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J D Stittsworth

Publications and source records attributed to J D Stittsworth.

11 recordsLinked to original sources
PubMed1998

Conduction velocity versus amplitude analysis: evidence for demyelination in diabetic neuropathy.

Motor conduction velocities (CVs) were correlated with distal compound muscle action potential (CMAP) amplitudes for tibial, peroneal, and median nerves in patients with biopsy-proven chronic inflammatory demyelinating polyneuropathy (CIDP), diabetic neuropathy, and amyotrophic lateral sclerosis. Only in the diabetic patients did CV significantly correlate with CMAP amplitude. The data show that diabetic neuropathy produces conduction velocity slowing that cannot be explained by axon loss alone, and that differentiation between diabetic neuropathy and CIDP in an individual nerve is difficult.

Action Potentials↗
PubMed1994

Comparison of neuronal responses to experimental ischemia in gerbil and rat hippocampal slices.

The present study utilized in vitro gerbil and rat hippocampal slices to compare responses to experimental ischemia without species differences in the cerebrovasculature as a variable. Ischemic depolarization occurred faster in the gerbil (2.53 +/- 0.05 min) than in the rat (4.59 +/- 1.1 min). These results indicate that the gerbil's greater propensity to neuronal damage following short ischemic periods may be due to greater sensitivity of the gerbil brain itself.

Animals↗
PubMed1994

Resistance to epileptic, but not anoxic, depolarization in the gerbil hippocampal slice preparation.

The Mongolian gerbil displays spontaneous seizures and is used as a model for global ischemia. This study investigated the electrophysiological events associated with 0-Mg(2+)-induced seizures in gerbil hippocampal slices. In the rat hippocampal slice, 0-Mg2+ medium leads to rapid extracellular epileptic depolarization (ED) accompanied by long-term synaptic failure. Both evoked and spontaneous epileptiform activity was observed in the gerbil hippocampal slice after the introduction of the 0-Mg2+ aCSF. However, unlike the rat, ED was rarely observed in the gerbil hippocampal slice (2/17). When ED occurred, synaptic responses recovered (75%) within 20 min. This resistance to epileptic depolarization did not generalize to experimental ischemia-induced depolarization. Anoxia in 2 mM D-glucose produced anoxic depolarization in all gerbil hippocampal slices tested (6/6).

Animals↗
PubMed1993

Lactate mimics only some effects of D-glucose on epileptic depolarization and long-term synaptic failure.

Lactate supports normal synaptic function and may be neuroprotective following an anoxic insult. The present study investigated the effects of lactate on epileptic depolarization and long-term synaptic failure during a zero-magnesium-induced epileptic insult using the hippocampal slice preparation. In artificial cerebrospinal fluid (aCSF) containing 10 mM D-glucose, no epileptic depolarization was observed. At lower concentrations of D-glucose, epileptic depolarization occurred and often was followed by long-term synaptic failure. Low concentrations of lactate, in place of D-glucose, supported normal synaptic transmission. However, no concentration of lactate tested (up to 30 mM) blocked the occurrence of epileptic depolarization. High concentrations of lactate allowed for partial recovery of synaptic responses following epileptic depolarization. Reinstatement of D-glucose was necessary to observe this recovery. The results confirm that lactate can replace D-glucose in maintaining synaptic responses, but demonstrate that lactate cannot replace D-glucose in blocking an insult-induced depolarization. The inability of lactate to mimic all the effects of D-glucose is consistent with the notion of compartmentation of energy utilization within neurons.

Animals↗
PubMed1990

Cholecystokinin octapeptide potentiates the inhibitory response mediated by D2 dopamine receptors in slices of the ventral tegmental area of the brain in the rat.

The ability of cholecystokinin octapeptide (CCK8) to modulate dopamine (DA)-induced inhibition of the firing of neurons in the ventral tegmental area of the rat was examined. Extracellular recordings were obtained from putative DA-containing neurons, identified on the basis of their electrophysiological characteristics and response to DA, in an in vitro slice preparation from the ventral tegmental area of the brain. Application of DA produced a concentration-dependent reduction in firing rate. This DA-induced inhibition was mimicked by the D2 selective agonist, LY 171555 (trans-(-)-4,4a,5,6,7,8,8a,9-octahydro-5-propyl-2H- pyrazolo[3,4-g]quinoline), but not by the D1 selective agonist, SKF 38393 (R-(+)-2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine). The DA-induced inhibition was antagonized selectively by the D2 antagonist, l-sulpiride, but not by the D1 antagonist, SCH 23390 (R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7- ol). However, CCK8 elicited a transient increase in firing rate in some neurons and, in addition, potentiated the inhibitory response evoked by DA or LY 171555. Again SKF 38393 was without effect following the administration of CCK8. Taken together, these results suggest that DA-induced inhibition of DA-containing neurons in the ventral tegmental area of the brain of the rat is mediated by activation of D2-receptors and that CCK8 potentiates this D2-mediated inhibition.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1983

[3H]dopamine depletion from osmotically defined storage sites: effects of reserpine, 53 mM KCl, and d-amphetamine.

A crude synaptosome-containing fraction (P2') prepared from rat striatal slices incubated with [3H]dopamine was exposed to hypoosmotic conditions and rapidly subjected to Millipore filtration. P2'-associated [3H]dopamine trapped on the filters was defined as hypoosmotic resistant, whereas P2'-associated [3H]dopamine that washed through the filters was defined as hypoosmotic sensitive. Electron microscopic examination of sections prepared from a P2' pellet that had been exposed to hypoosmotic conditions revealed extensive synaptosomal lysis. [3H]Dopamine accumulation and retention by the hypoosmotic-resistant fraction were reduced by reserpine. The proportional distribution of [3H]dopamine between hypoosmotic-resistant and -sensitive fractions was measured following in vitro exposure of the preloaded P2' fraction to reserpine, 53 mM KCl, and d-amphetamine. Each of these treatments resulted in a time-dependent loss of [3H]dopamine from the loaded P2' fraction without eliciting an alteration in the proportional distribution of [3H]dopamine between hypoosmotic-resistant and -sensitive fractions. Release induced by reserpine and d-amphetamine was independent of extrasynaptosomal Ca2+, whereas 53 mM KCl-induced release was dependent on extrasynaptosomal Ca2+. These results suggest that dopamine may be rapidly equilibrated between osmotically defined storage compartments, and thus specific compartmental depletion of loaded [3H]dopamine cannot be identified on the basis of osmotic lability.

Animals↗
PubMed1980

Comparative effects of pentylenetetrazol on the sensory responsiveness of lateral geniculate and reticular formation neurons.

The responses of bulbar and mesencephalic reticular formation (MRF) neurons to visual, auditory and/or somatosensory stimuli were considerably enhanced after subconvulsant doses of pentylenetetrazol (PTZ) in a similar fashion suggesting a general action of PTZ on reticular formation (RF) neurons. PTZ enhanced MRF responses evoked by electrical stimuli in the lateral geniculate nucleus (LGN) or cochlear nucleus but only modestly enhanced LGN neuronal responses. These findings indicate that the effects of this convulsant on the first brain sensory 'relay' nuclei and primary sensory receptors do not appear to be sufficient to account for the extensive PTZ-induced enhancement of RF neuronal responses, and direct effects of PTZ on the reticular formation may play a major role in this enhancement.

Animals↗
PubMedDate not supplied

Electrodiagnostic patterns in MGUS neuropathy.

Monoclonal gammopathies of undetermined significance (MGUS) are frequently associated with neuropathies, particularly in the elderly. To better characterize the electrodiagnostic findings in MGUS-associated neuropathies, we analyzed electrodiagnostic data from 35 patients with MGUS-associated neuropathies (mean age 70.6; 12 IgM, 19 IgG, 4 IgA) who had no other cause for their neuropathies. Data was also analyzed for 29 age-matched patients (mean age 69.8) with diabetic neuropathies. Using electrodiagnostic criteria, studies were classified as being consistent with demyelination; 9 patients had findings consistent with axonal injury; and, in 3 patients, criteria for both demyelination and axonal injury were present. However, 24 of the 35 patients with MGUS-associated neuropathies had dyssummetric findings. In contrast, only 4 of the 29 patients with only diabetes had a dyssymmetric process (p < 0.0001). In MGUS-associated neuropathies, dyssymmetry is the most common, definable abnormal electrodiagnostic pattern.

Aged↗