Localized surface optical phonons in a layered crystal: GaSe(001).
Explore the source record for details and available documents.
Journal Article↗
Biomedical subjects
G Benedek
Publications and source records attributed to G Benedek.
Physiological properties of visually responsive neurones in the insular cortex of the cat.
Extracellularly recorded responses of neurones in the insula and the adjoining rostroventral bank of the anterior ectosylvian sulcus to moving bars of light and to electrical stimulation of the superior colliculus and suprageniculate nucleus were recorded in barbiturate-anaesthetized cats. Insular cortical neurones had extremely large receptive fields, exhibited a high incidence of directional selectivity, responded best to high or medium velocity movements of the stimulus and some displayed fairly powerful end-inhibitions. Orthodromically elicited responses from the superior colliculus and suprageniculate nucleus were obtained at latencies of 5-6.5 ms and 3.0-6.0 ms, respectively. No polysensory responses were obtained from visually sensitive neurones. These data provide evidence that a population of neurones in the dorsal rim of the insula comprise a visual area which may be closely related anatomically and functionally to the recently described anterior ectosylvian visual area.
Acoustic Stimulation↗
Connections of the anterior ectosylvian visual area (AEV).
We have previously described a visual area situated in the cortex surrounding the deep infolding of the anterior ectosylvian sulcus of the cat (Mucke et al. 1982). Using orthograde and retrograde transport methods we now report anatomical evidence that this anterior ectosylvian visual area (AEV) is connected with a substantial number of both cortical and subcortical regions. The connections between AEV and other cortical areas are reciprocal and, at least in part, topographically organized: the rostral AEV is connected with the bottom region of the presylvian sulcus, the lower bank of the cruciate sulcus, the rostral part of the ventral bank of the splenial sulcus, the rostral portion of the lateral suprasylvian visual area (LS) and the lateral bank of the posterior rhinal sulcus; the caudal AEV is connected with the bottom region of the presylvian sulcus, the caudal part of LS, the ventral part of area 20 and the lateral bank of the posterior rhinal sulcus. Subcortically, AEV has reciprocal connections with the ventral medial thalamic nucleus (VM), with the medial part of the lateralis posterior nucleus (LPm), as well as with the lateralis medialis-suprageniculate nuclear (LM-Sg) complex. These connections are also topographically organized with more rostral parts of AEV being related to more ventral portions of the LPm and LM-Sg complex. AEV also projects to the caudate nucleus, the putamen, the lateral amygdaloid nucleus, the superior colliculus, and the pontine nuclei. It is concluded that AEV is a visual association area which functionally relates the visual with both the motor and the limbic system and that it might play a role in the animal's orienting and alerting behavior.
Afferent Pathways↗
Potentiating effect of morphine on seizures induced by kainic acid in rats. An electroencephalographic study.
The effect of morphine pretreatment on kainic acid-induced seizures in rats was investigated by electroencephalographic recording. Seizure activity was quantified by counting the number of spikes in the EEG of freely-moving rats during 2 min periods at 30 min intervals after the intraperitoneal administration of 8, 10 or 12 mg/kg kainic acid. Pretreatment with morphine (1-10 mg/kg s.c.) 10 min before kainic acid administration significantly increased the number of spikes in the EEG in a dose-dependent manner. The potentiating effect of morphine on kainic acid-induced seizures was reduced considerably, but not abolished completely by pretreatment with naloxone (2-5 mg/kg s.c.). The results indicate that the potentiating action of morphine on kainic acid-induced seizures may be exerted in both a specific, naloxone-reversible manner and a non-specific, naloxone-resistant manner.
Animals↗
Observation of surface optical phonons in NaF(001) by inelastic He-atom scattering.
Explore the source record for details and available documents.
Journal Article↗
Effects of acute and chronic treatment with amitryptyline on the sleep-wake activity of rats.
Amitriptyline (1, 5 or 15 mg/kg intraperitoneally, twice a day) was administered to rats and the sleep-wake activity was recorded for either 24 hr (1 mg/kg) or 12 hr (5 or 15 mg/kg) on the day before treatment with amitriptyline, on days 1 and 5 of the treatment and on day 6, when the drug was withdrawn. In the first 3 hr amitriptyline increased non-REM sleep (NREMS), and decreased REM sleep (REMS) and wakefulness; the effects were dose-dependent. The changes in non-REM sleep and wakefulness (W) were followed by a compensatory reaction 6-12 hr after the treatment. The effects of chronic injection of amitriptyline on non-REM sleep revealed a definite decrease only in the case of the 15 mg/kg dose. Rebound of REM sleep appeared after withdrawal of the 5 and 15 mg/kg doses. Amitriptyline at 1 mg/kg had no effect on the sleep-wake activity during the dark period. The results show that the increase in non-REM sleep is as characteristic of amitriptyline as the reduction of REM sleep, and that these effects are resistant to chronic treatment when the dose is small.
Amitriptyline↗
Non-opiate analgesia following stressful acoustic stimulation.
The change in the nociceptive reactions of rats was characterized after stressful acoustic (115 dB) stimulation. Acoustic loading for five minutes resulted in considerable analgesia in the hot-plate test, whereas a significant analgesic response was not observed in the tail-flick test. The analgesic reaction after acoustic stimulation was resistant to naloxone pretreatment and was also found in morphine-tolerant rats, but the acute thermoregulatory and analgesic effects of morphine were greatly potentiated by simultaneous acoustic loading. Substance P or cholecystokinin treatment likewise failed to prevent the analgesic effect of auditory stimulation. No tolerance developed to the analgesic effect on repeated stressing. Diltiazem, a slow calcium channel blocker, facilitated the analgesia. The data suggest a stress-induced analgesia with obviously non-opiate properties, although an indirect involvement of opiate effects could not be excluded.
Acoustic Stimulation↗
Sensitization or tolerance to morphine effects after repeated stresses.
Rats were subjected to prolonged footshock, intensive acoustic stress, cold water swim and restraint over a period of 10 days. The analgesic and thermoregulatory properties of morphine (2, 4 and 8 mg/kg, sc.) were tested on the 11th day. Analgesia assessment was performed by means of hot-plate (HP) and tail-flick (TF) tests, and body temperature (Tb) changes was measured. Prolonged footshock and acoustic stress increased the sensitivity to morphine, while repeated restraint lessened morphine's effect. Cold water swim caused ambiguous consequences, facilitated the effect of a small dose of morphine, but reduced that of a large dose. It was concluded that the sensory components of the stressful exposure determine the effects of repeated stress on morphine sensitivity. Whereas painful interventions led to sensitization, and non-painful procedures result in tolerance to morphine's effects. The finding that analgesic and thermoregulatory effects of morphine were simultaneously enhanced supports the contention that the mechanism of sensitization to opiates involves a site where pathways mediating opiate analgesia and thermoregulatory effects converge.
Acoustic Stimulation↗
Potentiation of thermoregulatory and analgesic effects of morphine by calcium antagonists.
Diltiazem, a calcium slow channel blocker, greatly potentiated and prolonged the antinociceptive effect of morphine in rats. Hypothermia, the primary thermoregulatory effect of morphine, was also potentiated. Verapamil, another calcium blocker elicited corresponding changes in the analgetic and thermoregulatory effects of morphine. These findings seem to be in concert with the suggestions that opiate effects on thermoregulation and nociception are exerted via modulation of calcium fluxes across neural membranes.
Analgesics↗
Electrophysiological and anatomical demonstration of an overlapping striate and tectal projection to the lateral posterior-pulvinar complex of the cat.
Extracellular unit activity was recorded in the lateral posterior (LP)-pulvinar complex. The responses of 254 neurons after electrical stimulation of the central-paracentral part of cortical area 17 and of 84 neurons after stimulation of both area 17 and the superior colliculus (SC) were investigated. Neurons in the LP-pulvinar complex responded to area 17-stimulation with excitatory-inhibitory effects; in some cases only with inhibition. Neurons affected by striate stimulation were found in the caudal region of the complex in a region that extended widely into the medial part of the lateralis posterior nucleus (LPm), the so-called tectorecipient part of the lateral posterior nucleus. Accordingly, 26 of the 84 neurons in which electrical stimulation of area 17 and of the SC was tested, were found to react to both types of stimulation. Cells responding only to SC-stimulation were found in the ventral region of the anterior LP-Pulvinar complex. Anatomical studies supported the finding that striate and tectal inputs overlap considerably in the LP-pulvinar complex. After depositing horseradish peroxidase (HRP) into various regions of the LP-pulvinar complex, retrogradely labeled cells were found in area 17 (layer V) as well as in the superficial layers of the SC. These results were confirmed by orthograde transport autoradiography after injection of labeled amino-acids into area 17. Our findings indicate that cortical and collicular inputs into the caudal part of the LP-pulvinar complex overlap considerably and that, in these overlapping regions, individual neurons may receive converging afferent excitation from both regions.
Animals↗
Impaired thermoregulation against cold in capsaicin pretreated rats.
A study was made of the effects of pretreatment with fractionated capsaicin on the changes in body temperature (Tb) induced in rats by exposure to cold and to warm environments, and by administration of histamine (40 mg X kg-1) or of pentobarbital (20 mg X kg-1). At the ambient temperature of 22 degrees C the Tb of capsaicin pretreated rats was lower than that of rats treated only with solvent (p less than 0.001). The capsaicin pretreated rats showed impairment of thermoregulation at both high and low environmental temperatures: their Tb rose to a higher level in a warm environment, while in a cold environment their Tb was lower than that of the control rats. Histamine and pentobarbital caused larger drops in the Tb of capsaicin pretreated rats than in the controls. These findings challenge the concept that capsaicin treatment acts exclusively on thermoregulatory mechanisms concerned with warmth sensation.
Animals↗
Morphine tolerance and withdrawal in capsaicin--pretreated rats.
Thermoregulatory reactions to warm exposure and naloxone treatment, as well as behavioral reactions to morphine withdrawal, were recorded in morphine tolerant rats after capsaicin pretreatment. Enhanced behavioural reactions to morphine withdrawal were found in capsaicin pretreated rats, although no differences in degree of withdrawal hypothermia were seen. Morphine tolerant rats displayed increased thermal tolerance; this was partially prevented by capsaicin pretreatment. The results provide further evidence concerning the interference of neural mechanisms sensitive to capsaicin and opiates.
Animals↗
Stress-related changes of opiate sensitivity in thermoregulation.
Body temperature reactions to morphine were tested in freely-moving adult rats reared without any previous experience to human handling. These animals reacted to 8 mg/kg morphine s.c. with a biphasic hypo-hyperthermic response. When the rats had been handled for six days, the same dose of morphine induced a monophasic hyperthermic reaction. The results are regarded as evidence that stress-related factors interfere with the thermoregulatory effects of morphine.
Animals↗
Capsaicin pretreatment interferes with the thermoregulatory effect of morphine.
Body temperature changes after the administration of 8 mg/kg morphine sulphate were studied in freely-moving and restrained rats, which were pretreated with capsaicin (300 mg/kg). Morphine caused a hyperthermic response irrespective of the previous capsaicin treatment in freely-moving rats; the lag time from the application of morphine to the hyperthermic maximum was, however, significantly delayed in capsaicin pretreated rats. A careful habituation to the experimental procedure (including injections, taking temperature, etc.) facilitated the hyperthermic response both in the pretreated and the control groups. Restrained rats typically showed a hypothermic response to the same dose of morphine. The drop of body temperature in habituated animals was significantly larger in the case of capsaicin pretreated rats. This potentiation of the hypothermic effect of morphine can be regarded as the primary site of interaction between capsaicin and morphine. Since capsaicin pretreated rats also showed an exaggerated thermoregulatory response to experimental stress, we conclude that the thermoregulatory effects of morphine and endogenous opiates are facilitated after capsaicin pretreatment.
Animals↗
Thermoregulatory effects of D-met2-pro5-enkephalinamide.
Changes elicited in the body temperature by subcutaneous injection of the synthetic D-met2-pro5-enkephalinamide (D-met2-pro5-EA) were studied in CFY rats. D-met2-pro5-EA in doses of 8, 20 and 40 mg/kg caused hyperthermia. If the animals were restrained, this hyperthermic effect was attenuated. Ten mg/kg naloxone completely prevented the elevation of body temperature. Previous administration of 300 mg/kg capsaicin in fractionated daily doses resulted in a facilitation of the hyperthermic reaction. In contrast to other opioids, hypothermia was never observed. Our observations support the concept of multiple opiate-sensitive mechanisms in thermoregulation.
Animals↗
Physiologic and anatomic investigation of a visual cortical area situated in the ventral bank of the anterior ectosylvian sulcus of the cat.
In this paper a cortical area is described that covers approximately the posterior two-thirds of the ventral bank of the anterior ectosylvian sulcus of the cat and is called anterior ectosylvian visual area (AEV). In cats anesthetized with a combination of N2O and barbiturate we explored this area by recording extracellularly the responses of AEV neurons to visual and electric stimulation as well as by injecting HRP into physiologically verified points. AEV neurons were found to be highly sensitive to small light stimuli moving rapidly in a particular direction through their large receptive fields. The properties of 74 neurons were quantitatively analyzed. Increasing the length of the stimulus within the receptive field to more than 2 deg strongly inhibited the responses, whereas increasing the speed of the stimulus movement up to 72-120 deg/s enhanced the neuronal responsiveness. Although the majority of neurons responded to a wide range of possible directions, one clearly preferred direction could usually be found for each neuron. There was predominance of preferred directions toward the contralateral hemifield. Anatomic and electrophysiologic connectivity studies showed that AEV receives its main afferent inputs from the lateral suprasylvian visual area (LS) and from the tecto-pulvinar complex. Although these studies suggested some topographical organization within the projection from LS to AEV, the large receptive fields in AEV, the great majority of which included the central area, did not reveal a clear retinotopic order. It is concluded that AEV is a specific visual area and that functionally the extrageniculate inputs predominate.
Animals↗
Elevation of thermoregulatory vasodilatation threshold in the rat after capsaicin treatment.
In control and capsaicin-treated (300 mg/kg) rats tail skin vasodilatation was studied while the body temperature was raised to 38 degrees C, 39 degrees C or 40 degrees C and held at these levels. In the capsaicin-treated rats, at 38 degrees C vasodilatation was weaker than in the controls but at temperatures of 39 degrees C and 40 degrees C a delayed increase in tail vasodilatation occurred to the level observed in the controls. It is concluded that the threshold of vasodilatation response to heat is elevated after capsaicin treatment.
Animals↗
Thermal and chemical stimulations of the hypothalamic heat detectors: the effects of the EEG.
In acute immobilized rats, the effect on the EEG of thermal and chemical (capsaicin microinjection) stimulation of the warm sensors in the preoptic region, mid-hypothalamic area and posterior hypothalamus were studied. Both localized heating and capsaicin resulted in a sleep-like EEG with spindles and slow waves. Stimulation of the posterior hypothalamus was the most effective and stimulation in the mid-hypothalamus was the least effective in inducing spindle activity. Since capsaicin is regarded as a specific stimulant for the hypothalamic warm sensors, the results suggest that the EEG effect, and probably the sleep-inducing effect, of heat are mediated via the central thermoreceptors, and cannot be due to a non-specific activation of the basal forebrain hypnogenic mechanisms.
Animals↗