A1 Neurons Research Articles

Encoding of sound envelope transients in the auditory cortex of juvenile rats and adult rats

Accurate neural processing of time-varying sound amplitude and spectral information is vital for species-specific communication. During postnatal development, cortical processing of sound frequency undergoes progressive refinement; however, it is not clear whether cortical processing of sound envelope transients also undergoes age-related changes. We determined the dependence of neural response strength and first-spike latency on sound rise–fall time across sound levels in the primary auditory cortex (A1) of juvenile (P20–P30) rats and adult (8–10 weeks) rats. A1 neurons were categorized as “all-pass”, “short-pass”, or “mixed” (“all-pass” at high sound levels to “short-pass” at lower sound levels) based on the normalized response strength vs. rise–fall time functions across sound levels. The proportions of A1 neurons within each of the three categories in juvenile rats were similar to that in adult rats. In general, with increasing rise–fall time, the average response strength decreased and the average first-spike latency increased in A1 neurons of both groups. At a given sound level and rise–fall time, the average normalized neural response strength did not differ significantly between the two age groups. However, the A1 neurons in juvenile rats showed greater absolute response strength, longer first-spike latency compared to those in adult rats. In addition, at a constant sound level, the average first-spike latency of juvenile A1 neurons was more sensitive to changes in rise–fall time. Our results demonstrate the dependence of the responses of rat A1 neurons on sound rise–fall time, and suggest that the response latency exhibit some age-related changes in cortical representation of sound envelope rise time.

Morphological and physiological evidence of a synaptic connection between the lateral parabrachial nucleus and neurons in the A7 catecholamine cell group in rats.

BackgroundThe descending noradrenergic (NAergic) system is one of the important endogenous analgesia systems. It has been suggested that noxious stimuli could activate descending NAergic system; nevertheless, the underlying neuronal circuit remains unclear. As NAergic neurons in the A7 catecholamine cell group (A7) are a part of the descending NAergic system and the lateral parabrachial nucleus (LPB) is an important brainstem structure that relays ascending nociceptive signal, we aimed to test whether LPB neurons have direct synaptic contact with NAergic A7 neurons.ResultsStereotaxic injections of an anterograde tracer, biotinylated dextran-amine (BDA), were administered to LPB in rats. The BDA-labeled axonal terminals that have physical contacts with tyrosine hydroxylase-positive (presumed noadrenergic) neurons were identified in A7. Consistent with these morphological observations, the excitatory synaptic currents (EPSCs) were readily evoked in NAergic A7 neurons by extracellular stimulation of LPB. The EPSCs evoked by LPB stimulation were blocked by CNQX, a non-NMDA receptor blocker, and AP5, a selective NMDA receptor blocker, showing that LPB-A7 synaptic transmission is glutamatergic. Moreover, the amplitude of LPB-A7 EPSCs was significantly attenuated by DAMGO, a selective μ-opioid receptor agonist, which was associated with an increase in paired-pulse ratio.ConclusionsTaken together, the above results showed direct synaptic connections between LPB and A7 catecholamine cell group, the function of which is subject to presynaptic modulation by μ-opioid receptors.

Hindbrain Catecholamine Neurons Activate Orexin Neurons During Systemic Glucoprivation in Male Rats.

Hindbrain catecholamine neurons are required for elicitation of feeding responses to glucose deficit, but the forebrain circuitry required for these responses is incompletely understood. Here we examined interactions of catecholamine and orexin neurons in eliciting glucoprivic feeding. Orexin neurons, located in the perifornical lateral hypothalamus (PeFLH), are heavily innervated by hindbrain catecholamine neurons, stimulate food intake, and increase arousal and behavioral activation. Orexin neurons may therefore contribute importantly to appetitive responses, such as food seeking, during glucoprivation. Retrograde tracing results showed that nearly all innervation of the PeFLH from the hindbrain originated from catecholamine neurons and some raphe nuclei. Results also suggested that many catecholamine neurons project collaterally to the PeFLH and paraventricular hypothalamic nucleus. Systemic administration of the antiglycolytic agent, 2-deoxy-D-glucose, increased food intake and c-Fos expression in orexin neurons. Both responses were eliminated by a lesion of catecholamine neurons innervating orexin neurons using the retrogradely transported immunotoxin, anti-dopamine-β-hydroxylase saporin, which is specifically internalized by dopamine-β-hydroxylase-expressing catecholamine neurons. Using designer receptors exclusively activated by designer drugs in transgenic rats expressing Cre recombinase under the control of tyrosine hydroxylase promoter, catecholamine neurons in cell groups A1 and C1 of the ventrolateral medulla were activated selectively by peripheral injection of clozapine-N-oxide. Clozapine-N-oxide injection increased food intake and c-Fos expression in PeFLH orexin neurons as well as in paraventricular hypothalamic nucleus neurons. In summary, catecholamine neurons are required for the activation of orexin neurons during glucoprivation. Activation of orexin neurons may contribute to appetitive responses required for glucoprivic feeding.

A Neural Substrate for Rapid Timbre Recognition? Neural and Behavioral Discrimination of Very Brief Acoustic Vowels.

The timbre of a sound plays an important role in our ability to discriminate between behaviorally relevant auditory categories, such as different vowels in speech. Here, we investigated, in the primary auditory cortex (A1) of anesthetized guinea pigs, the neural representation of vowels with impoverished timbre cues. Five different vowels were presented with durations ranging from 2 to 128 ms. A psychophysical experiment involving human listeners showed that identification performance was near ceiling for the longer durations and degraded close to chance level for the shortest durations. This was likely due to spectral splatter, which reduced the contrast between the spectral profiles of the vowels at short durations. Effects of vowel duration on cortical responses were well predicted by the linear frequency responses of A1 neurons. Using mutual information, we found that auditory cortical neurons in the guinea pig could be used to reliably identify several vowels for all durations. Information carried by each cortical site was low on average, but the population code was accurate even for durations where human behavioral performance was poor. These results suggest that a place population code is available at the level of A1 to encode spectral profile cues for even very short sounds.

Spatial organization of excitatory synaptic inputs to layer 4 neurons in mouse primary auditory cortex.

Layer 4 (L4) of primary auditory cortex (A1) receives a tonotopically organized projection from the medial geniculate nucleus of the thalamus. However, individual neurons in A1 respond to a wider range of sound frequencies than would be predicted by their thalamic input, which suggests the existence of cross-frequency intracortical networks. We used laser scanning photostimulation and uncaging of glutamate in brain slices of mouse A1 to characterize the spatial organization of intracortical inputs to L4 neurons. Slices were prepared to include the entire tonotopic extent of A1. We find that L4 neurons receive local vertically organized (columnar) excitation from layers 2 through 6 (L6) and horizontally organized excitation primarily from L4 and L6 neurons in regions centered ~300–500 μm caudal and/or rostral to the cell. Excitatory horizontal synaptic connections from layers 2 and 3 were sparse. The origins of horizontal projections from L4 and L6 correspond to regions in the tonotopic map that are approximately an octave away from the target cell location. Such spatially organized lateral connections may contribute to the detection and processing of auditory objects with specific spectral structures.

Behavioral detection of intra-cortical microstimulation in the primary and secondary auditory cortex of cats.

Although neural responses to sound stimuli have been thoroughly investigated in various areas of the auditory cortex, the results electrophysiological recordings cannot establish a causal link between neural activation and brain function. Electrical microstimulation, which can selectively perturb neural activity in specific parts of the nervous system, is an important tool for exploring the organization and function of brain circuitry. To date, the studies describing the behavioral effects of electrical stimulation have largely been conducted in the primary auditory cortex. In this study, to investigate the potential differences in the effects of electrical stimulation on different cortical areas, we measured the behavioral performance of cats in detecting intra-cortical microstimulation (ICMS) delivered in the primary and secondary auditory fields (A1 and A2, respectively). After being trained to perform a Go/No-Go task cued by sounds, we found that cats could also learn to perform the task cued by ICMS; furthermore, the detection of the ICMS was similarly sensitive in A1 and A2. Presenting wideband noise together with ICMS substantially decreased the performance of cats in detecting ICMS in A1 and A2, consistent with a noise masking effect on the sensation elicited by the ICMS. In contrast, presenting ICMS with pure-tones in the spectral receptive field of the electrode-implanted cortical site reduced ICMS detection performance in A1 but not A2. Therefore, activation of A1 and A2 neurons may produce different qualities of sensation. Overall, our study revealed that ICMS-induced neural activity could be easily integrated into an animal’s behavioral decision process and had an implication for the development of cortical auditory prosthetics.

Responses of neurons in the marmoset primary auditory cortex to interaural level differences: comparison of pure tones and vocalizations.

Interaural level differences (ILDs) are the dominant cue for localizing the sources of high frequency sounds that differ in azimuth. Neurons in the primary auditory cortex (A1) respond differentially to ILDs of simple stimuli such as tones and noise bands, but the extent to which this applies to complex natural sounds, such as vocalizations, is not known. In sufentanil/N2O anesthetized marmosets, we compared the responses of 76 A1 neurons to three vocalizations (Ock, Tsik, and Twitter) and pure tones at cells' characteristic frequency. Each stimulus was presented with ILDs ranging from 20 dB favoring the contralateral ear to 20 dB favoring the ipsilateral ear to cover most of the frontal azimuthal space. The response to each stimulus was tested at three average binaural levels (ABLs). Most neurons were sensitive to ILDs of vocalizations and pure tones. For all stimuli, the majority of cells had monotonic ILD sensitivity functions favoring the contralateral ear, but we also observed ILD sensitivity functions that peaked near the midline and functions favoring the ipsilateral ear. Representation of ILD in A1 was better for pure tones and the Ock vocalization in comparison to the Tsik and Twitter calls; this was reflected by higher discrimination indices and greater modulation ranges. ILD sensitivity was heavily dependent on ABL: changes in ABL by ±20 dB SPL from the optimal level for ILD sensitivity led to significant decreases in ILD sensitivity for all stimuli, although ILD sensitivity to pure tones and Ock calls was most robust to such ABL changes. Our results demonstrate differences in ILD coding for pure tones and vocalizations, showing that ILD sensitivity in A1 to complex sounds cannot be simply extrapolated from that to pure tones. They also show A1 neurons do not show level-invariant representation of ILD, suggesting that such a representation of auditory space is likely to require population coding, and further processing at subsequent hierarchical stages.

Selective optogenetic stimulation of the retrotrapezoid nucleus in sleeping rats activates breathing without changing blood pressure or causing arousal or sighs.

Combined optogenetic activation of the retrotrapezoid nucleus (RTN; a CO2/proton-activated brainstem nucleus) with nearby catecholaminergic neurons (C1 and A5), or selective C1 neuron stimulation, increases blood pressure (BP) and breathing, causes arousal from non-rapid eye movement (non-REM) sleep, and triggers sighs. Here we wished to determine which of these physiological responses are elicited when RTN neurons are selectively activated. The left rostral RTN and nearby A5 neurons were transduced with channelrhodopsin-2 (ChR2(+)) using a lentiviral vector. Very few C1 cells were transduced. BP, breathing, EEG, and neck EMG were monitored. During non-REM sleep, photostimulation of ChR2(+) neurons (20s, 2-20 Hz) instantly increased V̇e without changing BP (13 rats). V̇e and BP were unaffected by light in nine control (ChR2(-)) rats. Photostimulation produced no sighs and caused arousal (EEG desynchronization) more frequently in ChR2(+) than ChR2(-) rats (62 ± 5% of trials vs. 25 ± 2%; P < 0.0001). Six ChR2(+) rats then received spinal injections of a saporin-based toxin that spared RTN neurons but destroyed surrounding catecholaminergic neurons. Photostimulation of the ChR2(+) neurons produced the same ventilatory stimulation before and after lesion, but arousal was no longer elicited. Overall (all ChR2(+) rats combined), ΔV̇e correlated with the number of ChR2(+) RTN neurons whereas arousal probability correlated with the number of ChR2(+) catecholaminergic neurons. In conclusion, RTN neurons activate breathing powerfully and, unlike the C1 cells, have minimal effects on BP and have a weak arousal capability at best. A5 neuron stimulation produces little effect on breathing and BP but does appear to facilitate arousal.

Role of A1 and A2 Noradrenergic Neurons and Median Preoptic Nucleus in Cardiovascular Recovery Induced by Hypertonic Saline Infusion in Hypovolemic Hemorrhagic Rats

Previous studies showed the involvement of Median Preoptic Nucleus (MnPO) and medullary catecholaminergic neurons (A1 and A2) in cardiovascular responses to changes in plasma osmolality. The present study examines the role of A1 and A2 noradrenergic neurons and MnPO in cardiovascular recovery induced by hypertonic saline infusion (HSI) in hypovolemic hemorrhagic rats. All experiments were performed in Wistar rats. Lesions of A1 and A2 neurons were obtain by nanoinjections of anti‐DBH‐saporin (6.3 ng/60nl). In other group nanoinjections muscimol (GABA agonist ‐ 4 mM) were used to blockade MnPO. Bleeding was induced by the withdrawal of blood for over 10 min until MAP reaches approximately 60 mmHg. After 20 min of hemorrhagic period, HSI administration was performed (3M NaCl; 1.8 ml/kg; i.v). On the day of experiment, rats were anesthetized with thiopental (40 mg/kg, i.v.) and instrumented for mean arterial pressure (MAP) recording. In sham‐rats we observed a recovery of MAP (112 ± 4.6 mmHg, 10 min after HSI). The blockade of MnPO prevented restoration of MAP induced by HSI (60 ± 6.2, 10 min after HSI; p &lt;0.05). Similar to observed in sham rats, HSI induced a recovery of MAP in A1 (101 ± 8.5 mmHg; 10 min after HSI) and A2 lesioned rats (121.4 ± 5.3 mmHg, 10 min after HSI). In A2 pressor response was greatest. The MnPO injections sites and A1 or A2 lesions extensions were confirmed by histology analysis. These results showed that the MnPO plays an important role in HSI induced resuscitation in hemorrhagic shock. However, A1 and A2 noradrenergic neurons seem not to be directly involved in the cardiovascular recovery induced by HSI in hemorrhagic rats.Financial Support: CNPq, FAPEG

Localization and production of peptide endocannabinoids in the rodent CNS and adrenal medulla

The endocannabinoid system (ECS) comprises the cannabinoid receptors CB1 and CB2 and their endogenous arachidonic acid-derived agonists 2-arachidonoyl glycerol and anandamide, which play important neuromodulatory roles. Recently, a novel class of negative allosteric CB1 receptor peptide ligands, hemopressin-like peptides derived from alpha hemoglobin, has been described, with yet unknown origin and function in the CNS. Using monoclonal antibodies we now identified the localization of RVD-hemopressin (pepcan-12) and N-terminally extended peptide endocannabinoids (pepcans) in the CNS and determined their neuronal origin. Immunohistochemical analyses in rodents revealed distinctive and specific staining in major groups of noradrenergic neurons, including the locus coeruleus (LC), A1, A5 and A7 neurons, which appear to be major sites of production/release in the CNS. No staining was detected in dopaminergic neurons. Peptidergic axons were seen throughout the brain (notably hippocampus and cerebral cortex) and spinal cord, indicative of anterograde axonal transport of pepcans. Intriguingly, the chromaffin cells in the adrenal medulla were also strongly stained for pepcans. We found specific co-expression of pepcans with galanin, both in the LC and adrenal gland. Using LC-MS/MS, pepcan-12 was only detected in non-perfused brain (∼40 pmol/g), suggesting that in the CNS it is secreted and present in extracellular compartments. In adrenal glands, significantly more pepcan-12 (400–700 pmol/g) was measured in both non-perfused and perfused tissues. Thus, chromaffin cells may be a major production site of pepcan-12 found in blood. These data uncover important areas of peptide endocannabinoid occurrence with exclusive noradrenergic immunohistochemical staining, opening new doors to investigate their potential physiological function in the ECS.This article is part of the Special Issue entitled ‘Fluorescent Tools in Neuropharmacology’.

Cross-modal and multisensory training may distinctively shape restored senses.

Cross-modal and multisensory training may distinctively shape restored senses.

Thresholding of auditory cortical representation by background noise.

It is generally thought that background noise can mask auditory information. However, how the noise specifically transforms neuronal auditory processing in a level-dependent manner remains to be carefully determined. Here, with in vivo loose-patch cell-attached recordings in layer 4 of the rat primary auditory cortex (A1), we systematically examined how continuous wideband noise of different levels affected receptive field properties of individual neurons. We found that the background noise, when above a certain critical/effective level, resulted in an elevation of intensity threshold for tone-evoked responses. This increase of threshold was linearly dependent on the noise intensity above the critical level. As such, the tonal receptive field (TRF) of individual neurons was translated upward as an entirety toward high intensities along the intensity domain. This resulted in preserved preferred characteristic frequency (CF) and the overall shape of TRF, but reduced frequency responding range and an enhanced frequency selectivity for the same stimulus intensity. Such translational effects on intensity threshold were observed in both excitatory and fast-spiking inhibitory neurons, as well as in both monotonic and nonmonotonic (intensity-tuned) A1 neurons. Our results suggest that in a noise background, fundamental auditory representations are modulated through a background level-dependent linear shifting along intensity domain, which is equivalent to reducing stimulus intensity.

Hierarchical effects of task engagement on amplitude modulation encoding in auditory cortex.

We recorded from middle lateral belt (ML) and primary (A1) auditory cortical neurons while animals discriminated amplitude-modulated (AM) sounds and also while they sat passively. Engagement in AM discrimination improved ML and A1 neurons' ability to discriminate AM with both firing rate and phase-locking; however, task engagement affected neural AM discrimination differently in the two fields. The results suggest that these two areas utilize different AM coding schemes: a "single mode" in A1 that relies on increased activity for AM relative to unmodulated sounds and a "dual-polar mode" in ML that uses both increases and decreases in neural activity to encode modulation. In the dual-polar ML code, nonsynchronized responses might play a special role. The results are consistent with findings in the primary and secondary somatosensory cortices during discrimination of vibrotactile modulation frequency, implicating a common scheme in the hierarchical processing of temporal information among different modalities. The time course of activity differences between behaving and passive conditions was also distinct in A1 and ML and may have implications for auditory attention. At modulation depths ≥ 16% (approximately behavioral threshold), A1 neurons' improvement in distinguishing AM from unmodulated noise is relatively constant or improves slightly with increasing modulation depth. In ML, improvement during engagement is most pronounced near threshold and disappears at highly suprathreshold depths. This ML effect is evident later in the stimulus, and mainly in nonsynchronized responses. This suggests that attention-related increases in activity are stronger or longer-lasting for more difficult stimuli in ML.

Mesencephalic dopaminergic neurons express a repertoire of olfactory receptors and respond to odorant-like molecules.

BackgroundThe mesencephalic dopaminergic (mDA) cell system is composed of two major groups of projecting cells in the Substantia Nigra (SN) (A9 neurons) and the Ventral Tegmental Area (VTA) (A10 cells). Selective degeneration of A9 neurons occurs in Parkinson’s disease (PD) while abnormal function of A10 cells has been linked to schizophrenia, attention deficit and addiction. The molecular basis that underlies selective vulnerability of A9 and A10 neurons is presently unknown.ResultsBy taking advantage of transgenic labeling, laser capture microdissection coupled to nano Cap-Analysis of Gene Expression (nanoCAGE) technology on isolated A9 and A10 cells, we found that a subset of Olfactory Receptors (OR)s is expressed in mDA neurons. Gene expression analysis was integrated with the FANTOM5 Helicos CAGE sequencing datasets, showing the presence of these ORs in selected tissues and brain areas outside of the olfactory epithelium. OR expression in the mesencephalon was validated by RT-PCR and in situ hybridization. By screening 16 potential ligands on 5 mDA ORs recombinantly expressed in an heterologous in vitro system, we identified carvone enantiomers as agonists at Olfr287 and able to evoke an intracellular Ca2+ increase in solitary mDA neurons. ORs were found expressed in human SN and down-regulated in PD post mortem brains.ConclusionsOur study indicates that mDA neurons express ORs and respond to odor-like molecules providing new opportunities for pharmacological intervention in disease.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-729) contains supplementary material, which is available to authorized users.

Hindbrain medulla catecholamine cell group involvement in lactate-sensitive hypoglycemia-associated patterns of hypothalamic norepinephrine and epinephrine activity

Cell-type compartmentation of glucose metabolism in the brain involves trafficking of the oxidizable glycolytic end product, l-lactate, by astrocytes to fuel neuronal mitochondrial aerobic respiration. Lactate availability within the hindbrain medulla is a monitored function that regulates systemic glucostasis as insulin-induced hypoglycemia (IIH) is exacerbated by lactate repletion of that brain region. A2 noradrenergic neurons are a plausible source of lactoprivic input to the neural gluco-regulatory circuit as caudal fourth ventricular (CV4) lactate infusion normalizes IIH-associated activation, e.g. phosphorylation of the high-sensitivity energy sensor, adenosine 5′-monophosphate-activated protein kinase (AMPK), in these cells. Here, we investigated the hypothesis that A2 neurons are unique among medullary catecholamine cells in directly screening lactate-derived energy. Adult male rats were injected with insulin or vehicle following initiation of continuous l-lactate infusion into the CV4. Two hours after injections, A1, C1, A2, and C2 neurons were collected by laser-microdissection for Western blot analysis of AMPKα1/2 and phosphoAMPKα1/2 proteins. Results show that AMPK is expressed in each cell group, but only a subset, e.g. A1, C1, and A2 neurons, exhibit increased sensor activity in response to IIH. Moreover, hindbrain lactate repletion reversed hypoglycemic augmentation of pAMPKα1/2 content in A2 and C1 but not A1 cells, and normalized hypothalamic norepinephrine and epinephrine content in a site-specific manner. The present evidence for discriminative reactivity of AMPK-expressing medullary catecholamine neurons to the screened energy substrate lactate implies that that lactoprivation is selectively signaled to the hypothalamus by A2 noradrenergic and C1 adrenergic cells.

Frequency transformation in the auditory lemniscal thalamocortical system.

The auditory lemniscal thalamocortical (TC) pathway conveys information from the ventral division of the medial geniculate body to the primary auditory cortex (A1). Although their general topographic organization has been well characterized, functional transformations at the lemniscal TC synapse still remain incompletely codified, largely due to the need for integration of functional anatomical results with the variability observed with various animal models and experimental techniques. In this review, we discuss these issues with classical approaches, such as in vivo extracellular recordings and tracer injections to physiologically identified areas in A1, and then compare these studies with modern approaches, such as in vivo two-photon calcium imaging, in vivo whole-cell recordings, optogenetic methods, and in vitro methods using slice preparations. A surprising finding from a comparison of classical and modern approaches is the similar degree of convergence from thalamic neurons to single A1 neurons and clusters of A1 neurons, although, thalamic convergence to single A1 neurons is more restricted from areas within putative thalamic frequency lamina. These comparisons suggest that frequency convergence from thalamic input to A1 is functionally limited. Finally, we consider synaptic organization of TC projections and future directions for research.

State‐dependent regulation of breathing by the retrotrapezoid nucleus (872.10)

In this study we stimulated the retrotrapezoidal neurons (RTN) by optogenetics in behaving animals to determine ventilatory responses across sleep and wake states. We targeted the rostral RTN region (n=12) with a PRSX8 promoter lentivirus and limited ChannelRhodopsin expression to RTN neurons and noradrenergic A5 neurons. A subset of rats (n=6) also received intraspinal anti‐DBH‐saporin, a catecholaminergic‐specific neurotoxin, to eliminate A5 neurons. We observed no significant differences for the resting or evoked ventilatory behavior after effective lesion. In quiet awake and non‐rapid eye movement (nREM; quiet asleep) states, RTN stimulation increased respiratory frequency and tidal volume, and could entrain respiratory rate between 1.2Hz ‐ 2Hz. We also observed active expiration in the wake state only. The increase in breathing by RTN stimulation was occluded by hypercapnia (6% CO2), but not hypoxia (12% O2). Surprisingly, RTN stimulation in REM (active sleep) failed to increase or pace respiratory rate and only tidal volume was significantly increased. This REM phenomenon draws an intriguing parallel to voluntary breathing (active wake), where homeostatic mechanisms are limited to adjusting the depth of each cortically‐triggered breath.Grant Funding Source: Supported by NIH (HL28785, HL74011)

Neural correlates of hearing in noise in macaque auditory cortex

The perception of sound in a noisy environment is a critical function of the auditory system. Here, we describe results from our study into the link between neural activity in the auditory cortex and the hearing-in-noise tasks described above. We recorded neural activity from single neurons in the core auditory cortex (i.e., A1) while monkeys were participating in these tasks. Neural recordings were conducted with tetrodes, and the frequency of the target matched the best frequency of the recorded auditory neuron. We found that the relative intensity of the target tone in the presence of the noise masker significantly modulated the response of A1 neurons. In contrast, the presentation of the target sound alone did not elicit a significant response from A1 neurons. This suggests a task-relevant contextual modulation of A1 responses during hearing in noise. Additionally we found no correlation between the monkey's behavioral choices—as assessed by their responses on choice trials—and A1 activity. Our results suggest that the encoding of a sound of interest in the presence of a noise masker is an active process, providing new insights into the neural basis for hearing in noise in the auditory system.

Ventral tegmental area activation promotes firing precision and strength through circuit inhibition in the primary auditory cortex.

The activation of the ventral tegmental area (VTA) can rebuild the tonotopic representation in the primary auditory cortex (A1), but the cellular mechanisms remain largely unknown. Here, we investigated the firing patterns and membrane potential dynamics of neurons in A1 under the influence of VTA activation using in vivo intracellular recording. We found that VTA activation can significantly reduce the variability of sound evoked responses and promote the firing precision and strength of A1 neurons. Furthermore, the compressed response window was caused by an early hyperpolarization as a result of enhanced circuit inhibition. Our study suggested a possible mechanism of how the reward system affects information processing in sensory cortex: VTA activation strengthens cortical inhibition, which shortens the response window of post-synaptic cortical neurons and further promotes the precision and strength of neuronal activity.

Learning-Stage-Dependent Plasticity of Temporal Coherence in the Auditory Cortex of Rats

Temporal coherence among neural populations may contribute importantly to signal encoding, specifically by providing an optimal tradeoff between encoding reliability and efficiency. Here, we considered the possibility that learning modulates the temporal coherence among neural populations in association with well-characterized map plasticity. We previously demonstrated that, in appetitive operant conditioning tasks, the tone-responsive area globally expanded during the early stage of learning, but shrank during the late stage. The present study further showed that phase locking of the first spike to band-specific oscillations of local field potentials (LFPs) significantly increased during the early stage of learning but decreased during the late stage, suggesting that neurons in A1 were more synchronously activated during early learning, whereas they were more asynchronously activated once learning was completed. Furthermore, LFP amplitudes increased during early learning but decreased during later learning. These results suggest that, compared to naïve encoding, early-stage encoding is more reliable but energy-consumptive, whereas late-stage encoding is more energetically efficient. Such a learning-stage-dependent encoding strategy may underlie learning-induced, non-monotonic map plasticity. Accumulating evidence indicates that the cholinergic system is likely to be a shared neural substrate of the processes for perceptual learning and attention, both of which modulate neural encoding in an adaptive manner. Thus, a better understanding of the links between map plasticity and modulation of temporal coherence will likely lead to a more integrated view of learning and attention.