Changes in glutamate immunoreactivity in the somatic sensory cortex of adult monkeys induced by nerve cuts

Abstract

Antibodies to glutamate (Glu) were used to study the effects of reduced afferent input on excitatory neurons in the somatic sensory cortex of adult monkeys. In each monkey, immunocytochemical staining was compared to thionin and cytochrome oxidase (CO) staining in adjacent sections. In the cervical spinal cord, dorsal column nuclei, ventroposterior thalamus, and primary somatic sensory cortex (SI), Glu immunoreactivity (Glu-ir) was analogous to that described in normal animals; regions with reduced or absent Glu-ir were never observed and no appreciable differences were noted between the experimental and normal side. There were also no differences in CO or thionin-stained sections from the affected hemisphere. In the insuloparietal operculum, sections in the hemisphere contralateral to the nerve cut showed that most cortical fields had a normal pattern of Glu-ir (pattern a), some exhibited a reduction of Glu-ir (pattern b), and that in the central portion of the upper bank of the central sulcus, which corresponds to the general location of the hand representation of the second somatic sensory cortex (SII), Glu-ir had virtually disappeared (pattern c). Adjacent sections processed for CO or stained with thionin showed that in the regions corresponding to those characterized by pattern c, CO was slightly decreased and that glial cells had increased in number. In the regions of SII characterized by pattern c, small intensely stained glial cells displayed Glu-ir. These findings indicate that Glu-ir is regulated by afferent activity and suggest that changes in Glu levels in neurons as well as in glial cells may trigger the biochemical processes underlying the functional and structural changes occurring during a slow phase of reorganizational plasticity in the cerebral cortex of adult monkeys.

Cooperative changes in GABA, glutamate and activity levels: the missing link in cortical plasticity

“…Given the correlation between glutamate concentration and neuronal activity (Carder & Hendry, 1994; Conti et al ., 1996) one would expect to see parallel changes in neuronal activity at the border of the ‘unresponsive’ cortex. Extracellular multiple recordings of single units in 2‐week cats confirmed that expectation.…”

“…Whether changes in the excitatory circuitry itself are involved in the potentiation of existing connections has not yet been studied. In fact, the excitatory neurotransmitter glutamate could play a role in cortical reorganization because of the activity‐dependent nature of its neuronal concentration (Carder & Hendry, 1994; Conti et al ., 1996) and the involvement of various glutamate receptors in neuronal plasticity (Roche et al ., 1994; Kamishita et al ., 1995; Garraghty & Muja, 1996; Kaczmarek et al ., 1997). To investigate the possibility that glutamate is indeed involved in cortical plasticity, we used immunocytochemical and bioanalytical methods to examine the glutamate levels in area 17 of normal cats and cats with retinal lesions.…”

Mechanisms of Cortical Reorganization in Lower-Limb Amputees

“…Although experiments in animals have shown that reorganization can occur at multiple levels, including the cortex (Pons et al, 1988;Recanzone et al, 1992;Merzenich and Jenkins, 1993;Gilbert, 1994, 1995), thalamus (Garraghty and Kass, 1991;Pons et al, 1991;Nicolelis et al, 1993), brainstem (Pons et al, 1991;Florence and Kaas, 1995), and spinal cord (C arp and Wolpaw, 1994;Florence and Kaas, 1995), the site of motor reorganization in humans is not known. Whereas animal studies have shown that GABAergic (Hendry and Jones, 1986;Welker et al, 1989;Jacobs and Donoghue, 1991), glutaminergic (Anw yl, 1991;Garraghty et al, 1993;Conti et al, 1996), and cholinergic mechanisms (Juliano et al, 1991) are involved in different forms of cortical plasticity, the mechanisms of human plasticity are also unclear. Understanding of these mechanisms is crucial to the design of rational strategies to modulate plasticity and to enhance recovery of function.…”

Localization of NMDA receptors in the cerebral cortex: a schematic overview

“…These receptors can monitor Glu release by neighboring axon terminals (35,36) of thalamic (25) and corticocortical (70) origin, as well as from axon collaterals of cortical Gluergic neurons (71), and therefore they can mediate part of the neuron-glia signaling mechanisms that regulate gene expression and responses to pathological elevations of Glu levels of astrocytes, and may participate in the mechanism(s) subserving activity-dependent cortical plasticity (72).…”