Abstract:Hearing loss induces plasticity in excitatory and inhibitory neurotransmitter systems in auditory brain regions. Excitatory-inhibitory balance is also influenced by a range of neuromodulatory regulatory systems, but less is known about the effects of auditory damage on these networks. In this work, we studied the effects of acoustic trauma on neuromodulatory plasticity in the auditory midbrain of CBA/J mice. Quantitative PCR was used to measure the expression of serotonergic and GABAergic receptor genes in the… Show more
“…[ 23 ] Acoustic trauma in an animal model induced substantial hearing loss and caused selective upregulation of serotonin receptor genes in the inferior colliculus. [ 24 ] These 3 studies have demonstrated that hearing loss may induce plasticity in the excitatory and inhibitory neurotransmitter systems in the central auditory brain regions. However, information on networks and etiologic mechanisms between auditory damage and depression via the serotonin pathway is scant.…”
Acquired sensory hearing loss (SHL) is suggested to be associated with depression. However, some studies have reported conflicting results. Our study investigated the relationship between the prevalence of SHL and the incidence of depression over 12 years of follow-up by using data from the Taiwan National Health Insurance Research Database (NHIRD). We sought to determine the association between SHL and subsequent development of depression and discuss the pathophysiological mechanism underlying the association.Patients with SHL were identified from the NHIRD (SHL cohort). A non-SHL cohort, comprising patients without SHL frequency-matched with the SHL patients according to age group, sex, and the year of diagnosis of SHL at the ratio of 1:4, was constructed, and the incidence of depression was evaluated in both cohorts. A multivariable model was adjusted for age, sex, and comorbidity.The SHL cohort and non-SHL cohort comprised 5043 patients with SHL and 20,172 patients without SHL, respectively. The incidences density rates were 9.50 and 4.78 per 1000 person-years in the SHL cohort and non-SHL cohort, respectively. After adjustment for age, sex, and comorbidities, the risk of depression was higher in the SHL cohort than in the non-SHL cohort (hazard ratio = 1.73, 95% confidence interval = 1.49–2.00).Acquired SHL may increase the risk of subsequent depression. The results demonstrated that SHL was an independent risk factor regardless of sex, age, and comorbidities. Moreover, a strong association between hearing loss and subsequent depression among Taiwanese adults of all ages, particularly those aged ≤49 and >65 years and without using steroids for the treatment of SHL was observed. Prospective clinical and biomedical studies on the relationship between hearing loss and depression are warranted for determining the etiopathology.
“…[ 23 ] Acoustic trauma in an animal model induced substantial hearing loss and caused selective upregulation of serotonin receptor genes in the inferior colliculus. [ 24 ] These 3 studies have demonstrated that hearing loss may induce plasticity in the excitatory and inhibitory neurotransmitter systems in the central auditory brain regions. However, information on networks and etiologic mechanisms between auditory damage and depression via the serotonin pathway is scant.…”
Acquired sensory hearing loss (SHL) is suggested to be associated with depression. However, some studies have reported conflicting results. Our study investigated the relationship between the prevalence of SHL and the incidence of depression over 12 years of follow-up by using data from the Taiwan National Health Insurance Research Database (NHIRD). We sought to determine the association between SHL and subsequent development of depression and discuss the pathophysiological mechanism underlying the association.Patients with SHL were identified from the NHIRD (SHL cohort). A non-SHL cohort, comprising patients without SHL frequency-matched with the SHL patients according to age group, sex, and the year of diagnosis of SHL at the ratio of 1:4, was constructed, and the incidence of depression was evaluated in both cohorts. A multivariable model was adjusted for age, sex, and comorbidity.The SHL cohort and non-SHL cohort comprised 5043 patients with SHL and 20,172 patients without SHL, respectively. The incidences density rates were 9.50 and 4.78 per 1000 person-years in the SHL cohort and non-SHL cohort, respectively. After adjustment for age, sex, and comorbidities, the risk of depression was higher in the SHL cohort than in the non-SHL cohort (hazard ratio = 1.73, 95% confidence interval = 1.49–2.00).Acquired SHL may increase the risk of subsequent depression. The results demonstrated that SHL was an independent risk factor regardless of sex, age, and comorbidities. Moreover, a strong association between hearing loss and subsequent depression among Taiwanese adults of all ages, particularly those aged ≤49 and >65 years and without using steroids for the treatment of SHL was observed. Prospective clinical and biomedical studies on the relationship between hearing loss and depression are warranted for determining the etiopathology.
“…Gene expression relative to the housekeeping gene (Rpl13a) was calculated with the method used by [ 93 ], in which corrections for different efficiencies between target gene and housekeeping gene are made: in which RE is the relative expression, Ekhg is the efficiency of the housekeeping gene, CThkg is the Ct value of the housekeeping gene, Etg is the efficiency of the target gene, and CTtg is the Ct value of the target gene.…”
Detecting regular patterns in the environment, a process known as statistical
learning, is essential for survival. Neuronal adaptation is a key mechanism in
the detection of patterns that are continuously repeated across short (seconds
to minutes) temporal windows. Here, we found in mice that a subcortical
structure in the auditory midbrain was sensitive to patterns that were repeated
discontinuously, in a temporally sparse manner, across windows of minutes to
hours. Using a combination of behavioral, electrophysiological, and molecular
approaches, we found changes in neuronal response gain that varied in mechanism
with the degree of sound predictability and resulted in changes in frequency
coding. Analysis of population activity (structural tuning) revealed an increase
in frequency classification accuracy in the context of increased overlap in
responses across frequencies. The increase in accuracy and overlap was
paralleled at the behavioral level in an increase in generalization in the
absence of diminished discrimination. Gain modulation was accompanied by changes
in gene and protein expression, indicative of long-term plasticity.
Physiological changes were largely independent of corticofugal feedback, and no
changes were seen in upstream cochlear nucleus responses, suggesting a key role
of the auditory midbrain in sensory gating. Subsequent behavior demonstrated
learning of predictable and random patterns and their importance in auditory
conditioning. Using longer timescales than previously explored, the combined
data show that the auditory midbrain codes statistical learning of temporally
sparse patterns, a process that is critical for the detection of relevant
stimuli in the constant soundscape that the animal navigates through.
“…Moreover, activating serotonergic pathways in the IC strongly influences responses of IC neurons to playbacks of squeaks. Activating the 5-HT1A receptor, a type which is strongly expressed within the IC (Thompson et al 1994;Peruzzi and Dut 2004;Smith et al 2014), greatly decreases the responses of IC neurons to squeaks (Hurley and Nigam 2014). 5-HT1A activation also consolidates squeak-evoked action potentials in time, so that information on the temporally varying acoustic structure of squeaks is also reduced.…”
Section: Model Of Contextual Feedback To the Auditory Midbrainmentioning
Context is critical to the adaptive value of communication. Sensory systems such as the auditory system represent an important juncture at which information on physiological state or social valence can be added to communicative information. However, the neural pathways that convey context to the auditory system are not well understood. The serotonergic system offers an excellent model to address these types of questions. Serotonin fluctuates in the mouse inferior colliculus (IC), an auditory midbrain region important for species-specific vocalizations, during specific social and non-social contexts. Furthermore, serotonin is an indicator of the valence of event-based changes within individual social interactions. We propose a model in which the brain's social behavior network serves as an afferent effector of the serotonergic dorsal raphe nucleus in order to gate contextual release of serotonin in the IC. Specifically, discrete vasopressinergic nuclei within the hypothalamus and extended amygdala that project to the dorsal raphe are functionally engaged during contexts in which serotonin fluctuates in the IC. Since serotonin strongly influences the responses of IC neurons to social vocalizations, this pathway could serve as a feedback loop whereby integrative social centers modulate their own sources of input. The end result of this feedback would be to produce a process that is geared, from sensory input to motor output, toward responding appropriately to a dynamic external world.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.