Effects of Aging on Properties of the Local Circuit in Rat Primary Somatosensory Cortex (S1) In Vitro

Abstract

During aging receptive field properties degrade, the ability of the circuit to process temporal information is impaired and behaviors mediated by the circuit can become impaired. These changes are mediated by changes in the properties of neural circuits, particularly the balance of excitation and inhibition, the intrinsic properties of neurons, and the anatomy of connections in the circuit. In this study, properties of thalamorecipient pyramidal neurons in layer 3 were examined in the hindpaw region of rat primary somatosensory cortex (S1) in vitro. Excitatory and inhibitory postsynaptic currents (IPSCs) resulting from trains of electrical stimulation of thalamocortical afferents were recorded. Excitatory postsynaptic currents were larger in old S1, but showed no difference in temporal dynamics; IPSCs showed significantly less suppression across the train in old S1, partly due to a decrease in GABAB signaling. Neurons in old S1 were more likely to exhibit burst firing, due to an increase in T-current. Significant differences in dendritic morphology were also observed in old S1, accompanied by a decrease in dendritic spine density. These data directly demonstrate changes in the properties of the thalamorecipient circuit in old S1 and help to explain the changes observed in responses during aging.

A complementary role of intracortical inhibition in age-related tactile degradation and its remodelling in humans

“…Furthermore, in-vitro studies showed that both excitation and inhibition were affected during aging43. Based on these findings, and the enhanced activation in SI (see Fig.…”

Age-Related Deterioration of Perineuronal Nets in the Primary Auditory Cortex of Mice

“…A consistent finding across the sensory cortex is a decline in inhibitory neurotransmission with age (Leventhal et al, 2003; Caspary et al, 2008; Syka, 2010; Hickmott and Dinse, 2013). Processing of rapidly changing spectrotemporal cues, such as those present in speech, depends on interactions between excitatory and inhibitory components of the auditory neuron receptive field (Zhang et al, 2003; Razak and Fuzessery, 2006, 2008, 2009; Sadagopan and Wang, 2010; Trujillo et al, 2013).…”

Dissecting mechanisms of brain aging by studying the intrinsic excitability of neurons

“…AP threshold is the critical level to which the membrane potential must be depolarized in order to initiate an AP and hence it is often used as a measure for neuron excitability. Recent studies have reported an age-related increase in the AP threshold of the rat hippocampal CA1 pyramidal cell (HP-CA1-PC; Matthews et al, 2009 ) and primary somatosensory cortex layer 3 pyramidal cell (S1-PC) (Hickmott and Dinse, 2013 ), mice (Randall et al, 2012 ) and rabbit HP-CA1-PC (Power et al, 2002 ) and also in the ventral pleural ganglion sensory neuron (PVC-SN) and buccal ganglion sensory neuron (BSC-SN) of aging Aplysia (Kempsell and Fieber, 2014 ). While the basis of this change has not yet been clarified, age-related depolarization of the AP threshold could likely be ascribed to alterations of voltage-gated Na + channel (Na v channel) activation properties or channel subtype expression patterns (Randall et al, 2012 ).…”