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Lisa Tanner 1 Effects of early acoustic stimulatio n on prepulse inhibition in mice Lisa Tanner Audiology Doctoral Project Submitted to the Faculty of the University of South Florida In partial fulfillment of the requirement for the degree of Doctor of Audiology James Willott, Ph.D., Chair Jennifer Lister, Ph.D., Co-Chair Raymond Hurley, Ph.D., Member December 6, 2003 Tampa, Florida Keywords: Augmented Acoustic Environment, Ne onatal Intensive Care Unit, Noise Exposure, Auditory Development, Animal Modeling
Lisa Tanner 2 Abstract The purpose of this study was to determine th e effects of an atypi cal pattern of early acoustic stimulation on auditory development. Previous human research suggests that the acoustic environment of pre-term human infant s in the Neonatal Intensive Care Unit (NICU) negatively affects some aspects of auditory development. An imal research suggests that premature auditory stimulation interrupts auditory development. Because mice are born before their auditory systems are developed, they make an excellent model for research on fetal and postnatal plasticity of the auditory system. Th e premature auditory state of newborn mice is similar to that of the NICU pre-te rm infant, albeit, natural for mice C57 mouse pups were exposed to an augmente d acoustic environment (AAE) of a nightly 12-hour regiment of 70 dB SPL noise burst, beginni ng before age 12 days ( onset of hearing) and lasting for one month. The prepulse inhibition (P PI) of mice exposed to the AAE was compared to that of non-exposed mice to observe short-term and long-term effects. Results showed that the prepulse inhibition of the AAE exposed mice did not differ signi ficantly from that of the nonexposed mice. However, it is possible that th e measurement used, PPI, may not have been appropriate or that the AAE may not have b een an appropriate simulation of the NICU environment.
Lisa Tanner 3 Introduction Pre-term infants in the typical neonatal intensive care unit (NICU) are exposed to continuous light and a variety of necessary, but noisy equipment such as incubators, high frequency ventilators, and EKG monitors. The American Academy of Pediatrics (1997) raised concerns regarding the exposure of pre-term infants to high and continuous sound levels in the NICU. They reported sound levels inside incuba tors ranged from 50 dBA of background noise to 120 dBA of impact noise. These noise levels ar e in excess of the Environmental Protection Agency (EPA) recommendations for hospital le vels of 45 dBA during the day and 35 dBA at night (Kahn, Cook, Carlisle, Nelson, Kramers, & Millman, 1998). This environment is very different, both visually and acoustically, from th at experienced by a full-term infant during the same developmental period in the womb. Recen tly, the Study Group on Neonatal Intensive Care Unit Sound, convened by the Center for the Phys ical and Developmental Environment of the High Risk Infant, reviewed research on human a nd animal auditory development, including the effects of environmental light a nd noise exposure at different ma turity levels in fetuses and neonates (Graven, 2000). Animal studies show that neurosensory development follows a certain pattern of development, a patter n that likely parallels that of human neurological development (Graven, 2000). This pattern begins with the sense of touch and is followed by vestibular, chemical, auditory, and, finally, visual development (Lickliter, 2000). Pre-term birth does not alter this sequence. Animal models indicate that prenatal vi sual stimulation and augmented auditory stimulation interrupts auditory development (e.g., Lickliter, 1994; Lickliter, 1990; Lickliter and Stoumbos, 1992). For example, bobwhite quail chicks exposed prenata lly to patterned light or to an unnatural pattern of auditory stimulation did no t exhibit normal auditory responsiveness to the
Lisa Tanner 4 maternal quail call (Lickliter, 1990; Lickliter and Stoumbos, 1992). It seems that, when a sensory system is typically, natu rally stimulated at a pa rticular period of devel opment, that stimulation becomes essential for normal development. Howeve r, if the same stimulus is too intense, too early, or out of sequence, it can interfere with the normal pattern of neurosensory development. Therefore, the Study Group concluded that stimul ation of the developing sensory system is dependant on the amount, type, and timing of s timulation (Graven, 2000). Pre-term infants are often exposed to patterned light and unfiltered sound at a stage in development when such stimulation is inappropriate. This suggests that visual and auditory e xposure in the NICU may have long-term auditory effects. Due to the ethical and practical issues surr ounding studies of the effects of the early sensory environment on human infants, animal mode ls are required for such studies. The use of animal models reduces between-subject variab les and allows the cont rol of environmental conditions. The use of inbred mice as a particul ar animal model for auditory research is advantageous because of the vast amount of information available on mouse genetics and on the mouse auditory system (Willott, 2001). In the present study, a mouse model was used to address the issue of possible long-term effects from moderately intense (70 dB SPL) aud itory stimulation during early development. The C57BL/6J (C57) inbred strain of mice was selected because it has been well studied. C57 mice hear normally during the first few months of lif e and into early adulthood. However, due to the Ahl gene, they exhibit gradual, progressive high frequency hearing lo ss parallel to that experienced by many humans as they age (Willott, 2001; Willott, Carson, & Chen, 1994). Thus, the present experiment may also shed light on the effects of early ac oustic stimulation on the course of adult prog ressive hearing loss.
Lisa Tanner 5 It should be noted that the timetable of a uditory system development of the C57 mouse differs from that of humans. During a 36-40 week gestational period, the human auditory system begins to develop by the end of the third week after conception (Peck, 1994). Between week 10 and week 21 of gestation, the organ of Corti begi ns to form, and hair cells begin to mature. By the seventh fetal month, all neural synapses are formed. At this time, the fetus is experiencing sound. Electrophysiological data indicat e that, at birth, the full term infant has mature middle and inner ear structures, while the central auditory system continues to develop for the next 18 months (Ruben & Rapin, 1980; Hall, 1992; Hood, 1998). The human visual system begins to devel op by 22 days gestation. However, more than nine months of development are required for the visual system to reach completion. In fact, the eyelids, which fuse at the third gestational month, will not re-open until the fifth gestational month. The retinal vessels will not reach full matu rity until after the ninth month. Some fetuses may demonstrate a response to light as early as the eighth gestational m onth indicating that at least some central nervous system pathways are established early (Sadler, 1985; Cibis, Anderson, Chew, Fishman, Kardon, Tripathi, Van Kujik, Weleber, & Balyeat, 1994). In contrast, the gestational period for mice is 17 to 22 days and, at birth, the peripheral fibers within the auditory organ are still not orie nted. It is not until the mouse is a few days old that the inner spiral bundle de velops (Sobkowicz & Rose, 1983). By 12 days after birth, the eyes and external auditory canals open (Shnerson & Pu jol, 1983). By 14 days, th e cochlea is relatively mature, but the central auditory system continue s to mature (Webster & Webster, 1980). Because mice are born before their periph eral auditory systems are fully developed, they make an excellent model for research on fetal and postnat al plasticity of the auditory system. The
Lisa Tanner 6 premature auditory state of newborn mice is simila r to that of the NICU pre-term infant, albeit, natural for mice. In this study, the auditory behavior meas ured was prepulse inhibition (PPI) of the acoustic startle response (ASR). The ASR is e licited by an intense noise (e.g., 100 dB SPL) of abrupt onset. PPI occurs when a tone that does not have the pote ntial to startle (e.g.. 70 dB SPL) is presented within 10 to 200 ms pr ior to the startle stimulus. If the prepulse tone is successful, a reduction, inhibition, of ASR amplitude will occur (Willott et al., 1994). PPI occurs readily in both humans and mice (Swerdlow & Geyer, 1999). PPI is the ratio of the startle with a prepulse to the baseline startle response, and can be used to assess the behavioral salience of sound. If the tone produces PPI, it can be heard by the animal, is assumed to be salient, and vice versa. In mice and in humans, the inhibition of the startle re sponse when a prepulse is presented at a short interval prior to the startle stimulus can help determine the integrity of auditory pathways in the central nervous system (Blumentha l, 1999). Structures involved in the modification of the startle are the inferior colliculus along with other hi gher-order structures (Willott, Sundin & Jeskey, 2001). Thus, if normal PPI occurs, pathways in the auditory brainstem must be functional. Past studies performed by Willott and colleagues have examined the effects of controlled auditory stimulation on the auditory function of mice. They found th at auditory neural plasticity was induced by exposing adolescent/young a dult C57 mice to an augmented acoustic environment (AAE), a broadband noise (rise/fall = 10 ms, duration = 200 ms, rate = 2/sec.) of 70 dB SPL presented nightly for 12 hours over a period of a few days to several weeks. Willott and colleagues have demonstrated that appropriate stimulation of the degene rating cochlea and the central auditory system by an appropriate AAE may have ameliorative effects, similar to the effects of "exercise" or increased neural activ ity in other neural systems (Willott et al., 2001;
Lisa Tanner 7 Willott & Turner, 2000). PPI became stronger in mi ce when the AAE was maintained for a long period of time. This suggests that changes o ccur in the physiological and or anatomical properties of the central auditory system in response to chronic AAE treatment. Thus far, studies of AAE have initiated treatm ent after weaning, at age 25 days. It is not known if very early AAE exposure might have weak er, stronger, or lasting effects on PPI and the ASR. Therefore, the goal of this project was to use an animal model to determine the effects of an atypical pattern of early acoustic stimulati on on auditory development. The animal model used was the C57BL/6J (C57) inbred mouse. Th e testing procedures included the ASR and PPI. Specifically, mouse pups were exposed to a ni ghtly 12-hour regimen of 70 dB SPL noise burst beginning before age 12 days (onset of hear ing) and lasting for one month. Then the PPI of mice exposed to the AAE was compared to that of non-exposed mice to observe short-term effects. Secondly, the mice were retested at severa l intervals after termina tion of noise exposure, with a maximum age of nine months to observe long-term effects of early exposure. It was expected that results of this study may have im plications for early acoustic exposures found in the NICU.
Lisa Tanner 8 Methods Subjects C57BL/6J mice of either sex were obtained fr om the University of South Florida rodent colony. Mice from this colony were the offspri ng of stock obtained from Jackson Laboratory (Bar Harbor, ME). They were randomly selected to form two groups: those that were exposed to an AAE (7 males and 10 females) and a non-exposed group (7 males and 6 females) housed in the vivarium. Housing Mice were kept with their mother until w eaning. In the exposed group, the mother was also exposed to the AAE from the time the pups we re 11 days old until weaning at 21-23 days of age. After weaning, the mice were separated into same sex c ohort groups. Mice in exposed and non-exposed groups were kept in plastic shoebox cag es with wire lids for unlimited access to tap water and rodent chow. Room temper ature was maintained at 23 to 24 C A 12-hour night-day schedule was maintained. The exposed group re ceived 12 hours of AAE treatment during their nocturnal active period, beginning at 11 days ol d. The non-exposed groups were kept in a relatively quiet vivarium. AAE Treatment The AAE was digitally synthesized and reco rded on a compact disk (rise/fall= 10 ms, duration= 200 ms, rate= 2 noise bursts per sec.). The noise was amplifie d and sent to a Radio Shack Super tweeter, which was positioned over th e top of each cage. The AAE was calibrated to 70 dB SPL using a sound level meter at variou s positions within the cage. The groups were exposed to a total of 30 days of the AAE envir onment, after which they were returned to the vivarium with the non-exposed groups.
Lisa Tanner 9 Startle and PPI measurements The stimulus used to elicit the startle was a 100 dB SPL broadband noise burst (4k 25k range spectrum, 10 ms duration, 1 ms rise/fall time, delivered at a va riable rate of 3 to 8 ms). The prepulse stimulus was a 70 dB SPL tone bur st (4 kHz, 12 kHz or 20 kHz) with a 10 ms duration, and a 3 ms rise/fall time. The prepulse stimulus preceded the startle stimulus by 100 ms. A Med Associates startle meas uring system was used to pro cess and present the stimuli and record the startle responses. A speaker was m ounted in the ceiling of a sound attenuated box. Beneath the speaker, the mouse was placed in a 32 ounce plastic cup placed on a movementsensitive load cell to measure the mouses movements. Procedures PPI testing began after one week of AAE exposure. For the first month, mice (exposed and non-exposed groups) were tested once per wee k. Thereafter, both groups were tested once per month for four months and once again when the mice were 9 months old. Each test included two runs. Each run consisted of 40 trials to test PPI. Trials consisting of startle stimulus only and trials consisting of the prepulse stimulus pair ed with the startle stimulus were presented in random order. For each session, the mean PPI fo r each frequency was calculated as a percent reduction of the startle amplitude with respect to that produced by the startle stimulus only. Statistics The PPI data were analyzed using separate 3-way mixed analyses of variance (ANOVA) for each prepulse frequency condition. For each ANOVA, age (1 month, 2 month and 9 month) was a repeated measure and environment conditi on (AAE, control) and gender (male, female) were between-groups measur es. The alpha level was 0.05.
Lisa Tanner 10 Results The pattern of age-related change in PPI wa s different for each prepulse frequency. As shown in Figure 1, PPI improves with age for the 4 kHz prepulse, particularly for the female mice. This was true for both the AAE exposed group and the control group. These observations are supported by the statistical analysis. The main effect of age (F (2,52) = 11.97; p < 0.0001) and the interaction between gender and age (F (2,52) = 3.76; p < 0.0297) were statistically significant. Tukey post-hoc analyses revealed that PPI at 1 month was significantly poorer than PPI at 2 or 9 months (p < 0.0001) but PPI at 2 and 9 months di d not differ significantly (p > 0.05). Also, the PPI of female mice was poorer th an that of male mice at 2 months but the reverse was true at 9 months (p < 0.05). For the 12 kHz prepulse (Figure 2), PPI appears similar across age and environment groups. None of the main effect s or the interactions was statistically significant (p > 0.05). For the 20 kHz prepulse (Figure 3), PPI app ears to worsen with age for mice of both genders, however the PPI of the female mice is poor er than that of the male mice. There are no apparent differences in PPI between the AAE a nd control groups for either gender. The main effects of age (F (2,52) = 5.26; p < 0.0083) and gender (F (1,26) = 4.79; p< 0.0377) were statistically significant. Tukey pos t-hoc analyses revealed that the PPI of the female mice was poorer than that of the male mice (p = 0.037) and PPI was poorer at 9 months than at 2 months (p = 0.005). The PPI at 1 month and 2 months did not differ, nor did PPI at 1 month and 9 months (p > 0.05)
Lisa Tanner 11 Figure 1. PPI amplitude for the 4 kHz prepul se stimuli across age. Filled circles represent the female C57 mice exposed to the AAE. Open circles represent the female C57 mice not exposed to the AAE. Filled squares represent the male C57 mice exposed to the AAE. Open squares represent the male C57 mice not exposed to the AAE. Standard error bars are shown for each group.
Lisa Tanner 12 Figure 2. PPI amplitude for the 12 kHz pre pulse stimuli across age. Symbols and legend as shown in Figure 1.
Lisa Tanner 13 Figure 3. PPI amplitude for the 20 kHz pre pulse stimuli across age. Symbols and legend as shown in Figure 1. To summarize, PPI changed across age, but the AAE had no signifi cant effect on PPI. Gender differences were present, but these inte racted with prepulse frequency. Females (both AAE and control) showed greater improvement of PPI with age for the 4 kHz prepulse as compared to males. By contrast, females (AAE and control) exhibited w eaker PPI for the 20 kHz prepulse than males. PPI with the 12 kHz pre pulse was unaffected by age, gender, or AAE.
Lisa Tanner 14 Discussion Previous studies have shown that PPI with a 4 kHz prepulse improves with age in C57 mice, as found in the present study (Willott et al., 1994; Willott & Turner, 2000). Gender differences were not analyzed, however. The im provement probably reflects central auditory plasticity previously demonstrated in this st rain. As high frequency sensitivity is lost, the auditory salience of low frequencies has been shown to improve (Jeskey & Willott, 2000; Willott & Turner, 2000; Willott & Carlson, 1995; Willo tt, 1984). Worsening of PPI using a highfrequency prepulse, shown here with 20 kHz, was also observed in the earlier studies (Willott et al., 1994; Willott & Turner, 2000), and presumably reflects the loss of sensitivity to high frequencies. The improvement seen in the salie nce of the 4 kHz prepulse for female mice, coupled with the poorer PPI for the higher (20 kHz) prepulse frequency suggests that the female mice suffered more high frequency hearing loss (a nd resultant plasticity fo r 4 kHz) than did the male mice. Whereas age and gender effects were found in the present study, the results do not support the hypothesis that early acoustic stimulation affects a uditory development. Even immediately following exposure (1 month of ag e), AAE-exposed and control mice had similar PPI. Of course, it is possible that an effect mi ght be demonstrable using exposure parameters different from those employed here. It is possibl e that the testing method used (i.e., PPI) was not the appropriate testing method; th erefore, another testing method, su ch as the auditory brainstem response may have a higher sensitivity. The question still remains: does the NICU e nvironment affect the auditory development of pre-term infants? The traditional American NI CU environment consists of patterned light and continuous sound. The sounds are airborne, intens e, continuous, and cover a wide range of
Lisa Tanner 15 frequencies. These sounds are generally lack ing in pattern and r hythm, unlike the sounds experienced in utero (for revi ew see Philbin, 2000). Typical NI CU sound levels vary from 50 to 75 dBA with peaks of 105 dBA and frequent prol onged sounds in the 70-80 dBA range. Because conversational speech falls between 60 and 75 dBA, maternal speech is often masked and rendered less intelligible by NICU sounds (for review see Morris, Philb in & Bose, 2000). Thus, it is possible that the pre-term infant may experi ence a disrupted pattern of auditory learning due to the auditory deprivation caused by the ma sking (League, Parker, Robertson, Valentine & Powell, 1972; Peltzman, Kitterman, Os twald, Manchester, & Heath, 1970). In contrast, the fetus in the womb is exposed to low frequency and temporal aspects of speech (e.g., intonation, stress, rhythm), but not li ght. Prenatal animal research has shown that early visual experience can alter postnatal percep tion in the visual modality as well as earlier developing sensory systems (e.g., olf actory and auditory). Studies of precocial birds showed that embryos do not exhibit prenatal auditory le arning when the maternal call is presented simultaneously with visual experience. This s uggests that early expos ure or deprivation of normal or typical sensory stimulation can ha ve negative effects on auditory development (Lickliter, 2000). In an attempt to determine the effects of early acoustic stimulation on auditory development using C57 mice exposed to an AAE, th e analyzed data indicated that early acoustic stimulation of the auditory syst ems of C57 mice does not affect th e auditory processing of tonal stimuli in three frequency regions (4k Hz, 12k Hz and 20k Hz). It is possible that it is the early visual stimulation that disrupt s the auditory development of premature human infants in the NICU and not the early exposure to instrument noise. These results ar e supportive of such a hypothesis. Of course, the results ill ustrate the need for more resear ch within the area of auditory
Lisa Tanner 16 development of premature infants in the NICU, such as, the synergism effects of noise, drugs, oxygen, low-birth weight and ea rly visual stimulation.
Lisa Tanner 17 References American Academy of Pediatrics, Committee on E nvironmental Health. (1997) Noise: A hazard for the fetus and newborn. Pediatrics, 100, (4), 724-727. Blumenthal, T. D. (1999). Short lead interval startle modification. (51-71). New York: Cambridge University Press. Cibis, G., Anderson, R., Chew, E., Fishman, G ., Kardon, R., Tripathi, R., Van Kujik, F., Weleber, R. & Balyeat, H. (1994). Em bryology. Fundamentals and Principles of Ophthamology. San Francisco: Amer ican Academy of Opthamology. Graven, S. N. (2000). The full-term and pr emature newborn. Sound and the developing infant in the NICU: Conclusions and recommendations for care. Journal of Perinatology, 20, S88-S93. Hall, J. W. (1992). Handbook of auditory evoked responses. Boston: Ally and Bacon. Hood, L.. (1998). Clinical Application of the auditory brainstem response. San Diego: Singular Publishing Group, Inc. Jeskey, J. E. & Willott, J. F. (2000). M odulation of prepulse inhibition by an augmented acoustic environment in DBA/2J mice. Behavioral Neuroscience, 114, (5), 991-997. Kahn, D. M., Cook, T. E., Carlisle, C. C., Nelson, D. L., Kramer, N. R. & Millman, R. P. (1998). Identification and modification of environmental noise in an ICU setting Chest, 114, (2), 535-540. League, R., Parker, J., Robertson, M., Valen tine, V., & Powell, J. (1972). Acoustical environments in incubators and infant oxygen tents. Preventive Medicine, 1 231-239. Lickliter, R. (1990). Premature visual stimula tion accelerates intersensory functioning in
Lisa Tanner 18 bobwhite quail neonates. Developmental Psychobiology, 23, 15-27. Lickliter, R. (1994). Prenatal vi sual experience alters postnatal sensory dominance hierarchy in bobwhite quail chicks. Infant Behavior and Development, 17 185-193. Lickliter, R. (2000). The fetus. Atypical perina tal sensory stimulation and early perceptual development: Insights from developmental psychobiology. Journal of Perinatology, 20 S45-S54. Lickliter, R. & Stoumbos, J. (1992) Modification of prenatal audito ry experience alters postnatal auditory preference of bobwhite quail chicks. Quarterly Journal of Experimental Psychology, 44B 199-241. Morris, B., Philbin, M. K., & Bose. C. (2000). Physiological effects of sound on the newborn. Journal of Perinatology, 20 S55-S60. Peck, J. E. (1994). Development of hearing. Part II. Embryology. Journal of the American Academy of Audiology 5, (6), 359-365. Peltzman, P. Kitterman, J., Ostwald, P., Manchester, D., & Heath, L. (1970). Effects of incubator noise on human hearing. The Journal of Auditory Research, 10 335-339. Philbin, M. K. (2000). The influence of audito ry experience on the behavior of preterm newborns. Journal of Perinatology, 20 S77-S87. Ruben, R. J. & Rapin, I. (1980). Plastici ty of the developing auditory system. The Annals of Otology, Rhinology & Laryngology, 89, 303-309. Sadler, T. (1985). Eye. Langmans Medical Embryology 5th Ed. Baltimore: Williams and Wilkins. Shnerson, A. & Pujol, R. (1983). Development: an atomy, electrophysiololgy and behavior. In J.
Lisa Tanner 19 F. Willott (Ed.), The Auditory Psychobiology of the Mouse. (395-425). Springfield, Illinois: Charles C. Thomas. Swerdlow, N. R. & Geyer, M. A. (1999). Ne urophysiology and Neuropharmacology of short lead interval startle modifi cation. In M. Dawson, A. M. Schell & A. H. Bohmelt (Ed.), Startle Modification. (114133). New York: Cambridge University Press. Sobkowicz, H. M. & Rose, J. E. (1983). Innervati on of the Organ of Corti of the fetal mouse in culture. In R. Romand (Ed.), Development of Auditory and Vestibular Systems. (27-45). New York: Academic Press. Webster, D. B. & Webster, M. (1980). M ouse brainstem auditory nuclei development. The Annals of Otology, Rhinology & Laryngology, 89, 254-256. Willott, J. F. (2001). Preface. In J. F. Willott, (Ed.), Handbook of Mouse Auditory Research from Behavior to Molecular Biology. New York: CRC Press. Willott, J. F. (1984). Changes in frequency repres entation in the auditory system of mice with age-related hearing impairment. Brain Research, 309, 159-162. Willott, J. F. & Carlson, S. (1995). Modificatio n of the acoustic startle response in hearingimpaired C57BL/6J mice: Prepulse augmentation and pr olongation of prepulse inhibition. Behavioral Neuroscience, 109, (3), 396-403. Willott, J. F., Carlson, S., & Chen, H. (1994). Prepulse inhibition of the startle response in mice: Relationship to hearing loss and auditory system plasticity. Behavioral Neuroscience, 108, (4), 703-713. Willott, J. F. & Turner, J. G. (2000). Neural pl asticity in the mouse inferior colliculus: Relationship to hearing loss, augments ac oustic stimulation, and prepulse inhibition. Hearing Research, 147, 275-281.
Lisa Tanner 20 Willott, J. F., Sundin, V., & Jeskey, J. (2001). Ef fects of exposure to an augmented acoustic environment on the mouse auditory system. In J. F. Willott, (Ed.), Handbook of Mouse Auditory Research from Be havior to Molecular Biology. (205-214). New York: CRC Press.
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Effects of early acoustic stimulation of prepulse inhibition in mice
h [electronic resource] /
by Lisa Tanner.
[Tampa, Fla.] :
University of South Florida,
Professional research project (Au.D.)--University of South Florida, 2003.
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ABSTRACT: The purpose of this study was to determine the effects of an atypical pattern of early acoustic stimulation on auditory development. Previous human research suggests that the acoustic environment of pre-term human infants in the Neonatal Intensive Care Unit (NICU) negatively affects some aspects of auditory development. Animal research suggests that premature auditory stimulation interrupts auditory development. Because mice are born before their auditory systems are developed, they make an excellent model for research on fetal and postnatal plasticity of the auditory system. The premature auditory state of newborn mice is similar to that of the NICU pre-term infant, albeit, natural for mice C57 mouse pups were exposed to an augmented acoustic environment (AAE) of a nightly 12-hour regiment of 70 dB SPL noise burst, beginning before age 12 days (onset of hearing) and lasting for one month. The prepulse inhibition (PPI) of mice exposed to the AAE was compared to that of non-exposed mice to observe short-term and long-term effects. Results showed that the prepulse inhibition of the AAE exposed mice did not differ significantly from that of the non-exposed mice. However, it is possible that the measurement used, PPI, may not have been appropriate or that the AAE may not have been an appropriate simulation of the NICU environment.
Adviser: F.Willott, James
Co-adviser: Lister, Jennifer
Auditory perception in children.
Mice as laboratory animals.
neonatal intensive care unit.
augmented acoustic environment.
t USF Electronic Theses and Dissertations.