It has been well documented that neurons in the auditory cortex of anaesthetized animals generally display transient responses to acoustic stimulation, and typically respond to a brief stimulus with one or fewer action potentials. The number of action potentials evoked by each stimulus usually does not increase with increasing stimulus duration. Such observations have long puzzled researchers across disciplines and raised serious questions regarding the role of the auditory cortex in encoding ongoing acoustic signals. Contrary to these long-held views, here we show that single neurons in both primary (area A1) and lateral belt areas of the auditory cortex of awake marmoset monkeys (Callithrix jacchus) are capable of firing in a sustained manner over a prolonged period of time, especially when they are driven by their preferred stimuli. In contrast, responses become more transient or phasic when auditory cortex neurons respond to non-preferred stimuli. These findings suggest that when the auditory cortex is stimulated by a sound, a particular population of neurons fire maximally throughout the duration of the sound. Responses of other, less optimally driven neurons fade away quickly after stimulus onset. This results in a selective representation of the sound across both neuronal population and time.

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Direct dynamics simulations, utilizing the RM1 semiempirical electronic structure theory, were performed to study the thermal dissociation of the doubly protonated tripeptide threonine-isoleucine-lysine ion, TIK(H), for temperatures of 1250-2500 K, corresponding to classical energies of 1778-3556 kJ/mol. The number of different fragmentation pathways increases with increase in temperature. At 1250 K there are only three fragmentation pathways, with one contributing 85% of the fragmentation. In contrast, at 2500 K, there are 61 pathways, and not one dominates. The same ion is often formed via different pathways, and at 2500 K there are only 14 m/z values for the product ions. The backbone and side-chain fragmentations occur by concerted reactions, with simultaneous proton transfer and bond rupture, and also by homolytic bond ruptures without proton transfer. For each temperature the TIK(H) fragmentation probability versus time is exponential, in accord with the Rice-Ramsperger-Kassel-Marcus and transition state theories. Rate constants versus temperature were determined for two proton transfer and two bond rupture pathways. From Arrhenius plots activation energies E and A-factors were determined for these pathways. They are 62-78 kJ/mol and (2-3) × 10 s for the proton transfer pathways and 153-168 kJ/mol and (2-4) × 10 s for the bond rupture pathways. For the bond rupture pathways, the product cation radicals undergo significant structural changes during the bond rupture as a result of hydrogen bonding, which lowers their entropies and also their E and A parameters relative to those for C-C bond rupture pathways in hydrocarbon molecules. The E values determined from the simulation Arrhenius plots are in very good agreement with the reaction barriers for the RM1 method used in the simulations. A preliminary simulation of TIK(H) collision-induced dissociation (CID), at a collision energy of 13 eV (1255 kJ/mol), was also performed to compare with the thermal dissociation simulations. Though the energy transferred to TIK(H) in the collisions is substantially less than the energy for the thermal excitations, there is substantial fragmentation as a result of the localized, nonrandom excitation by the collisions. CID results in different fragmentation pathways with a significant amount of short time nonstatistical fragmentation. Backbone fragmentation is less important, and side-chain fragmentation is more important for the CID simulations as compared to the thermal simulations. The thermal simulations provide information regarding the long-time statistical fragmentation.

We studied the influences of the temporal firing patterns of presynaptic cat visual cortical cells on spike generation by postsynaptic cells. Multiunit recordings were dissected into the activity of individual neurons within the recorded group. Cross-correlation analysis was then used to identify directly coupled neuron pairs. The 22 multiunit groups recorded typically showed activity from two to six neurons, each containing between 1 and 15 neuron pairs. From a total of 241 neuron pairs, 91 (38%) had a shifted cross-correlation peak, which indicated a possible direct connection. Only two multiunit groups contained no shifted peaks. Burst activity, defined by groups of two or more spikes with intervals of

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Burst activity, defined by groups of two or more spikes with intervals of < or = 8 ms, was analyzed in responses to drifting sinewave gratings elicited from striate cortical neurons in anesthetized cats. Bursting varied broadly across a population of 507 simple and complex cells. Half of this population had > or = 42% of their spikes contained in bursts. The fraction of spikes in bursts did not vary as a function of average firing rate and was stationary over time. Peaks in the interspike interval histograms were found at both 3-5 ms and 10-30 ms. In many cells the locations of these peaks were independent of firing rate, indicating a quantized control of firing behavior at two different time scales. The activity at the shorter time scale most likely results from intrinsic properties of the cell membrane, and that at the longer scale from recurrent network excitation. Burst frequency (bursts per s) and burst length (spikes per burst) both depended on firing rate. Burst frequency was essentially linear with firing rate, whereas burst length was a nonlinear function of firing rate and was also governed by stimulus orientation. At a given firing rate, burst length was greater for optimal orientations than for nonoptimal orientations. No organized orientation dependence was seen in bursts from lateral geniculate nucleus cells. Activation of cortical contrast gain control at low response amplitudes resulted in no burst length modulation, but burst shortening at optimal orientations was found in responses characterized by supersaturation. At a given firing rate, cortical burst length was shortened by microinjection of gamma-aminobutyric acid (GABA), and bursts became longer in the presence of N-methyl-bicuculline, a GABA(A) receptor blocker. These results are consistent with a model in which responses are reduced at nonoptimal orientations, at least in part, by burst shortening that is mediated by GABA. A similar mechanism contributes to response supersaturation at high contrasts via recruitment of inhibitory responses that are tuned to adjacent orientations. Burst length modulation can serve as a form of coding by supporting dynamic, stimulus-dependent reorganization of the effectiveness of individual network connections.

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Blocking GABAA-receptor-mediated inhibition reduces the selectivity of striate cortical neurons for the orientation of a light bar primarily by reducing the selectivity of their onset transient (initial 200 ms) response. Blocking GABAB-receptor-mediated inhibition with phaclofen, however, is not reported to reduce the orientation selectivity of these neurons when it is measured with a light bar. We hypothesized that blocking GABAB-receptor-mediated inhibition would instead affect the orientation selectivity of cortical neurons by reducing the selectivity of their sustained response to a prolonged stimulus. To test this hypothesis, we stimulated 21 striate cortical neurons with drifting sine-wave gratings and measured their orientation selectivity before, during, and after iontophoretic injection of 2-hydroxy-saclofen (2-OH-S), a selective GABAB-receptor antagonist. 2-OH-S reduced the orientation selectivity of six of eight simple cells by an average of 28.8 (± 13.2)% and reduced the orientation selectivity of eight of 13 complex cells by an average of 32.3 (± 27.4)%. As predicted, 2-OH-S reduced the orientation selectivity of the neurons' sustained response, but did not reduce the orientation selectivity of their onset transient response. 2-OH-S also increased the length of spike “bursts” (two or more spikes with interspike intervals ≤ 8 ms) and eliminated the orientation selectivity of these bursts for six cells. These results are the first demonstration of a functional role for GABAB receptors in visual cortex and support the hypothesis that two GABA-mediated inhibitory mechanisms, one fast and the other slow, operate within the striate cortex to shape the response properties of individual neurons.