Developmental decline in modulation of glutamatergic synapses in layer IV of the barrel cortex by group II metabotropic glutamate receptors

Abstract

Previously, we demonstrated that group II mGluRs reduce glutamate release from thalamocortical synapses during early postnatal development (P7–11). To further examine the role of group II mGluRs in the modulation of somatosensory circuitry, we determined whether group II mGluRs continue to modulate thalamocortical synapses until adulthood and whether these receptors also modulate intra-cortical synapses in the barrel cortex. To address these issues, we examined the effect of the group II mGluR agonists on thalamocortical EPSCs and intra-barrel EPSCs in slices from animals of different ages (P7–53). We found that the depression of thalamocortical EPSCs by stimulation group II mGluRs rapidly declined after the second postnatal week. In contrast, adenosine continued to depress thalamocortical EPSCs via a presynaptic mechanism in young adult mice (P30–50). Activation group II mGluRs also reduced intra-barrel EPSCs through a postsynaptic mechanism in young mice (P7–11). Similar to the thalamocortical synapses, the group II mGluR modulation of intra-barrel excitatory synapses declined with development. In young adult animals (P30–50), group II mGluR stimulation had little effect on intra-barrel EPSCs but did hyperpolarize the neurons. Together our results demonstrate that group II mGluRs modulate barrel cortex circuitry by presynaptic and postsynaptic mechanisms depending on the source of the synapse and that this modulation declines with development.

Adenosine Differentially Modulates Synaptic Transmission of Excitatory and Inhibitory Microcircuits in Layer 4 of Rat Barrel Cortex

“…In cortical L4, adenosine suppresses excitatory thalamocortical input to both L4 inhibitory and excitatory neurons (Fontanez and Porter 2006;Mateo and Porter 2015). In the neocortex, our previous (van Aerde et al 2015) and present work reveals a more selective role for adenosine in modulating neuronal excitability and neurotransmission.…”

“…In the primary somatosensory (barrel) cortex of rodents, layer 4 (L4) neurons are the major targets of thalamocortical afferents from the ventroposterior medial nucleus of thalamus (Bosman et al 2011;Feldmeyer 2012;Feldmeyer et al 2013). Previous work has shown that thalamocortical excitation of L4 excitatory and inhibitory neurons is down-regulated by presynaptic adenosine A1 receptors in juvenile and adult mouse barrel cortex (Fontanez and Porter 2006;Mateo and Porter 2015). However, the effect of adenosine on the local intracortical synapses between L4 excitatory and inhibitory neurons has not yet been investigated.…”

Chronic stimulation of group II metabotropic glutamate receptors in the medulla oblongata attenuates hypertension development in spontaneously hypertensive rats

“…The electrophysiological properties of RVLM neurons and their responses to angiotensin II differ between WKYs and SHRs, even in the neonatal stage [21]. mGluRs, especially postsynaptic ones, do not exhibit any function at younger (juvenile) stages in some cases [22][23][24] but regulate various neuronal functions at different developmental stages [25][26][27][28][29][30][31][32][33][34]. Furthermore, mGluR2/3 agonists hyperpolarize neurons in normotensive rats [35], while the agonists effects seemed to be attenuated in adult SHRs (authors' observation).…”

Nicotine Exposure during Adolescence Leads to Changes of Synaptic Plasticity and Intrinsic Excitability of Mice Insular Pyramidal Cells at Later Life

“…The repeated exposure of nicotine during adolescence may affect the maturation of mice insular circuitry and lead to changes in the insular circuitry that may last for a lifetime. It has been shown that the enhanced spike-timing dependent plasticity caused by adolescent nicotine exposure in the rat prefrontal layer V PNs was mediated by a long-term decrease in the expression of synaptic metabotropic glutamate receptor 2 (mGluR2) [ 31 ], which was present in presynaptic terminal and reduces excitatory synaptic transmission [ 32 , 33 ]. Thus, it is possible that adolescent nicotine exposure reduces synaptic mGluR2 expression in the mice insular cortex at later life, which may increase synaptic potentiation in insular layer V PNs.…”