamprey central pattern generator (CPG) is described as a chain of coupled nonlinear oscillators; experimentally, entrainment of fictive locomotion by imposed movement has been investigated. Interpretation of the results in the context of the theory has allowed conclusions to be drawn about the nature of ascending and descending coupling in the lamprey spinal CPG. 3. Theory predicts and data show that 1) the greater the number of oscillators in the chain, the smaller is the entrainment frequency range and 2) it is possible to entrain both above and below the rest frequency at one end but only above or below at the other end. 4. In the context of the experimental results, the theory indicates the following: 1) ascending coupling sets the intersegmental phase lags, whereas descending coupling changes the frequency of the coupled oscillators; 2) there are differences in the ascending and descending coupling other than strength; and it also suggests that 3) coupling slows down the oscillators.

Afferent Pathways↗
PubMed1989

Systemic carbachol used in radiation-controlled focal brain pharmacology can decrease rat running.

Radiation-controlled focal brain pharmacology is a method to concentrate a neuropharmacologic agent in any selected portion of the brain by irradiating that selected area and thereby lowering the BBB in that area. Then, when a drug that does not cross the normal BBB is administered systemically, the drug will preferentially penetrate and act only in the selected part of the brain. Rats received 20 Gy to the brainstem and then were tested with normal 0.9% saline 1 ml/kg, GABA 400 mg/kg, taurine 200 mg/kg, carbachol 1 mg/kg, amphetamine 2 mg/kg, and bicuculline methiodide 27 mg/kg. Opening the BBB produced no change in the average amount of running following the injection of saline. With the BBB closed, carbachol, bicuculline methiodide and taurine produced no statistically significant effect compared to saline. Comparing the effects of a drug when the BBB is open to that of saline when the BBB is open showed no significant effect of bicuculline methiodide, taurine and GABA. Carbachol produced a 73% reduction, significant at p less than .0001. Comparing a drug when the BBB is open to the same drug when the BBB is closed showed no significant effect of bicuculline methiodide, taurine and GABA. Carbachol produced a 65% reduction, significant at p less than .001. This shows that radiation-controlled focal brain pharmacology with carbachol can decrease the complex behavior of running.

Animals↗
PubMed1986

The late effects of radiation on the blood brain barrier.

Rats were irradiated with 60 to 20 Gy in a single dose focussed to a volume of 0.5 cc in the center of the left hemisphere. Breakdown of the BBB was detected by the presence of spikes on EEG after subcutaneous injection of Bicuculline methiodide, and the presence of staining following Evans Blue dye injection. Breakdown of the BBB (mean and standard deviation) occurred in 38/46 of the 60 Gy rats at 98 +/- 16 days, 7/11 of the 50 Gy rats at 128 +/- 25 days, 11/18 of the 40 Gy rats at 162 +/- 3 days, 5/11 of the 30 Gy rats at 178 +/- 5 days and, 7/12 of the 20 Gy rats at 217 +/- 7 days post irradiation. This study suggests that endothelial damage could be the principle mechanism mediating the late radiation syndrome.

Animals↗
PubMed1973

A semiquantitative theory of synaptic vesicle movements.

Under the assumption that vesicles are the anatomic correlate of quantal release, the forces governing the movement of synaptic vesicles inside neurons are analyzed. Semiquantitative calculations are presented to show that a diffuse layer field penetrates a few Debye lengths into the axoplasm. This field binds tightly a monolayer of water to the membrane forming the potential barrier for miniature end-plate potential (mepp) release. The action potential destroys the monolayer and pulls the vesicle to the membrane. The vesicles are brought to the synaptic zone and held there by a Na(+) leak in the synaptic membrane. A stochastic theory of synaptic vesicle release is presented to explain experimental results. The rate of vesicle release is fractionated into a rate of membrane contacts by a vesicle and a rate of vesicle discharge per contact.

Action Potentials↗
PubMedDate not supplied

Bicuculline methiodide in the blood-brain barrier-epileptogen model of epilepsy.

Focal epilepsy can be produced by a blood-brain barrier (BBB)-excluded systemic convulsant (penicillin, folic acid, etc.) in the presence of a focal BBB lesion. Bicuculline methiodide, a gamma-aminobutyric acid blocking epileptogen, crosses the normal BBB of rats poorly and produces no consistent abnormality behaviorally or on EEG at 36 mg/kg. When the BBB is opened in 0.25 ml of cortex by 6,000 rad of alpha particles, by a pin trauma lesion, or by a heat lesion, the rats are normal clinically and on EEG. When these lesioned rats are challenged with bicuculline methiodide, 36 mg/kg, an intense, highly localized epileptiform discharge results that begins approximately 20 min after injection and lasts 30-90 min. The plausibility and experimental utility of the BBB-epileptogen model of epilepsy are enhanced by these observations.

Animals↗
PubMedDate not supplied

Systemic focal epileptogenesis.

Rats that receive radiation to 0.25 cc of one cerebral hemisphere are clinically and electroencephalographically normal until there is a breakdown of the blood-brain barrier (BBB) at 3 to 6 months postradiation. This BBB lesion can be detected by transient focal seizure activity produced by the BBB-excluded systemic convulsant bicuculline methiodide. In two rats the seizure activity induced by this one injection was self-sustaining. In seven of 15 other rats tested, the subsequent administration of repeated 2 mg/kg injections created a chronic focus that continued to spike with great frequency for 3 weeks or more without further administration of any convulsant. In three of eight other rats, implanted minipumps delivering 180 micrograms/h of bicuculline methiodide produced self-sustaining epileptic activity.

Animals↗
PubMedDate not supplied

Pharmacological response of systemically derived focal epileptic lesions.

Focal epileptic lesions were made in rats by systemic focal epileptogenesis. In this method, a focal lesion of the blood-brain barrier (BBB) is produced by focal alpha irradiation followed by repeated systemic injection of a convulsant drug that cannot cross the normal BBB, resulting in a chronic epileptic focus. Changes in the spike frequency of these foci in response to various drugs was recorded. The controls, saline and chlorpromazine, produced no change. Phenytoin, phenobarbital, chlordiazepoxide, and valproic acid produced the expected decrease in spike frequency. Pentobarbital and diazepam produced a paradoxical increase in spike frequency.

Action Potentials↗