We have succeeded in recording short and middle latency vestibular evoked responses in human subjects. The head was held rigidly in a special, patented head holder, constructed individually for each subject, which gripped the teeth of the upper jaw. The stimulus consisted of 2/sec steps of angular acceleration impulses produced by a special motor with intensities of about 10,000 degrees/sec 2 and with a rise time of 1-2 msec. The electrical activity was recorded as the potential difference between special forehead and mastoid electrodes having a large, secure contact area with the skin. The activity was digitally filtered and averaged in 2 separate channels by means of a Microshev 2000 evoked response system. The short latency responses, with peaks at about 3.5 msec (forehead positive), 6.0 msec (forehead negative) and 8.4 msec (forehead positive; bandpass: 200-2000 Hz; average of 1024 trials), had amplitudes of about 0.5 microV. The middle latency responses had peaks at about 8.8 msec (forehead positive), 18.8 msec (forehead negative) and 26.8 msec (forehead positive; 30-300 Hz; N = 128 trials), with larger amplitudes (about 15 microV). These responses were consistently recorded in the same subject at different times and were similar in different normal subjects. Strenuous control experiments were conducted in order to ensure that these responses are not artefacts due to the movement of conducting media (head, electrodes and leads) in the electromagnetic field of the motor and are elicited by activation of normal labyrinths.(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗

PubMedDate not supplied

Atriopeptin prevents angiotensin II-stimulated glucose utilization in the subfornical organ.

Previous studies have shown that angiotensin II (ANG II) increases glucose utilization in the subfornical organ and stimulates drinking behavior. We investigated with the deoxyglucose method whether atriopeptin III, an atrial natriuretic peptide (ANP), would prevent this enhanced glucose metabolism and interfere with the drinking response in the presence of ANG II. Two rat models with high circulating levels of ANG II were studied: the homozygous Brattleboro and ANG II-infused Sprague-Dawley rats. ANP decreased the normally enhanced glucose utilization in the subfornical organ in the Brattleboro rat and inhibited ANG II-stimulated glucose metabolism in the subfornical organ of Sprague-Dawley rats. This effect was accompanied by decreased ANG II-stimulated water intake. These findings indicate that ANP may act at the level of subfornical organ to antagonize the dipsogenic action of ANG II.

Angiotensin II↗

PubMedDate not supplied

Sequence polymorphism of HLA DR beta 1 alleles relating to T-cell-recognized determinants.

HLA class II molecules are a highly polymorphic family of dimeric cell-surface proteins primarily involved in regulating T-cell responses to extrinsic antigens. To define regions of class II molecules involved in T-cell recognition, we have now compared sequences of three HLA DR beta cDNA clones obtained from cells that all express the same serologically defined determinants but differ in terms of T-cell-recognized specificities. The comparisons indicate that very few (one to four) nucleotides differ between what are almost certainly alleles of the DR beta 1 locus. All differences were in the first domain of the molecule and all localized to a region from amino acids 71-86. Because all differences were found only in this region of the molecule, and because DR alpha-chains seem to be relatively non-polymorphic, these positions in the DR beta-chain must have a major role in influencing T-cell recognition of the DR molecule.

Alleles↗

PubMedDate not supplied

When leukemia complicates pregnancy.

Explore the source record for details and available documents.

Adolescent↗

PubMedDate not supplied

Development of transient evoked otoacoustic emissions in the neonatal rat.

Otoacoustic emissions (OAEs) represent acoustic energy generated by the cochlear amplifier which contributes to auditory sensitivity and frequency discrimination. Therefore the OAEs can serve as a noninvasive tool to study the cochlear amplifier. While transient evoked OAEs (TEOAEs) are generally recorded clinically in man, it has been difficult to record them in animals and instead cubic distortion product OAEs (DPOAEs) have been experimentally studied in animals. In a previous study, we perfected a method of recording TEOAEs routinely in rats and this technique was used here to study the development of OAEs in neonatal rats. TEOAEs were recorded and compared to the DPOAEs on several postnatal days. With increasing postnatal age, TEOAE peak-to-peak amplitude and spectral energy in the 2- to 4-kHz band increased, their threshold decreased and their input-output functions became less monotonic with a change in slope (notch and/or plateau) in the mid-intensity region. The DPOAEs to higher frequencies appeared first, then the TEOAEs, followed by the DPOAEs to lower frequencies. With age, their amplitude also increased, thresholds decreased and a notch appeared in their input-output functions. The TEOAEs were measurable during the continuum of the appearance of the DPOAEs and the developmental sequences of both types of OAEs were similar. This may be evidence that similar mechanisms account for their maturation which probably initially involves a reduction in the air-bone gap with maturation of the outer and middle ears, and then elevation of the endocochlear potential and additional micromechanical maturations.

Age Factors↗

PubMedDate not supplied

Effect of temperature on the transient evoked and distortion product otoacoustic emissions in rats.

In order to study the energy dependence of the cochlear amplifier, transient evoked otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs) were recorded in rats during gradual cooling to 27 degrees C and heating to 40 degrees C. In the range 33-39 degrees C, the TEOAEs and DPOAEs were maximal in amplitude and almost insensitive to temperature. However, they were significantly depressed (reversibly) at higher and lower temperatures. Intensity functions were plotted at 37, 27 and 40 degrees C for both types of oto-acoustic emissions. At 37 degrees C intensity functions were nonlinear, with a notch at mid-intensity regions. At 27 degrees C, the magnitudes were depressed more at the lower intensities and threshold elevations were observed. As a result, the intensity functions were more linear and the notch was no longer seen. This result provides further evidence for a more active, energy-dependent component of the otoacoustic emissions at lower intensities for both TEOAEs and DPOAEs. The cooling probably affects the lower intensity otoacoustic emissions by inducing a depression in the endocochlear potential, by reducing the motility of the outer hair cells and by introducing a small conductive hearing loss.

Animals↗

PubMedDate not supplied

Effect of long-term noise exposure on the developing and developed ear in the Rat.

There have been reports that the developing ear is more sensitive than the adult ear to noise-induced hearing loss. This was investigated by testing auditory function in rats, both electrophysiologically and histologically, following exposure to broad-band noise (12 h/day for 15 days) at different stages of auditory development (neonates and adults), and also in age-matched controls. An exposure of 90 dB SPL broad-band noise caused no long-term change in auditory function in either age group. A higher exposure (102 dB SPL) caused greater long-term changes in hearing in the adult compared to the young noise-exposed rats, although histology showed greater damage to hair cells in the younger animals. Therefore, functionally, the developing ear does not seem more vulnerable than the developed ear to acoustic trauma.

Age Factors↗

PubMedDate not supplied

The effect of various durations of noise exposure on auditory brainstem response, distortion product otoacoustic emissions and transient evoked otoacoustic emissions in rats.

This study was designed to investigate the effect of various durations of noise exposure in animals on physiological responses from the cochlea which are also used clinically in humans: auditory brainstem response (ABR), transient evoked otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs). Rats were exposed to 113 dB SPL broad-band noise (12 h on/12 h off) for durations of 3, 6, 9, 12, 15 and 21 days, and tested 24 h after cessation of the noise and again after a period of 6 weeks. ABR threshold to click stimuli and to a 2-kHz tone burst (TB), TEOAE energy content and DPOAE amplitude in the exposed rats were compared to those in a group of control rats not exposed to noise. ABR thresholds (click and TB) were significantly elevated in all exposure duration groups compared to control rats. DPOAE amplitudes and TEOAE energy content were significantly reduced. The mean ABR thresholds following 21 days exposure were significantly greater (click = 100 dB pe SPL; TB = 115 dB pe SPL) than those following 3 days exposure (click = 86 dB pe SPL; TB = 91 dB pe SPL). Linear regression analysis between recorded responses and duration of noise exposure (days) showed a significant increase in ABR thresholds of approximately 0.8-- 1.4 dB/day. TEOAE and DPOAE responses showed no such dependence on noise duration and were already maximally reduced after only 3 days of exposure. This can be explained by the possibility that short noise exposures may cause damage to the early, more active stages of cochlear transduction (as shown by TEOAEs and DPOAEs). As the noise exposure continues, further damage may be induced at additional, later stages of the cochlear transduction cascade (as shown by ABR). Thus, ABR seems more sensitive to noise duration than OAE measures.

Animals↗