GABAergic organization of the auditory cortex in the mustached bat (Pteronotus p. parnellii).

The structure and distribution of neurons and axon terminals (puncta) immunostained for gamma-aminobutyric acid (GABA) in the parietotemporal neocortex of the mustached bat (Pteronotus p. parnellii) was studied. The types of GABAergic neurons and puncta (putative terminals) were analyzed, and the immunocytochemical patterns were compared to those in cat auditory cortex (AC). The classic map of mustached bat primary auditory cortex (AI) corresponds to a belt of granular six-layered cortex on the temporal convexity. This area encompasses the Doppler-shifted constant frequency 60 kHz domain (DSCF) described in physiological investigations, as well as its flanking, low-frequency, posterior field (AIp) and the anterior high-frequency region (AIa). Many types of GABAergic neurons correspond to those in cat primary AC. However, the bat had a significantly lower proportion of such cells in five of the six layers. The classes of GABAergic neurons in most layers were small, medium-sized, and large multipolar cells, and bipolar and bitufted neurons. Types found in only one or two layers included horizontal cells (layers I and VI) or extraverted multipolar neurons (layer II). Only layer IV had comparable percentages (∼ 26%), suggesting that the GABAergic influence on lemniscal thalamocortical input is conserved phylogenetically. While the cellular basis for GABAergic cortical processing may reflect shared neural circuits and common modes of inhibitory processing, laminar differences could underlie adaptations specific to microchioptera.

Focal projections of cat auditory cortex to the pontine nuclei.

The pontine nuclei (PN) receive projections from the auditory cortex (AC) and they are a major source of mossy fibers to the cerebellum. However, they have not been studied in detail using sensitive neuroanatomical tracers, and whether all AC areas contribute to the corticopontine (CP) system is unknown. We characterized the projection patterns of 11 AC areas with WGA-HRP. We also compared them with their corticothalamic and corticocollicular counterparts. A third objective was to analyze the structure of the CP axons and their terminals with BDA. Both tracers confirm that all AC areas projected to lateral, central, and medial ipsilateral pontine divisions. The strongest CP projections were from nontonotopic and polymodal association areas. Preterminal fibers formed single terminal fields having many boutons en passant as well as terminal endings, and there was a specific morphological pattern for each pontine target, irrespective of their areal origin. Thus, axons in the medial division had a simpler terminal architecture (type 1 terminal plexus); both the central and lateral pons received more complex endings (type 2 terminal plexus). Auditory CP topographical distribution resembled visual and somatosensory CP projections, which preserve retinotopy and somatotopy in the pons, respectively. However, the absence of pontine tonotopy suggests that the AC projection topography is unrelated to tonotopy. CP input to the medial and central pons coincides with the somatosensory and visual cortical inputs, respectively, and such overlap might subserve convergence in the cerebellum. In contrast, lateral pontine input may be exclusively auditory.

Acetylcholinesterase level and molecular isoforms are altered in brain of Reelin Orleans mutant mice.

In this study we examined changes in acetylcholinesterase (AChE) pattern in the brain of adult Reelin Orleans (RelnOrl) homozygous mutant mice. The AChE histochemistry firstly revealed an abnormal distribution of AChE-positive cells in several areas of the reeler brain, including cortices; the strongest labelling was observed in cerebellum and hippocampus when compared with controls. Biochemical determinations demonstrated an increase of 80-90% in AChE specific activity from cerebellar and hippocampal extracts. We also report that the AChE tetrameric form (G4) was selectively increased in the RelnOrl brain. The relationship between AChE and Reelin and suggested morphogenetic functions are also discussed.

Hypothyroidism prevents developmental neuronal loss during auditory organ development.

The deficit of thyroid hormone leads to several structural and physiological modifications in the auditory receptor: the outer hair cells present an immature morphology, abnormal persistence of the afferent dendrites and incomplete development of the efferent terminals. The aim of this work was to perform a quantitative and morphometric study of the spiral ganglion neurons in control and hypothyroid animals. The cochleae from both experimental groups were processed in order to obtain plastic sections. In control animals the size of the neurons increased throughout development and was larger in the basal than in the apical portion of the cochlea. In hypothyroid animals, the cell death that takes place normally during development did not occur, and there was no differentiation into types I and II neurons. The size of the neurons also increased with development in treated animals, but they were smaller than in control animals, and in this case the neurons in the apex were larger than in the base. This study shows that hypothyroidism alters the normal development of the spiral ganglion neurons.