Unilateral and bilateral projections from cortical cells to the inferior colliculus in guinea pigs

Coomes, Diana L.; Schofield, Ryan M.; Schofield, Brett R.

doi:10.1016/j.brainres.2005.02.015

Cited by 47 publications

(50 citation statements)

References 25 publications

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“…A change in the balance between LTP and LTD may explain the decreased responsiveness of ACx in sound-deprived mice (21) and the decline of electrically evoked responses observed in congenitally deaf cats (45). L5 synaptic plasticity may have a significant impact on subthalamic processing because of the massive descending projection from ACx (28,(46)(47)(48)(49)(50). Furthermore, the specific complement of cortical plasticity mechanisms may support the functional takeover of ACx by other sensory modalities.…”

Section: Discussionmentioning

confidence: 99%

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Kotak

Breithaupt

Sanes³

2007

Proc. Natl. Acad. Sci. U.S.A.

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Severe hearing loss during early development is associated with deficits in speech and language acquisition. Although functional studies have shown a deafness-induced alteration of synaptic strength, it is not known whether long-term synaptic plasticity depends on auditory experience. In this study, sensorineural hearing loss (SNHL) was induced surgically in developing gerbils at postnatal day 10, and excitatory synaptic plasticity was examined subsequently in a brain slice preparation that preserves the thalamorecipient auditory cortex. Extracellular stimuli were applied at layer 6 (L6), whereas evoked excitatory synaptic potentials (EPSPs) were recorded from L5 neurons by using a whole-cell current clamp configuration. In control neurons, the conditioning stimulation of L6 significantly altered EPSP amplitude for at least 1 h. Approximately half of neurons displayed long-term potentiation (LTP), whereas the other half displayed long-term depression (LTD). In contrast, SNHL neurons displayed only LTD after the conditioning stimulation of L6. Finally, the vast majority of neurons recorded from control prehearing animals (postnatal days 9 -11) displayed LTD after L6 stimulation. Thus, normal auditory experience may be essential for the maturation of synaptic plasticity mechanisms.deafness ͉ long-term depression S evere hearing loss is known to affect auditory processing in humans. This loss includes impairments of signal detection in noise or in a multiple source environment, and disruption of intensity discrimination, frequency discrimination, and temporal resolution (1-4). Even transient bouts of conductive hearing loss can disrupt auditory processing, and months or years may be required for normal perception to resolve (5, 6). Because severe hearing loss during development is implicated in the deficient acquisition of auditory perceptual skills and language, which presumably require learning, we have examined whether synaptic plasticity is also affected.At a structural level, hearing impairments can lead to neuron death or atrophy and alter process outgrowth (7). Furthermore, direct examination of neuron function in brain slice preparations from deaf animals has revealed significant physiological changes to intrinsic and synaptic properties. In both the inferior colliculus and auditory cortex (ACx), early sensorineural hearing loss (SNHL) alters the balance of excitatory and inhibitory synaptic strength (8-10). A similar disruption in synaptic physiology and certain intrinsic properties also occurs in the auditory brainstem of the congenitally deaf mutant mouse (11,12).Both long-term potentiation (LTP) and depression (LTD) have been characterized in a series of studies on the rat ACx (13-18). For example, an NMDA receptor-mediated LTP in the ACx can be induced by stimulation of afferents innervating the ACx via the white matter (13), whereas thalamo-and corticocortical synapse activation can induce LTD (16). These cellular mechanisms may serve as a substrate for use-dependent alteration of coding properties in...

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Section: Discussionmentioning

confidence: 99%

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Kotak

Breithaupt

Sanes³

2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Double labeling experiments yielded no evidence for collateral projections to both targets among layer V cells (Wong and Kelly, 1981). A few scattered cortical cells located in layer VI next to the white matter project to the IC (Doucet et al, 2003;Bajo and Moore, 2005;Coomes et al, 2005), and it cannot be ruled out that these cells are among the layer VI cells that also project to the thalamus. Given their very small numbers relative to the numbers of cells in layer V, however, it does not seem likely that they would represent a significant source of inputs to the MG.…”

Section: Other Potential Sources Of the Bda-labeled Terminals And Axomentioning

confidence: 95%

Multiple topographically organized projections connect the central nucleus of the inferior colliculus to the ventral division of the medial geniculate nucleus in the gerbil, Meriones unguiculatus

Cant

Benson

2007

J of Comparative Neurology

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The ventral division of the medial geniculate nucleus (MGv) receives almost all of its ascending input from the ipsilateral central nucleus of the inferior colliculus (CNIC). In a previous study (Cant and Benson [2006] J. Comp. Neurol. 495:511-528), we made injections of biotinylated dextran amine into the CNIC of the gerbil and demonstrated that it can be divided into two parts. One part (zone 1) receives almost all of its ascending input from the cochlear nuclei, the nuclei of the lateral lemniscus, and the main nuclei of the superior olivary complex; the other part (zone 2) receives inputs from the cochlear nuclei and nuclei of the lateral lemniscus but few or no inputs from the main olivary nuclei. Here we show that these two parts of the CNIC project differentially to the MGv. Axons labeled anterogradely by injections in zone 1 project throughout the rostral two-thirds of the MGv, whereas axons from zone 2 project to the caudal third of the MGv. Throughout much of their extent, the terminal fields do not appear to overlap, although both parts of the CNIC project to medial and dorsal parts of the MGv, and there may be overlap in the most ventral part as well. The results indicate that two parallel pathways arising in the CNIC remain largely separate in the medial geniculate nucleus of the gerbil. It seems most likely that the neurons in the two terminal zones in the MGv perform different functions in audition.

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“…Thus, blocking the A1 may impair both auditory object/ feature-based attention and auditory spatial attention, leading to that attention-impaired rats do not exhibit any attentional modulations of PPI. Moreover, the A1 sends descending axonal projections to some important relay sites in the pathway mediating PPI, including the IC (Herbert et al, 1991;Druga et al, 1997;Coomes et al, 2005;Schofield, 2009), pedunculopontine tegmental nucleus (PPTg), and laterodorsal tegmental nucleus (Schofield and Motts, 2009;Schofield, 2010). Thus, the A1 may directly mediate the top-down modulations of PPI via its direct projections to the PPI pathway.…”

Section: Contributions Of the A1mentioning

confidence: 99%

Differentially Organized Top-Down Modulation of Prepulse Inhibition of Startle

Du¹,

Wu²,

Li³

2011

J. Neurosci.

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Prepulse inhibition (PPI) of startle is the suppression of the startle reflex when a weaker sensory stimulus (the prepulse) shortly precedes the startling stimulus. PPI can be attentionally enhanced in both humans and laboratory animals. This study investigated whether the following three forebrain structures, which are critical for initial cortical processing of auditory signals, auditory fear conditioning/ memories, and spatial attention, respectively, play a role in the top-down modulation of PPI in rats: the primary auditory cortex (A1), lateral nucleus of the amygdala (LA), and posterior parietal cortex (PPC). The results show that, under the noise-masking condition, PPI was enhanced by fear conditioning of the prepulse in a prepulse-specific manner, and the conditioning-induced PPI enhancement was further increased by perceptual separation between the conditioned prepulse and the noise masker. Reversibly blocking glutamate receptors in the A1 with 2 mM kynurenic acid eliminated both the conditioning-induced and perceptual separation-induced PPI enhancements. Blocking the LA eliminated the conditioning-induced but not the perceptual separation-induced PPI enhancement, and blocking the PPC specifically eliminated the perceptual separation-induced PPI enhancement. The two types of PPI enhancements were also eliminated by the extinction manipulation. Thus, the top-down modulation of PPI is differentially organized and depends on operations of various forebrain structures. Due to the fine-tuned modulation by higher-order cognitive processes, functions of PPI can be more flexible to complex environments. The top-down enhancements of PPI in rats are also useful for modeling some mental disorders, such as schizophrenia, attention deficit/hyperactivity disorder, and posttraumatic stress disorder.

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Unilateral and bilateral projections from cortical cells to the inferior colliculus in guinea pigs

Cited by 47 publications

References 25 publications

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Developmental hearing loss eliminates long-term potentiation in the auditory cortex

Multiple topographically organized projections connect the central nucleus of the inferior colliculus to the ventral division of the medial geniculate nucleus in the gerbil, Meriones unguiculatus

Differentially Organized Top-Down Modulation of Prepulse Inhibition of Startle

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