Biomedical subjects

R S Dyer

Publications and source records attributed to R S Dyer.

At least 19 recordsLinked to original sources

PubMed1992

Alterations in rat flash and pattern reversal evoked potentials after acute or repeated administration of carbon disulfide (CS2).

Because solvents may selectively alter portions of visual evoked potentials, we examined the effects of carbon disulfide (CS2) on flash (FEPs) and pattern reversal (PREPs) evoked potentials. Long-Evans rats were administered ip carbon disulfide either acutely or for 30 days. FEPs or PREPs were recorded prior to and 1, 2, 4, 8, or 24 hr after a single dose of CS2 (0, 100, 200, 400, or 500 mg/kg). Flash evoked potentials were also recorded 1, 2, 6, and 24 hr after the last of 30 doses of 200 mg CS2/kg/day. Acute exposure to CS2 consistently decreased the amplitude of FEP peak N160 at 1 hr, depressed peak N30 amplitude over 2-4 hr, and increased the latency of peaks P21, N30, P46, N56, and N160 for up to 4 hr after treatment. Carbon disulfide decreased the amplitude of PREP peaks P65, N83, P88, and N122 4 hr after treatment. Colonic temperature was depressed up to 8 hr after treatment. Administration of 200 mg CS2/kg/day decreased the amplitude of FEP peak N30 and increased the latencies of peaks P21, N30, P46, N56, and N160 up to 24 hr after the last dose. The differential effects of CS2 on portions of FEPs indicate that FEP peaks can be independently modulated. Changes in PREPs were temporally correlated with alterations in early FEP peaks, but FEP peak N160 was depressed at an earlier time point. Repeated CS2 exposure affected FEPs at lower doses and for a longer time than an acute exposure, similar to the reported greater severity of neurological disturbances following repeated CS2 exposures in humans.

Animals↗

PubMed1991

Rat flash-evoked potential peak N160 amplitude: modulation by relative flash intensity.

The flash-evoked potential (FEP) of rats has a large negative peak (N160) approximately 160 ms following stimulation. This peak has been reported to be modulated by the subject's state of behavioral arousal and influenced by several test parameters. These experiments examined the influences of repeated testing, the number of stimuli/session, interactions of ambient illumination and flash intensity, and the effect of pupillary dilation on the development and amplitude of peak N160. The amplitude of peak N160 increased with daily testing and reached an asymptotic amplitude by about day 10. This amplitude was affected by the intensity of the flash stimulus relative to the ambient illumination (RFI) and appeared to reach a "ceiling" amplitude at greater than 50 dB RFI. The number of stimuli/session and dilation of the subject's pupils did not have a large influence on the growth or asymptotic level of peak N160 amplitude. The data are consistent with the hypothesis that the growth of peak N160 may represent a sensitization-like phenomenon.

Animals↗

PubMed1989

Peak N160 of rat flash evoked potential: does it reflect habituation or sensitization?

Flash evoked potentials recorded from awake rats contain a negative peak occurring about 160 msec after the flash (N160). This peak has been associated with a specific level of arousal, and/or habituation by various authors. The current studies attempted to determine whether changes in N160 amplitude which accompany repeated testing reflect processes associated with sensitization or habituation. This paper describes experiments in Long-Evans hooded rats which demonstrate the effects of repeated testing, varying stimulus intensity, varying stimulus frequency, and discharging an alarm bell before and during a test session. Repeated testing produced increases in N160 amplitude which were greater at high than low stimulus intensities. Repeated exposure to the test chamber without flashing did not alter N160 amplitude, nor did altering stimulus rate within the range of 0.5 to 4.0 Hz. Discharging an alarm increased N160 amplitude. Taken together, the data suggest that amplitude of N160 more closely reflects sensitization to the stimulus than habituation to either the stimulus or any feature of the test situation.

Animals↗

PubMed1988

Convulsant properties of cyclotrimethylenetrinitramine (RDX): spontaneous audiogenic, and amygdaloid kindled seizure activity.

Dose-effect and time course relationships were determined for the effects of the explosive cyclotrimethylenetrinitramine (RDX) on seizure susceptibility. Male Long Evans rats treated with 0-60 mg/kg RDX po were monitored for spontaneous seizures during an 8-hr interval between dosing and audiogenic (AG) seizure testing. Blood samples for analyzing plasma RDX concentrations were obtained immediately thereafter. Spontaneous and AG seizures were observed at dosages as low as 10-12.5 mg/kg, with significant seizure incidence induced by dosages of 25.0 mg/kg (5.34 micrograms RDX/ml plasma) and 50.0 mg/kg (8.28 micrograms RDX/ml plasma), respectively. Spontaneous seizure incidence peaked at 2 hr for all RDX treatment groups, then decreased (12.5 and 25.0 mg/kg) or remained elevated (50.0 mg/kg) for the remaining 6 hr. In contrast, AG seizures (37.5 mg/kg) could be elicited only at 8 and 16 hr, despite significant elevation of plasma RDX concentrations at 2 and 4 hr. Because limbic system involvement was suggested by spontaneous seizure characteristics, the rate of amygdaloid kindling was measured following daily treatment with 6.0 mg/kg. This dosage significantly accelerated kindling development without inducing spontaneous seizures or producing an accumulation of RDX in plasma. These data provide preliminary evidence that limbic structures may participate in RDX-induced seizure susceptibility.

Acoustic Stimulation↗

PubMed1988

Temperature-dependent changes in visual evoked potentials of rats.

The effects of alterations in body temperature on flash and pattern reversal evoked potentials (FEPs and PREPs) were examined in hooded rats whose thermoregulatory capacity was compromised with lesions of the preoptic/anterior hypothalamic area and/or cold restraint. Body temperature, measured with a rectal thermometer, was manipulated via exposure to different ambient temperatures. To describe the data, a model was used in which both linear and quadratic relationships could be estimated. PREP amplitudes were not significantly influenced by body temperature over the range of 27-42 degrees C, although in one experiment FEP amplitudes did show a linear decline as temperatures fell below approximately 30 degrees C. Both FEP and PREP latencies were strongly influenced by temperature and became progressively longer as body temperature was lowered. The non-linear component affecting latencies became more prominent as body temperature decreased. These data demonstrate the temperature dependence of FEP and PREP latencies independent of anesthetic or other drugs.

Animals↗

PubMed1988

Ketamine alters rat flash evoked potentials.

Discovering the neurotransmitters involved in the generation of flash evoked potentials (FEPs) would enhance the use of FEPs in screening for and assessment of neurological damage. Recent evidence suggests that the excitatory amino acids, glutamate and aspartate, may be transmitters in the visual system. Ketamine selectively antagonizes the actions of excitatory amino acids on n-methyl-d-aspartate receptors and may be administered systemically. Two experiments were designed to test the effects of ketamine on rat FEPs. First, the effects of ketamine (37, 75, 150 mg/kg) on FEPs recorded in light and dark backgrounds were investigated at a single (10 min) posttreatment interval. Ketamine administration resulted in dose-dependent alterations in FEP peak amplitudes and latencies. Peak P1 amplitude increased by a factor of 4, in a dose-dependent manner. Peak N1 virtually disappeared at 150 mg/kg. Peak P2 amplitude increased by 50%, but only in the light background, and only at 150 mg/kg. Second, ketamine (150 mg/kg) effects on FEPs were investigated 5 min and 30 min following administration. The decrease in peak N1 amplitude was maximal 5 min after administration and the amplitude was recovering at 30 min. The effects on peak P1 and peak N3 amplitudes were maximal 5 min after ketamine administration, but were not recovering 30 min postinjection. The various peak latencies were also affected differently. The possible role of glutamate or aspartate in the generation of rat FEPs is discussed.

Animals↗

PubMed1987

Time-dependent neurobiological effects of colchicine administered directly into the hippocampus of rats.

Rats were given bilateral injections of colchicine into the dorsal and ventral hippocampus. Behavioral, neurochemical and histopathological measurements were taken, up to 12 weeks after surgery. Colchicine produced a consistent increase in spontaneous motor activity, enhanced acoustic startle reactivity, and accelerated acquisition of two-way shuttle box avoidance, but did not affect reactivity to a noxious thermal stimulus. Measurement of dynorphin in the hippocampus indicated that colchicine rapidly depleted this neuropeptide, which is thought to be contained preferentially in the mossy fibers of granule cells of the hippocampus. Colchicine also decreased Met-enkephalin in the hippocampus, but the magnitude of the change (22%) was less than that (89% depletion) observed for hippocampal dynorphin. Examination of hippocampal morphology using light microscopic techniques indicated that colchicine caused approximately 60% degeneration of granule cells in the hippocampus. Although the length of the pyramidal cells was decreased (12-16%), the width of the CA1 and CA3 region of the hippocampus was not affected. These data underscore the importance of the granule cells in the mediation of behavioral processes such as motor activity, startle reactivity and performance of shuttle box avoidance.

Acoustic Stimulation↗

PubMed1987

Possible role of the brainstem in the mediation of prepulse inhibition in the rat.

Bilateral stimulation of electrodes aimed at the cuneiform nucleus produced significant inhibition of the startle response produced by presentation of an 8-kHz, 110-dB tone. Stimulation of electrodes aimed at the deep mesencephalic nucleus also reduced the magnitude of the startle response, but the effect was less than that following stimulation sites near the cuneiform nucleus. Histological reconstruction of the electrode tip locations revealed a significant negative correlation between the maximum magnitude reduction of the acoustic startle response following an electrical prepulse stimulus and the distance from the cuneiform nucleus. Histological examination also indicated that some electrodes aimed at the cuneiform nucleus were located in or near the inferior colliculus or parabrachial nucleus, all of which are thought to be part of an inhibitory circuit parallel to the acoustic startle reflex arc. These experiments support the view that the prepulse inhibition of the acoustic startle reflex originates in the brainstem.

Acoustic Stimulation↗

PubMed1987

Focal lesions of visual cortex--effects on visual evoked potentials in rats.

Focal lesions were placed in the visual cortex of Long-Evans hooded rats, immediately below skull screw recording electrodes. Lesions were produced by heat, and extended an average depth of about 0.9 mm below the cortical surface. Evoked potentials recorded from the electrode overlying the cortical lesion were compared with simultaneously recorded potentials from a contralateral homotopic site. The effects of the lesion were selective. Flash-evoked potential peaks P1, P2, and N2 were depressed by the lesion, and peaks N1 and P3 were augmented; peak N3 was unaffected. Pattern reversal evoked potential peak N3 was depressed by the lesion, and peaks N1 and P2 were made more distinct. The results emphasized that different peaks have different generators, and suggest in particular that flash-evoked potential peaks P1 and N2, and peak N3 of the pattern reversal-evoked potential require the superficial layers of the cortex.

Animals↗

PubMed1987

Differential effects of caffeine, picrotoxin, and pentylenetetrazol on hippocampal afterdischarge activity and wet dog shakes.

We identified changes in hippocampal afterdischarge activity that follow administration of subcon vulsant doses (one-half the convulsant dose) of analeptic agents with known pharmacological action. Long-Evans rats (N = 104) with chronic bipolar electrodes implanted in the dorsal hippocampus, were injected i.p. with saline, caffeine (75 mg/kg), picrotoxin (2 mg/kg), or pentylenetatrazol (20 mg/kg) in 1 ml/kg volume 15 min before testing. Body temperature was measured at the beginning of the session to determine if significant change was associated with any of the treatments. Beginning at 10 microA, current (2-s train of 50-Hz biphasic pulses) was applied to hippocampal electrodes and intensity was increased in 10-microA steps until the afterdischarge sequence was elicited. Afterdischarge threshold, wet dog shake frequency, and the duration of the primary afterdischarge, the postprimary depression, and the rebound afterdischarge were measured. Caffeine administration produced a dramatic prolongation of the rebound afterdischarge, without affecting the duration of the primary afterdischarge. All other afterdischarge variables were unchanged by the caffeine treatment. Because caffeine blocks adenosine receptors at physiologic concentrations, adenosine action is implicated in the termination of the second, but not the first, spike train. Picrotoxin and pentylenetetrazol had no influence on the EEG, despite evidence of slight (1 degrees C) hypothermia. A decrease in wet dog shake frequency, however, was associated with picrotoxin administration. As picrotoxin and pentylenetetrazol are known gamma-aminobutyric acid (GABA) antagonists, the results suggest that GABA is involved minimally, if at all, in the hippocampal afterdischarge sequence.

Animals↗

PubMed1987

Urethane affects the rat visual system at subanesthetic doses.

Urethane is an anesthetic which is commonly used in neurophysiological studies because it is presumed to have minimal effects upon neuronal activity. This study investigated the influence of urethane anesthesia upon flash evoked potentials (FEPs) recorded from hooded rats. Subanesthetic dosages (25 g/kg and 0.5 g/kg) and an anesthetic dosage (1.0 g/kg) were administered, and subsequently recorded FEPs were compared to vehicle-injected controls. Urethane produced profound qualitative and quantitative effects upon the FEP. At 0.5 g/kg, the P1 (normal latency = 20 msec) and N1 (normal latency = 30 msec) peaks became unrecognizable. Peak N1 disappeared and peak P1 merged with P2 (normal latency = 45 msec). Peak P2 increased in amplitude by about 100%. The results indicate that in the visual system, urethane has a significant influence upon neuronal activity. Caution should be used in interpreting data obtained from urethane-anesthetized rats.

Anesthesia↗

PubMed1987

Surface distribution of flash-evoked and pattern reversal-evoked potentials in hooded rats.

Simultaneous recording from 21 electrode sites in a 4 X 4 mm area over the posterior cortex was used to determine the surface distribution of all major peaks which constitute flash-evoked potentials (FEPs) and pattern reversal evoked-potentials (PREPs) in hooded rats. Topographical maps were constructed with respect to Bregma and midline reference points. The data indicate that not all of the peaks which constitute either evoked potential have their greatest amplitude within the classically defined primary visual cortex. Further, since the FEPs were produced by uniform stimulation, the data suggest that surface regions of the rat visual cortex differ in ways other than simply the portion of the visual field from which information is received.

Animals↗

PubMed1987

Ontogeny of flash-evoked potentials in unanesthetized rats.

The effects of age and stimulation frequency (0.2/sec, 1.0/sec, 2.0/sec, or 4.0/sec) on flash-evoked potentials (FEPs) were investigated in awake, unsedated, unrestrained rats. Animals were tested daily from postnatal day (PND) 8 to PND 20, and every 3 or 4 days thereafter until PND 41. On PND 9, a single negative wave (N1a) was observed following 0.2/sec flash presentation. Animals tested on PND 10 exhibited a positive wave (P2) following the return of peak N1a to baseline. On PND 13 another negative wave (N1) appeared on the leading shoulder of peak N1a. Peak N1 became the dominant negative wave on PND 14. Peak N1a merged into N1 and had disappeared by PND 19. Peak N3 was first observed as a negative shift following peak P2 on PND 15. Peaks N2 and P3 were not observed in the group average waveforms until PND 34. Peak latencies decreased through the fifth postnatal week. Peak amplitudes increased with age until after eye opening (PND 15), but were variable thereafter. No FEPs were observed following higher than 0.2/sec flash presentation until PND 13. Increasing stimulation frequency decreased N1 and P2 peak amplitudes, but had no effect on peak latencies.

Aging↗

PubMed1986

Amygdaloid kindling increases enkephalin-like immunoreactivity but decreases dynorphin-A-like immunoreactivity in rat hippocampus.

The effects of amygdaloid kindling on the regional levels and distribution of enkephalin-like and dynorphin-A (DN)-like immunoreactivity (LI) were examined. One day after completion of kindling, radioimmunoassay revealed a 71% decrease in DN1-8-LI and a 43% increase in [Met5]-enkephalin-LI in the hippocampus. Immunostaining revealed a depletion of DN1-17-LI in the hippocampal mossy fiber pathway and an increase in [Leu5]-enkephalin-LI in the temporoammonic pathway. Four weeks after completion of kindling, the levels and immunostaining intensity of dynorphin and enkephalin in the hippocampus had returned to control values.

Amygdala↗

PubMed1986

Unrecognized errors due to analog filtering of the brain-stem auditory evoked response.

Analog filtering of the brain-stem auditory evoked response (BAER) and synthetic wave forms using steeply sloped filters are shown to produce significant distortion even when filter cut-off frequencies are well removed from the wave form spectrum. The degree of distortion is such that it may result in erroneous identification of peaks in the BAER. Reversal of the order of peaks may occur with high pass settings at only 1/4 the lowest constituent frequency. Filter effects were identified as a major source of cross-laboratory differences in BAERs recorded from laboratory rats. Filter transfer functions of a typical analog filter set were derived for both gain and phase as a function of frequency. Filtering of synthetic wave forms was used to elucidate and highlight distortion effects. A typical Long-Evans rat BAER wave form was spectrum analyzed and conclusions were drawn with respect to appropriate bandpass frequencies.

Analog-Digital Conversion↗

PubMed1986

Superior colliculus lesions and flash evoked potentials from rat cortex.

It is generally assumed that the primary response of the rat flash evoked potential (FEP) is activated by a retino-geniculate path, and that the secondary response reflects input to the cortex by way of the superior colliculus (SC) or other brainstem structures. In the present study, male Long-Evans rats were implanted with monopolar screw electrodes placed over the left visual cortex, and a pair of twisted monopolar depth electrodes, which were used to produce electrolytic lesions, were placed in each SC. One half of the animals did not receive the electrolytic treatment (controls). FEP waveforms were obtained from all animals prior to treatment, and 2 and 5 days after treatment. Histological analysis was performed to verify electrode placement and determine lesion size. Electrolytic lesions resulting in massive destruction of the SC produced no decrement in any portion of the rat FEP but did produce an increase in amplitude of the N2P3 component. The data show that the secondary response is not generated by SC in rats, but that SC may modulate amplitude of the response.

Animals↗

PubMed1986

Sulfolane-induced hypothermia enhances survivability in mice.

Mice injected intraperitoneally with sulfolane (tetrahydrothiophene-1,1-dioxide) underwent a significant decrease in metabolic rate and body temperature at ambient temperatures of 20 and 30 degrees C but not 35 degrees C. If given the opportunity, mice treated with sulfolane preferentially sought a cool ambient temperature. When given an LD50 dose of sulfolane (1270 mg/kg), the percentage mortality varied directly with ambient temperature. For example, at 35 degrees C mortality was 75% whereas at 25 degrees C mortality was only 8%. By undergoing an autonomically and behaviorally mediated decrease in body temperature (i.e., regulated hypothermia), sulfolane-treated mice appear to enhance their chance of survival.

Animals↗

PubMed1985

Chlordimeform produces contrast-dependent changes in visual evoked potentials of hooded rats.

Previous experiments found that acute exposure to the insecticide/acaricide, chlordimeform (CDM), produced large increases in the amplitude of pattern reversal evoked potentials (PREPs) without changing the amplitude of flash evoked potentials (FEPs) in the same rats (W. K. Boyes and R. S. Dyer, Exp. Neurol. 86: 434-447, 1984). Current work investigated the influence of physical characteristics of the evoking stimuli on the action of CDM. Adult male Long-Evans rats with epidural visual cortex electrodes were used. In experiment 1, PREPs were elicited with alternating gratings having equal contrast (99%) and a square wave spatial luminance profile at several spatial frequencies. Rats treated 1 h previously with 40 mg/kg CDM had increased PREP amplitudes at 0.1, 0.2, and 0.4 cycles per degree (cpd), but not at 0.8 cpd. No changes were found after 5 mg/kg CDM. In experiment 2, PREPs were elicited with gratings oriented at 0 degrees (horizontal), 45 degrees, 90 degrees, or 135 degrees. Treatment with 40 mg/kg CDM increased PREP amplitudes and latencies regardless of orientation. In experiment 3, FEPs elicited with strobe flashes spanning four log units of intensity showed a small but significant CDM dose X intensity interaction on P2N2 peak-to-peak amplitude. In experiment 4, PREPs were elicited with alternating gratings having a sinusoidal spatial luminance profile, spatial frequency of 0.2 or 0.8 cpd, and contrast ranging from noise levels to 65%. Rats treated with 40 mg/kg CDM showed increased peak-to-peak amplitudes only at 0.2 cpd and only at contrast values above 10%. The failure of CDM to alter PREPs at 0.8 cpd was attributed to low contrast sensitivity at that spatial frequency. The results demonstrated that the action of CDM on visual evoked potentials was dependent on the amount of contrast in the stimulus pattern, and suggested that CDM alters the encoding of visual contrast.

Amidines↗