A case of peripheral odontogenic fibroma arising in the mandibular premolar region of a teenager.

Peripheral odontogenic fibroma (POdF) is a rare, benign ectomesenchymal tumor. Herein, we report a case of a 15-year-old female patient who developed POdF in the mandible. The lesion was resected along with the periosteum. Histopathological findings revealed a small mass and cord-like epithelium. There was no recurrence 16 months postoperatively.

Distinct development of GABA system in the ventral and dorsal horns in the embryonic mouse spinal cord.

In the adult brain, γ-amino butyric acid (GABA) is an inhibitory neurotransmitter, whereas it acts as an excitatory transmitter in the immature brain, and may be involved in morphogenesis. In the present study, we immunohistochemically examined the developmental changes in GABA signaling in the embryonic mouse cervical spinal cord. Glutamic acid decarboxylase and GABA were markers for GABA neurons. Vesicular GABA transporter was a marker for GABAergic and glycinergic terminals. Potassium chloride cotransporter 2 was a marker for GABAergic inhibition. We found five points: (1) In the ventral part, GABA neurons were divided into three groups. The first differentiated group sent commissural axons after embryonic day 11 (E11), but disappeared or changed their transmitter by E15. The second and third differentiated groups were localized in the ventral horn after E12, and sent axons to the ipsilateral marginal zone. There was a distal-to-proximal gradient in varicosity formation in GABAergic axons and a superficial-to-deep gradient in GABAergic synapse formation in the ventral horn; (2) In the dorsal horn, GABA neurons were localized after E13, and synapses were diffusely formed after E15; (3) GABA may be excitatory for several days before synapses formation; (4) There was a ventral-to-dorsal gradient in the development of GABA signaling. The GABAergic inhibitory network may develop in the ventral horn between E15 and E17, and GABA may transiently play crucial roles in inhibitory regulation of the motor system in the mouse fetus; (5) GABA signaling continued to develop after birth, and GABAergic system diminished in the ventral horn.

GABA/glycine signaling during degeneration and regeneration of mouse hypoglossal nerves.

In the adult central nervous system (CNS), GABA and glycine (Gly) are predominant inhibitory neurotransmitters, negatively regulating glutamatergic transmission. In the immature CNS, on the other hand, they act as trophic factors, mediating morphogenesis. In the present study, to investigate their involvement in axonal regeneration, we morphologically examined changes in their signaling in mouse hypoglossal nuclei during degeneration and regeneration of hypoglossal nerves. We found that (1) expression and localization of presynaptic elements were not changed, (2) localization of gephyrin, which anchors GABA and Gly receptors, was spread on the surface of motor neuron cell bodies and dendrites, (3) KCC2-expression markedly decreased, (4) choline acetyltransferase, which mediates acetylcholine-synthesis, immediately disappeared from the motor neurons, and (5) the synaptic cleft of both excitatory and inhibitory synapses became irregularly wider, in the hypoglossal nuclei of the sutured side after the operation. These changes gradually normalized during regeneration. These results suggested that synthesis of acetylcholine may be stopped in the motor neuron after axotomy. GABA/Gly may be normally released from presynaptic terminals, be spilled over the original synaptic cleft, be diffused into the neighboring space, bind to extrasynaptically localized receptors, and mediate depolarization of the membrane potential of motor neurons during degeneration and regeneration. Furthermore, it was suggested that GABA/Gly signaling in postsynaptic motor neurons went back to being immature after axotomy, and may play an important role in axonal regeneration.