Biomedical subjects

Martin Pienkowski

Publications and source records attributed to Martin Pienkowski.

3 recordsLinked to original sources

PubMed2005

Tone responses in core versus belt auditory cortex in the developing chinchilla.

Single-unit responses to tone pip stimuli were isolated from numerous microelectrode penetrations of core primary auditory cortex (AI) and a dorsocaudal (DC) belt region in the ketamine-anesthetized chinchilla (laniger). Results are reported at postnatal day 3 (P3), P15, P30, and from adult animals. The AI core could be distinguished from the DC belt on the basis of its strict tonotopic organization, evident in all chinchillas studied (including the youngest). Averaged by age group and compared to their core counterparts, belt neurons generally had similar absolute (spike rate) thresholds and onset latencies (at a given sound pressure level), but lower maximum spike rates, broader tuning bandwidths, and more complex (multipeaked) receptive fields. Most notably, the fraction of complex belt units in the near-newborn (P3) group was high (approximately 50%), and did not systematically increase with age, while that of complex core units was approximately 10% at P3 and increased steadily to about 40% in adulthood. These results provide further evidence to support the hypothesis that, at least to some extent, core and belt auditory cortex may constitute parallel processing streams which represent different aspects of complex acoustic stimuli.

Aging↗

PubMed2005

Dynamics of real time DPOAE contralateral suppression in chinchillas and humans.

The dynamics of contralateral acoustic suppression were studied using real time (millisecond resolution) distortion product otoacoustic emissions (DPOAEs) in chinchillas and humans. Latency of DPOAE suppression onset is 26 ms in chinchillas and 45 ms in humans. After onset, suppression builds over time before tending to plateau, reflecting a temporal integration process with a time constant of 100 ms (chinchillas). In chinchillas, suppression persists for 40 ms even when elicited by stimuli as short as 5 ms. With stimuli >40 ms, offset and onset latencies are similar and duration of suppression equals that of the contralateral stimulus. A comparison of DPOAE suppression onset latency with neural latency data from the pathways involved suggests the following timing scheme: stimulus onset to activity in (ventral) cochlear nucleus, 4ms (15% of delay); transfer to olivocochlear efferents, 9 ms (35%); efferent conduction to presynaptic OHC site, 4ms (15%); synaptic and mechanical events at OHCs, 9 ms (35% of delay).

Adolescent↗

PubMed2004

Tone frequency maps and receptive fields in the developing chinchilla auditory cortex.

Single-unit responses to tone pip stimuli were isolated from numerous microelectrode penetrations of auditory cortex (under ketamine anesthesia) in the developing chinchilla (laniger), a precocious mammal. Results are reported at postnatal day 3 (P3), P15, and P30, and from adult animals. Hearing sensitivity and spike firing rates were mature in the youngest group. The topographic representation of sound frequency (tonotopic map) in primary and secondary auditory cortex was also well ordered and sharply tuned by P3. The spectral-temporal complexity of cortical receptive fields, on the other hand, increased progressively (past P30) to adulthood. The (purported) refinement of initially diffuse tonotopic projections to cortex thus seems to occur in utero in the chinchilla, where external (and maternal) sounds are considerably attenuated and might not contribute to the mechanism(s) involved. This compares well with recent studies of vision, suggesting that the refinement of the retinotopic map does not require external light, but rather waves of (correlated) spontaneous activity on the retina. In contrast, it is most probable that selectivity for more complex sound features, such as frequency stacks and glides, develops under the influence of the postnatal acoustic environment and that inadequate sound stimulation in early development (e.g., due to chronic middle ear disease) impairs the formation of the requisite intracortical (and/or subcortical) circuitry.

Acoustic Stimulation↗