Intracellular recordings reveal integrative function of the basolateral amygdala in acoustic communication.

The amygdala, a brain center of emotional expression, contributes to appropriate behavior responses during acoustic communication. In support of that role, the basolateral amygdala (BLA) analyzes the meaning of vocalizations through the integration of multiple acoustic inputs with information from other senses and an animal's internal state. The mechanisms underlying this integration are poorly understood. This study focuses on the integration of vocalization-related inputs to the BLA from auditory centers during this processing. We used intracellular recordings of BLA neurons in unanesthetized big brown bats that rely heavily on a complex vocal repertoire during social interactions. Postsynaptic and spiking responses of BLA neurons were recorded to three vocal sequences that are closely related to distinct behaviors (appeasement, low-level aggression, and high-level aggression) and have different emotional valence. Our novel findings are that most BLA neurons showed postsynaptic responses to one or more vocalizations (31 of 46) but that many fewer neurons showed spiking responses (8 of 46). The spiking responses were more selective than postsynaptic potential (PSP) responses. Furthermore, vocal stimuli associated with either positive or negative valence were similarly effective in eliciting excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and spiking responses. This indicates that BLA neurons process both positive- and negative-valence vocal stimuli. The greater selectivity of spiking responses than PSP responses suggests an integrative role for processing within the BLA to enhance response specificity in acoustic communication.NEW & NOTEWORTHY The amygdala plays an important role in social communication by sound, but little is known about how it integrates diverse auditory inputs to form selective responses to social vocalizations. We show that BLA neurons receive inputs that are responsive to both negative- and positive-affect vocalizations but their spiking outputs are fewer and highly selective for vocalization type. Our work demonstrates that BLA neurons perform an integrative function in shaping appropriate behavioral responses to social vocalizations.

Unusual properties of α7 nicotinic acetylcholine receptor ion channels in B lymphocyte-derived SP-2/0 cells.

This study demonstrates the presence of α7 nicotinic acetylcholine receptors (nAChR) in B lymphocyte-derived SP-2/0 cells by means of flow cytometry and immunocytochemistry. According to lectin and sandwich ELISA, the α7 subunits expressed in SP-2/0 cells are more glycosylated compared to those expressed in the brain or normal B lymphocytes and are combined with ß2 subunits. At zero and negative pipette potentials, either acetylcholine or α7-specific agonist PNU282987 stimulated the ion channel activity in SP-2/0 cells revealed by single channel patch-clamp recordings. The conductivity was within the range of 19 to 39 pS and reversal potential was between -17 mV and +28 mV, the currents were potentiated by α7-specific positive allosteric modulator PNU120596 and were partially blocked by α7-specific antagonist methyllicaconitine (MLA). However, they were oriented downwards suggesting that the channels mediated the cation outflux rather than influx. As shown by Ca2+ imaging studies, PNU282987 did not stimulate immediate Ca2+ influx into SP-2/0 cells. Instead, Ca2+ influx through Ca-release-activated channels (CRACs) was observed within minutes after either PNU282987 or MLA application. It is concluded that SP-2/0 express α7ß2 nAChRs, which mediate the cation outflux under negative pipette potentials applied, possibly, due to depolarized membrane or negative surface charge formed by carbohydrate residues. In addition, α7ß2 nAChRs may influence CRACs in ion-independent way.

Developmental hearing loss impairs signal detection in noise: putative central mechanisms.

Listeners with hearing loss have difficulty processing sounds in noisy environments. This is most noticeable for speech perception, but is reflected in a basic auditory processing task: detecting a tonal signal in a noise background, i.e., simultaneous masking. It is unresolved whether the mechanisms underlying simultaneous masking arise from the auditory periphery or from the central auditory system. Poor detection in listeners with sensorineural hearing loss (SNHL) is attributed to cochlear hair cell damage. However, hearing loss alters neural processing in the central auditory system. Additionally, both psychophysical and neurophysiological data from normally hearing and impaired listeners suggest that there are additional contributions to simultaneous masking that arise centrally. With SNHL, it is difficult to separate peripheral from central contributions to signal detection deficits. We have thus excluded peripheral contributions by using an animal model of early conductive hearing loss (CHL) that provides auditory deprivation but does not induce cochlear damage. When tested as adults, animals raised with CHL had increased thresholds for detecting tones in simultaneous noise. Furthermore, intracellular in vivo recordings in control animals revealed a cortical correlate of simultaneous masking: local cortical processing reduced tone-evoked responses in the presence of noise. This raises the possibility that altered cortical responses which occur with early CHL can influence even simple signal detection in noise.

Intracellular recordings from combination-sensitive neurons in the inferior colliculus.

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.