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Biomedical subjects

M L Woodruff

Publications and source records attributed to M L Woodruff.

At least 55 records · Page 3Linked to original sources
PubMed1977

Epileptiform lesions in rat hippocampus and acquisition of two-way avoidance.

Three experiments were conducted to examine the effects on the acquisition of two-way active avoidance of implantation into the hippocampus of rats of two substances (aluminum hydroxide, penicillin) known to produce epileptogenic electrical discharges. In Experiment 1 bilateral deposits of aluminum hydroxide (ALOH) were placed in the hippocampus and the effects of this manipulation were compared to the effects of bilateral hippocampal aspiration. Sufficient postoperative time (130 days) was allowed such that epileptogenic discharges developed in the ALOH-implanted rats. Both bilateral hippocampal-ALOH deposits and bilateral hippocampal aspiration resulted in facilitated acquisition of the two-way avoidance. The results of Experiment 2 replicated this observation, but also indicated that bilateral hippocampal deposits of penicillin did not cause detectable effects on acquisition of the avoidance. Epileptiform activity produced by the penicillin was observed to disappear by postoperative Day 4. In Experiment 3 unilateral hippocampal aspiration was combined with contralateral implants of either ALOH or penicillin and avoidance training was begun 13 days postoperatively. Epileptiform activity was not observed in the ALOH-implanted rats and disappeared by postoperative Day 4 in the penicillin implanted rats. No significant changes were observed in the rate of acquisition of two-way active avoidance as a result of the manipulations done in Experiment 3. It is concluded that epileptiform discharge initiated focally within the hippocampus produces effects on the acquisition of two-way active avoidance which are similar to the effects produced by bilateral ablation.

Animals↗
PubMed1977

Guanosine 3',5'-cyclic monophosphate and the in vitro physiology of frog photoreceptor membranes.

Frog rod outer segments freshly detached from dark-adapted retinas contain approximately 1-2 molecules of guanosine 3',5'-cyclic monophosphate (cyclic GMP) for every 100 molecules of visual pigment present. This cyclic GMP decays to 5'-GMP, and the conversion is accelerated upon illumination of the outer segments. Bleaching one rhodopsin molecule can lead to the hydrolysis of 1,000-2,000 molecules of cyclic GMP within 100-300 ms. The decline in cyclic GMP concentration becomes larger as illumination increases, and varies with the logarithm of light intensity at levels which bleach between 5 X 10(2) and 5 X 10(5) rhodopsin molecules per outer segment-second. Light suppression of plasma membrane permeability, assayed in vitro as light suppression of outer segment swelling in a modified Ringer's solution, occurs over this same range of light intensity. The correlation between cyclic GMP and permeability or swelling is maintained in the presence of two pharmacological perturbations: papaverine, a phosphodiesterase inhibitor, increases both cyclic GMP levels and the dark permeability of the plasma membrane; and beta,gamma-methylene ATP increases the effectiveness of light in suppressing both permeability and cyclic GMP levels.

Animals↗
PubMed1976

Hyperemotionality and enhanced tonic immobility after septal lesions in the rabbit.

Large lesions of the septal region in the rabbit increased tonic immobility as measured by the number of successful inductions and by duration of immobility. Open field activity was also increased. Septally lesioned rabbits also exhibited increased emotionality, although the topography of the 'septal syndrome' in these rabbits was different from that described for rats. The septally lesioned rabbits exhibited increases in fear reactions such as thumping, escape responses and vocalization when caught, rather than increased aggressiveness. The results are discussed in terms of loss of inhibition of species-typical responses after septal damage.

Animals↗
PubMed1975

An economical operant space interface for the PDP-8 computer.

An inexpensive input/output transfer system between a PDP-8/1 Digital Equipment Corporation computer and two operant stations is described. An interrupt facility is included. Slight modification of this interface will also permit it to work with the newer PDP-8 series computers.

Animals↗
PubMed1975

Hippocampal ablation prolongs immobility response in rabbits (Oryctolagus cuniculus).

The present study was performed to test the hypothesis that damage to the hippocampus reduces tonic immobility in rabbits. Two measures were used: the number of successful inductions of tonic immobility in a test session and the duration of each successful immobilization. Both of these measures were found to increase in rabbits with hippocampal lesions rather than to decrease as expected. It is suggested that the hippocampus may act to suppress any ongoing dominant or prepotent response, whether the response involves movement or cessation of movement.

Analysis of Variance↗
PubMed1975

Cholinergic modulation of tonic immobility in the rabbit (Oryctolagus cuniculus).

The present study was performed to determine the effects of the anticholinergic agent scopolamine and the cholinergic agent physostigmine on tonic immobility in rabbits. Recordings of the electroencephalographic (EEG) activity from cortex and hippocampus were also made before, during, and after each test session. Scopolamine significantly prolonged the response and produced large amplitude slow wave activity in the EEG of both cortex and hippocampus. Physostigmine significantly shortened the duration of immobility and increased rhythmic slow activity in the frequency range of 5.5-9.1 Hz in the hippocampus while producing a desynchronized cortical rhythm. It is suggested that the cortex and hippocampus play a role in modulating tonic immobility duration by inhibiting the brain-stem structures thought to control this response.

Animals↗
PubMedDate not supplied

The time-course of trimethyltin-induced fiber and terminal degeneration in hippocampus.

Trimethyltin (TMT) produces prominent neuron death in the hippocampus. The time-course of TMT-induced damage was studied using reduced-silver procedures for impregnation of degenerating axons and their terminals, and a modified Timm's stain procedure for visualization of hippocampal transitional metals. Standard cell body stains were also used. Fifty-four, adult, Long-Evans rats were gavaged with 6.0 mg TMT/kg b.wt. and 10 rats were gavaged with distilled water as controls. Five TMT-gavaged rats and one saline-gavaged rat were sacrificed on either postgavage day 1, 3, 6, 9, 14, 19, 30, 45, 70 or 99. Histological examination revealed a band of degenerating terminals in the stratum lucidum, below the hippocampal subfields CA3a,b pyramidal cells, by postgavage day 3. This preceded dentate gyrus granule cell loss supplying the mossy fiber input to the stratum lucidum by several days. Hippocampal pyramidal cell necrosis continued through the examination period while dentate granule cell loss subsided between postgavage days 9 and 14. Fiber and terminal degeneration was more extensive in the dorsal hippocampus than in the ventral hippocampus, although Timm's-stained sections revealed "bleaching" of stainable metal in the mossy fiber pathway of the ventral hippocampus. These data suggest that loss of ventral dentate granule cells might reduce TMT-induced necrosis of pyramidal cells in the ventral (temporal) part of the Ammon's horn, possibly by preventing the spread of seizure activity in this region of the hippocampus. Additionally, although previous studies have reported the toxic effects of TMT to last approximately 60 days, the results of the present study indicate that TMT-induced degeneration continues for more than 3 months. Reduced-silver stains, such as the Fink-Heimer procedure, appear to be more sensitive indicators of enduring neuropathology than more traditional cell stains.

Animals↗
PubMedDate not supplied

Exposure to trimethyltin significantly enhances acetylcholinesterase staining in the rat dentate gyrus.

Trimethyltin (TMT) is known to produce substantial damage to the hippocampal formation. It also destroys neurons within the entorhinal cortex, thereby causing degeneration of perforant path afferents that terminate in the outer molecular layer (OML) of the dentate gyrus. Surgical destruction of the entorhinal cortex also causes the perforant path to degenerate. This leads to reactive synaptogenesis (axonal sprouting) of septal afferents to the dentate gyrus. The purpose of the present study was to determine whether administration of 6 mg/kg of TMT by gavage to rats would cause axonal sprouting within the septo-dentate projection. A histochemical stain for acetylcholinesterase (AChE) was used. Compared to control subjects rats given TMT exhibited significantly denser AChE staining in the dentate OML. This is putative indication of reactive synaptogenesis within the cholinergic projection to this layer of the dentate and is somewhat surprising because other neurotoxins, such as lead and ethanol, that affect neurons within the hippocampal formation reduce the capacity for reactive synaptogenesis in response to lesions of the entorhinal cortex.

Acetylcholinesterase↗
PubMedDate not supplied

Trimethyltin increases choline acetyltransferase in rat hippocampus.

The environmental neurotoxin trimethyltin (TMT) destroys parts of the hippocampal formation as well as the entorhinal cortex but leaves the septal cholinergic projection to the hippocampus and dentate gyrus intact. In this study we measured choline acetyltransferase (ChAT) activity in micropunch samples of the dentate gyrus, the CA1 region of Ammon's horn, and the caudate-putamen as a measure of density of cholinergic innervation in control rats and rats exposed to 7 mg/kg TMT by means of gastric intubation. Three months after the rats were exposed to a single dose of TMT both the dentate gyrus and CA1 demonstrated significantly higher ChAT activity in TMT-exposed rats than in control rats. No differences were found between groups for the caudate-putamen samples. These results support the hypothesis that exposure to TMT causes reactive synaptogenesis in the cholinergic septohippocampal system.

Animals↗
PubMedDate not supplied

Fetal Ammon's horn transplants improve acquisition of a radial arm maze and a low-rate operant schedule in trimethyltin-treated rats.

The results of previous studies indicated that block grafts of fetal hippocampal tissue made into cavities produced by aspiration lesions of the hippocampus in rats given the neurotoxin trimethyltin (TMT) significantly worsened the TMT-induced deficit in water maze acquisition. The purpose of the present study was to test the hypothesis that a procedure for transplantation that produced less destruction to the host brain and resulted in transplants with less mass might produce recovery in a spatial learning task in TMT-exposed rats. Acquisition of an externally cued (spatial) version of the radial arm maze (RAM), an internally cued version of the RAM, and of a differential reinforcement of low rate (DRL) operant schedule was assessed in normal rats, rats given TMT, and rats given TMT and stereotaxic implants of either fetal Ammon's horn or entorhinal cortex. The rats receiving Ammon's horn transplants made significantly fewer reentries into the baited arms in both maze configurations and fewer reentries into the nonbaited arms in the spatial RAM than rats in the TMT-only and TMT/entorhinal cortex transplant groups. The rats receiving transplants of Ammon's horn made significantly fewer responses and received more reinforcements during training on the DRL-20 schedule than rats receiving just TMT or rats receiving TMT and transplants of fetal entorhinal cortex. These results support the proposal that transplantation procedures that cause less damage to the host brain and result in transplants that do not occupy a large extent of the ventricular space increase the probability of behavioral recovery.

Animals↗