Balance beam crossing times are slower after noise exposure in rats.

Introduction: The vestibular system integrates signals related to vision, head position, gravity, motion, and body position to provide stability during motion through the environment. Disruption in any of these systems can reduce agility and lead to changes in ability to safely navigate one's environment. Causes of vestibular decline are diverse; however, excessive noise exposure can lead to otolith organ dysfunction. Specifically, 120 decibel (dB) sound pressure level (SPL) 1.5 kHz-centered 3-octave band noise (1.5 kHz 3OBN) causes peripheral vestibular dysfunction in rats, measured by vestibular short-latency evoked potential (VsEP) and reduced calretinin-immunolabeling of calyx-only afferent terminals in the striolar region of the saccule. The present study examined the functional impact of this noise exposure condition, examining changes in motor performance after noise exposure with a balance beam crossing task. Methods: Balance beam crossing time in rats was assessed for 19 weeks before and 5 weeks after noise exposure. Balance beam crossings were scored to assess proficiency in the task. When animals were proficient, they received a single exposure to 120 dB SPL 3-octave band noise. Results: During the initial training phase slower crossing times and higher scores, including multiple failures were observed. This was followed by a period of significant improvement leading to proficiency, characterized by fast and stable crossing times and consistently low scores. After noise exposure, crossing times were significantly elevated from baseline for 4-weeks. A total of 5 weeks after noise exposure, crossing times improved, and though still trending higher than baseline, they were no longer significantly different from baseline. Discussion: These findings show that the noise-induced peripheral vestibular changes we previously observed at cellular and electro-physiological levels also have an impact at a functional level. It has been previously shown that imbalance is associated with slower walking speed in older adults and aged rats. These findings in noise-exposed rats may have implications for people who experience noisy environments and for seniors with a history of noise exposure who also experience balance disorders and may be at increased fall risk.

Transient peripheral vestibular hypofunction measured with vestibular short-latency evoked potentials following noise exposure in rats.

Exposure to 120 dB sound pressure level (SPL) band-limited noise results in delayed onset latency and reduced vestibular short-latency evoked potential (VsEP) responses. These changes are still present 4 wk after noise overstimulation. Noise-induced hearing loss (NIHL) has been shown to vary in extent and duration based on the noise intensity. This study investigated whether noise-induced peripheral vestibular hypofunction (NPVH) would also decrease in extent and/or duration with less intense noise exposure. In the present study, rats were exposed to a less intense noise (110 dB SPL) but for the same duration (6 h) and frequency range (500-4,000 Hz) as used in previous studies. The VsEP was assessed 1, 3, 7, 14, 21, and 28 days after noise exposure. In contrast to 120 dB SPL noise exposure, the 110 dB SPL noise exposures produced smaller deficits in VsEP responses that fully recovered in 62% (13/21) of animals within 1 wk. These findings suggest that NPVH, a loss or attenuation of VsEP responses with a requirement for elevated stimulus intensity to elicit measurable responses, is similar to NIHL, that is, lower sound levels produce a smaller or transient deficit. These results show that it will be important to determine the extent and duration of vestibular hypofunction for different noise exposure conditions and their impact on balance.NEW & NOTEWORTHY This is the first study to show a temporary noise-induced peripheral vestibular hypofunction that recovers following exposure to continuous noise.

Exposure to Intense Noise Causes Vestibular Loss.

INTRODUCTION: The vestibular system is essential for normal postural control and balance. Because of their proximity to the cochlea, the otolith organs are vulnerable to noise. We previously showed that head jerks that evoke vestibular nerve activity were no longer capable of inducing a response after noise overstimulation. The present study adds a greater range of jerk intensities to determine if the response was abolished or required more intense stimulation (threshold shift). MATERIALS AND METHODS: Vestibular short-latency evoked potential (VsEP) measurements were taken before noise exposure and compared to repeated measurements taken at specific time points for 28 days after noise exposure. Calretinin was used to identify changes in calyx-only afferents in the sacculus. RESULTS: Results showed that more intense jerk stimuli could generate a VsEP, although it was severely attenuated relative to prenoise values. When the VsEP was evaluated 4 weeks after noise exposure, partial recovery was observed. CONCLUSION: These data suggest that noise overstimulation, such as can occur in the military, could introduce an increased risk of imbalance that should be evaluated before returning a subject to situations that require normal agility and motion. Moreover, although there is recovery with time, some dysfunction persists for extended periods.

Abnormal Locus Coeruleus Sleep Activity Alters Sleep Signatures of Memory Consolidation and Impairs Place Cell Stability and Spatial Memory.

Sleep is critical for proper memory consolidation. The locus coeruleus (LC) releases norepinephrine throughout the brain except when the LC falls silent throughout rapid eye movement (REM) sleep and prior to each non-REM (NREM) sleep spindle. We hypothesize that these transient LC silences allow the synaptic plasticity that is necessary to incorporate new information into pre-existing memory circuits. We found that spontaneous LC activity within sleep spindles triggers a decrease in spindle power. By optogenetically stimulating norepinephrine-containing LC neurons at 2 Hz during sleep, we reduced sleep spindle occurrence, as well as NREM delta power and REM theta power, without causing arousals or changing sleep amounts. Stimulating the LC during sleep following a hippocampus-dependent food location learning task interfered with consolidation of newly learned locations and reconsolidation of previous locations, disrupting next-day place cell activity. The LC stimulation-induced reduction in NREM sleep spindles, delta, and REM theta and reduced ripple-spindle coupling all correlated with decreased hippocampus-dependent performance on the task. Thus, periods of LC silence during sleep following learning are essential for normal spindle generation, delta and theta power, and consolidation of spatial memories.

Thermally activated magnetization reversal in monatomic magnetic chains on surfaces studied by classical atomistic spin-dynamics simulations.

We analyse the spontaneous magnetization reversal of supported monatomic chains of finite length due to thermal fluctuations via atomistic spin-dynamics simulations. Our approach is based on the integration of the Landau-Lifshitz equation of motion of a classical spin Hamiltonian in the presence of stochastic forces. The associated magnetization lifetime is found to obey an Arrhenius law with an activation barrier equal to the domain wall energy in the chain. For chains longer than one domain wall width, the reversal is initiated by nucleation of a reversed magnetization domain primarily at the chain edge followed by a subsequent propagation of the domain wall to the other edge in a random-walk fashion. This results in a linear dependence of the lifetime on the chain length, if the magnetization correlation length is not exceeded. We studied chains of uniaxial and triaxial anisotropy and found that a triaxial anisotropy leads to a reduction of the magnetization lifetime due to a higher reversal attempt rate, even though the activation barrier is not changed.