Comparison between offset and onset responses of primary auditory cortex ON-OFF neurons in awake cats. J Neurophysiol 97: [3421][3422][3423][3424][3425][3426][3427][3428][3429][3430][3431] 2007. First published March 23, 2007; doi:10.1152/jn.00184.2007. Primary auditory cortex (A1) neurons are believed not to carry much information about tonal offsets because A1 neurons in barbiturate-anesthetized animals are usually described as having only onset responses. We investigated tonal offset responses in comparison with onset responses in the caudal part of A1 of awake cats. Cells responding to both onsets and offsets were commonly found (59.2% of recorded cells). Offset responses usually co-occurred with phasic onset responses or phasic components of sustained responses. These ON-OFF cells had diverse combinations of offset-and onset-frequency-receptive field (FRF): offset-FRF was similar to onset-FRF, or narrower, wider, lower, or higher than onset-FRF. The distribution of FRF patterns was diffuse with no boundaries between the different FRF-pattern groups. The onset-versus offset-FRF pattern of each cell remained unchanged across multiple stimulus intensities. Mean offset response showed similar peak latency (19.5 vs. 21.5ms), longer half-decay time (74.5 vs. 48.5 ms), and lower peak amplitude (20.4 vs. 35.9 spikes/s) compared with the mean onset response. Although offset responses were facilitated when preceded by the suppression of spike activity, they were still elicited without preceding spike suppression. It is concluded that neurons showing paired onset and offset responses are predominant in the caudal A1. Their frequency-filtering property is usually not static but dynamic, changing between sound onsets and offsets. Offset responses are similarly precise and salient as onset responses for effectively encoding sound offsets. They may be elicited as active spike responses to sound offset rather than simple rebound facilitation.

Omnipause neurons (OPNs) are midline pontine neurons that are thought to control a number of oculomotor behaviors, especially saccades. Intracellular recordings were made from OPNs in alert cats to elucidate saccade-associated postsynaptic events in OPNs and thereby determine what patterns of afferent discharge impinge on OPNs to cause their saccadic inhibition. The membrane potential of impaled OPNs exhibited steep hyperpolarization before each saccade that lasted for the whole period of the saccade. The hyperpolarization was reversed to depolarization by intracellular injection of Cl- ions, indicating it consisted of temporal summation of inhibitory postsynaptic potentials (IPSPs). The duration of the saccade-related hyperpolarization was almost equal to the duration of the concurrent saccades. The time course of the hyperpolarization was similar to that of the radial eye velocity except for the initial phase. During the falling phase of eye velocity, the correlation between the instantaneous amplitude of hyperpolarization and the instantaneous eye velocity was highly significant. The amplitude of hyperpolarization at the eye velocity peak was correlated significantly with the peak eye velocity. The time integral of the hyperpolarization was correlated with the radial amplitude of saccades. The initial phase disparity between the hyperpolarization and eye velocity was due to the relative constancy of peak time (approximately 20 ms) of the initial steep hyperpolarization regardless of the later potential profile that covaried with the eye velocity. The initial steep hyperpolarization led the beginning of saccades by 15.9 +/- 3.8 (SD) ms, which is longer than the lead time for medium-lead burst neurons. These results demonstrate that the pause of activity in OPNs is caused by IPSPs initiated by an abrupt, intense input and maintained, for the whole duration of the saccade, by afferents conveying eye velocity signals. We suggest that the initial sudden inhibition originates from central structures such as the superior colliculus and frontal eye fields and that the eye velocity-related inhibition originates from the burst generator in the brain stem.

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Background: Primary auditory cortex (AI) neurons show qualitatively distinct response features to successive acoustic signals depending on the inter-stimulus intervals (ISI). Such ISI-dependent AI responses are believed to underlie, at least partially, categorical perception of click trains (elemental vs. fused quality) and stop consonant-vowel syllables (eg.,/da/-/ta/continuum).

1. Extracellular recordings were made from medium-lead burst neurons (MLBNs) in the paramedian pontomedullary reticular formation rostral and caudal to the abducens nucleus in the alert cat. 2. Single-pulse stimulation of the contralateral superior colliculus during intersaccadic intervals evoked no response in most MLBNs. When collicular stimulation was applied at the beginning of saccades, spikes of MLBNs were consistently evoked with short latencies. The shortest latency was 0.8 ms, indicating monosynaptic activation of MLBNs from the superior colliculus. 3. Results suggest that monosynaptic excitatory effects from the colliculus are concealed by inhibitory input from omnipause neurons (OPNs) during intersaccadic intervals and that the monosynaptic collicular activation is disclosed when this inhibition is removed by a pause in OPN activity at the beginning of saccades.