Title:Upregulation of Connexins in the Rat Hippocampal and Cortical Neurons
Following Blockade of NMDA Receptors During Postnatal Development
Volume: 30
Issue: 1
Author(s): Masoumeh Kourosh-Arami*, Mansoureh Soleimani, Mohammad Taghi Joghataei, Masoumeh Mosleh, Parisa Hayat and Alireza Komaki
Affiliation:
- Cellular and Molecular Research Center, School of Medical Sciences, Iran University of Medical Sciences, Tehran,
Iran
Keywords:
Connexin expression, hippocampus, cortex, NMDA receptor, postnatal development, cortical neurons.
Abstract:
Background: Interneural gap junctional coupling represents neural development that
decreases during the postnatal period. The decrease of gap junction function coincides with the main
period of chemical synapse creation and increment of synaptic activity during postnatal weeks 1 to 3.
Methods: Here, we have assessed the role of chemical synapses on connexin (Cx) expression in
neurons and glial cells of hippocampal and cortical neurons. We characterized the impact of NMDA
receptors blockade on the expression of Cx36 and Cx43 proteins by western blot analysis in postnatal
day (PND)14 and PND28. MK801 was injected subcutaneously from the first day of birth until 14 or 28
days, depending on the experimental groups. Saline was injected in the same volumes in the control
group.
Results: Early postnatal blockade of the NMDA subtype of glutamate receptors by the non-competitive
antagonist dizocilpine maleate (MK801) arrested the developmental reduction in gap junctions during
the initial postnatal weeks. Expression of Cx43 declined in PND28 compared to PND14 in visual cortex
(VC) neurons. Also, we found that the expression of Cx36 and Cx43 augmented in the rats' VC in
PND28 following the blockade of NMDA receptors. Expression of Cx36 declined in PND28 compared
to PND14 in hippocampal neurons. Also, we found that the expression of Cx36 augmented in the rats'
hippocampal neurons in PND14 and PND28 following a blockade of NMDA receptors.
Conclusion: These results suggest that the postnatal enhancement in glutamatergic synaptic activity is
associated with the loss of gap junctional connections and downregulation of Cx36 and Cx43 between
developing neurons and glial cells.