[Economical body platform for neonatal rats stereotaxic surgery]. / Plataforma economica para cirugia estereotaxica en rata neonata.

INTRODUCTION: Usually, most commercial platforms that adapt to the stereotaxic apparatus in neonatal rats or small animals, to carry out surgery are very expensive. Moreover, the operator must have certain experience in its handling. DEVELOPMENT: The present work presents two platforms, one of them made in acrylic and the other of expanded polystyrene. These adapt perfectly to conventional stereotaxic apparatus, while operator does not require a great entrainment to carry out the surgical procedure. Histological slides of the prefrontal cortex, ventral hippocampus and basolateral amygdala from adult rats (postnatal day 70), staining with cresyl violet are shown. The neonatal lesions were made at postnatal day 7 with ibotenic acid applied in the prefrontal cortex, ventral hippocampus or basolateral amygdala. CONCLUSIONS: The present data suggest that it is possible to carry out lesions or to apply drugs in neonatal rats, by using an acrylic or expanded polystyrene adaptor for the stereotaxic apparatus. These have the advantage of being economic and having a simple design. Also, the type of anesthesia used in neonatal lesion rats, is discussed.

Kainate receptor-mediated presynaptic inhibition converges with presynaptic inhibition mediated by Group II mGluRs and long-term depression at the hippocampal mossy fiber-CA3 synapse.

Kainate receptors (KARs) effect depression of glutamate release at hippocampal mossy fiber-CA3 (MF-CA3) synapses by a metabotropic action involving adenylyl cyclase (AC) inhibition, cAMP reduction, and diminished protein kinase A (PKA) activation. Using hippocampal slices, we show here that KAR activation interferes with the depression of glutamate release produced by Group II metabotropic glutamate receptor stimulation and low frequency stimulation (LFS)-induced long-term depression (LTD), also expressed through presynaptic AC/cAMP/PKA at MF-CA3 synapses. The mutual occlusion of depression mediated by presynaptic KARs, Group II mGluR and LFS-induced LTD suggests their mechanistic convergence at the MF-CA3 synapse and thus invokes KARs in synaptic plasticity manifest in LTD.