Midbrain local circuits shape sound intensity codes.
inferior colliculus; Animals; Mice; Neurons/physiology; Acoustic Stimulation; Auditory Perception/*physiology; Inferior Colliculi/*physiology; Auditory Pathways/*physiology; Auditory Threshold/physiology; high divalents; local circuits; monosynaptic; Neural Inhibition/*physiology; sound intensity
Hierarchical processing of sensory information requires interaction at multiple levels along the peripheral to central pathway. Recent evidence suggests that interaction between driving and modulating components can shape both top down and bottom up processing of sensory information. Here we show that a component inherited from extrinsic sources combines with local components to code sound intensity. By applying high concentrations of divalent cations to neurons in the nucleus of the inferior colliculus in the auditory midbrain, we show that as sound intensity increases, the source of synaptic efficacy changes from inherited inputs to local circuits. In neurons with a wide dynamic range response to intensity, inherited inputs increase firing rates at low sound intensities but saturate at mid-to-high intensities. Local circuits activate at high sound intensities and widen dynamic range by continuously increasing their output gain with intensity. Inherited inputs are necessary and sufficient to evoke tuned responses, however local circuits change peak output. Push-pull driving inhibition and excitation create net excitatory drive to intensity-variant neurons and tune neurons to intensity. Our results reveal that dynamic range and tuning re-emerge in the auditory midbrain through local circuits that are themselves variable or tuned.
Grimsley Calum Alex; Sanchez Jason Tait; Sivaramakrishnan Shobhana
Frontiers in neural circuits
2013
1905-7
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.3389/fncir.2013.00174" target="_blank" rel="noreferrer noopener">10.3389/fncir.2013.00174</a>
Lack of an inhibitory effect of hyperprolactinemia on androgen-dependent marking.
Animal/*physiology; Animals; Arousal/physiology; Brain/*physiology; Defecation/physiology; Inbred F344; Male; Mesencephalon/physiology; Neural Inhibition/*physiology; Neural Pathways/physiology; Preoptic Area/physiology; Prolactin/*physiology; Rats; Sex Attractants/*urine; Sexual Behavior; Testosterone/*physiology; Urination/*physiology
An experiment was performed to determine if hyperprolactinemia (chronically elevated serum prolactin levels), which inhibits testosterone-activated male sexual activity, also affects other androgen-dependent behaviors. Thus defecation and urine marking in response to a novel environment were examined in sham-operated and pituitary-grafted (hyperprolactinemic) male rats that had been castrated or castrated and given subcutaneous testosterone implants. Both castration and pituitary grafting significantly inhibited defecation, with the inhibitory effects of hyperprolactinemia being most pronounced in the castrated non-testosterone-treated animals. In contrast, castration significantly reduced the amount of urine marking observed, but pituitary grafting was without effect on this behavior. Thus, although hyperprolactinemia may inhibit sexual activity through an antagonism of the activational effects of testosterone, these results suggest that this effect is specific to sexual behavior and does not involve a more generalized inhibition of the effects of testosterone on androgen-dependent behaviors.
Doherty P C
Physiology & behavior
1991
1991-11
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0031-9384(91)90435-q" target="_blank" rel="noreferrer noopener">10.1016/0031-9384(91)90435-q</a>
Intracellular recordings from combination-sensitive neurons in the inferior colliculus.
Acoustic Stimulation/methods; Afferent/classification/*physiology; Animals; Auditory/physiology; Biological; Chiroptera; Evoked Potentials; Inferior Colliculi/*cytology; Membrane Potentials/physiology/radiation effects; Models; Neural Inhibition/*physiology; Neural Pathways/physiology; Neurons; Psychophysics; Reaction Time; Wakefulness
In vertebrate auditory systems, specialized combination-sensitive neurons analyze complex vocal signals by integrating information across multiple frequency bands. We studied combination-sensitive interactions in neurons of the inferior colliculus (IC) of awake mustached bats, using intracellular somatic recording with sharp electrodes. Facilitated combinatorial neurons are coincidence detectors, showing maximum facilitation when excitation from low- and high-frequency stimuli coincide. Previous work showed that facilitatory interactions originate in the IC, require both low and high frequency-tuned glycinergic inputs, and are independent of glutamatergic inputs. These results suggest that glycinergic inputs evoke facilitation through either postinhibitory rebound or direct depolarizing mechanisms. However, in 35 of 36 facilitated neurons, we observed no evidence of low frequency-evoked transient hyperpolarization or depolarization that was closely related to response facilitation. Furthermore, we observed no evidence of shunting inhibition that might conceal inhibitory inputs. Since these facilitatory interactions originate in IC neurons, the results suggest that inputs underlying facilitation are electrically segregated from the soma. We also recorded inhibitory combinatorial interactions, in which low frequency sounds suppress responses to higher frequency signals. In 43% of 118 neurons, we observed low frequency-evoked hyperpolarizations associated with combinatorial inhibition. For these neurons, we conclude that low frequency-tuned inhibitory inputs terminate on neurons primarily excited by high-frequency signals; these inhibitory inputs may create or enhance inhibitory combinatorial interactions. In the remainder of inhibited combinatorial neurons (57%), we observed no evidence of low frequency-evoked hyperpolarizations, consistent with observations that inhibitory combinatorial responses may originate in lateral lemniscal nuclei.
Peterson Diana Coomes; Voytenko Sergiy; Gans Donald; Galazyuk Alexander; Wenstrup Jeffrey
Journal of neurophysiology
2008
2008-08
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jn.90390.2008" target="_blank" rel="noreferrer noopener">10.1152/jn.90390.2008</a>
Ambient GABA-activated tonic inhibition sharpens auditory coincidence detection via a depolarizing shunting mechanism.
Animals; Chick Embryo; Patch-Clamp Techniques; Electric Stimulation; Neurons/*physiology; gamma-Aminobutyric Acid/*physiology; Membrane Potentials/physiology; Auditory Pathways/*physiology; Neural Inhibition/*physiology; Inhibitory Postsynaptic Potentials; Receptors; Blotting; Western; GABA-A/*physiology
Tonic inhibition mediated by extrasynaptic GABA(A) receptors (GABA(A)Rs) has emerged as a novel form of neural inhibition in the CNS. However, little is known about its presence and function in the auditory system. Using whole-cell recordings in brain slices, we identified a tonic current mediated by GABA(A)Rs containing the delta subunit in middle/high-characteristic-frequency neurons of the chicken nucleus laminaris, the first interaural time difference encoder that computes information for sound localization. This tonic conductance was activated by ambient concentrations of GABA released from synaptic vesicles. Furthermore, pharmacological manipulations of the conductance demonstrated its essential role in coincidence detection. Remarkably, this depolarizing tonic conductance was strongly inhibitory primarily because of its shunting effect. These results demonstrate a novel role for tonic inhibition in central auditory information processing.
Tang Zheng-Quan; Dinh Emilie Hoang; Shi Wei; Lu Yong
The Journal of neuroscience : the official journal of the Society for Neuroscience
2011
2011-04
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1523/JNEUROSCI.4733-10.2011" target="_blank" rel="noreferrer noopener">10.1523/JNEUROSCI.4733-10.2011</a>