Both for the pure and for the missing-fundamental tones, the Nb m

Both for the pure and for the missing-fundamental tones, the Nb middle-latency Ion Channel Ligand Library datasheet response was larger for pitch changes (tones preceded by tones of different pitch) than for pitch repetitions (tones preceded by tones

of the same pitch). This Nb enhancement was observed even for missing-fundamental tones preceded by repeated tones that had a different missing-fundamental pitch but included all harmonics of the subsequent tone with another missing-fundamental pitch. This finding rules out the possibility that the Nb enhancement in response to a change in missing-fundamental pitch was simply attributable to the activity of auditory cortex neurons responding specifically to the harmonics of missing-fundamental tones. The Nb effect presumably indicates pitch processing at or near the primary auditory cortex, and it was followed Nutlin-3a order by a change-related enhancement of the N1 response, presumably generated in the secondary auditory cortex. This N1 enhancement might have been caused by a mismatch negativity response overlapping with the N1 response. Processing of missing-fundamental pitch was also reflected by the distribution of Nb responses. Tones

with a higher missing-fundamental pitch elicited more frontally dominant Nb responses than tones with a lower missing-fundamental pitch. This effect of pitch, not seen for the pure tones, might indicate that the exact location of the Nb generator source in the auditory cortex depends on the missing-fundamental pitch of the eliciting tone. “
“The cAMP–protein

kinase A (PKA) pathway plays a critical role in regulating neuronal activity. Yet, how PKA signalling shapes the population activity of neurons that regulate respiratory rhythm and motor patterns in vivo is poorly defined. We determined the respiratory effects of focally inhibiting endogenous PKA activity in defined classes of respiratory neurons in the ventrolateral medulla and spinal cord by microinjection of the Astemizole membrane-permeable PKA inhibitor Rp-adenosine 3′,5′-cyclic monophosphothioate (Rp-cAMPS) in urethane-anaesthetized adult Sprague Dawley rats. Phrenic nerve activity, end-tidal CO2 and arterial pressure were recorded. Rp-cAMPS in the preBötzinger complex (preBötC) caused powerful, dose-dependent depression of phrenic burst amplitude and inspiratory period. Rp-cAMPS powerfully depressed burst amplitude in the phrenic premotor nucleus, but had no effect at the phrenic motor nucleus, suggesting a lack of persistent PKA activity here. Surprisingly, inhibition of PKA activity in the preBötC increased phrenic burst frequency, whereas in the Bötzinger complex phrenic frequency decreased.

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