Olfactory bulbectomy alters NMDA receptor levels in the rat prefrontal cortex

Differential characteristics of ketamine self-administration in the olfactory bulbectomy model of depression in male rats.

“…Lower NMDA receptor density was also found in several brain regions, for example, prefrontal and piriform cortexes, lateral amygdaloid nucleus, and thalamic nucleus (Harkin, Kelly, & Leonard, 2003; Song & Leonard, 2005). However, the exact nature of glutamatergic dysregulation seems to be much more complex, because some studies have shown increased NMDA density in the prefrontal cortex (Webster et al, 2000) and amygdala (Nakanishi et al, 1990). Furthermore, novelty-induced cortical glutamate release in the OBX model is believed to be responsible for some of the typical depressive-like phenotypes, especially irritability, hyperactivity in an unknown environment, and maladaptation to stress (Ho et al, 2000).…”

Differential characteristics of ketamine self-administration in the olfactory bulbectomy model of depression in male rats.

“…Lower NMDA receptor density was also found in several brain regions, for example, prefrontal and piriform cortexes, lateral amygdaloid nucleus, and thalamic nucleus (Harkin, Kelly, & Leonard, 2003; Song & Leonard, 2005). However, the exact nature of glutamatergic dysregulation seems to be much more complex, because some studies have shown increased NMDA density in the prefrontal cortex (Webster et al, 2000) and amygdala (Nakanishi et al, 1990). Furthermore, novelty-induced cortical glutamate release in the OBX model is believed to be responsible for some of the typical depressive-like phenotypes, especially irritability, hyperactivity in an unknown environment, and maladaptation to stress (Ho et al, 2000).…”

Mapping resting-state brain networks in conscious animals

“…For example, connections from the PFC to cingulate cortex and NAcc have been implicated in emotional processing (Hajos et al, 1998). While connections to the thalamus and cortical regions might be related to the modulatory function of the PFC on the thalamo-cortical input (Anderson and DeVito, 1987), connections to the olfactory bulb might be related to the finding that olfactory bulbectomy alters NMDA receptor levels in the rat PFC (Webster et al, 2000). In terms of the connections between the PFC and hippocampus, there are substantial evidences showing that the hippocampus projects densely to the medial PFC (Swanson, 1981; Ferino et al, 1987; Jay et al, 1989; Jay and Witter, 1991; Carr and Sesack, 1996; Ishikawa and Nakamura, 2003).…”

Brain NMDA Receptors in Schizophrenia and Depression

“…Chronic corticosterone administration, which emulates the endocrine response to stress, increased GRIN2A and GRIN2B mRNAs, which mediated the deleterious effects on the hippocampus [208]. Further, the olfactory bulbectomy model of depression reduces NMDA receptor binding in the prefrontal cortex and amygdala [209,210]. On the other hand, in the frontal cortex, BDNF deficiency, which occurs under chronic stress and is one of the leading causes of depression, also increased the density of GRIN1, GRIN2A and GRIN2B genes in the early stages of development [211].…”

Differential characteristics of ketamine self-administration in the olfactory bulbectomy model of depression in male rats.

“…Lower NMDA receptor density was also found in several brain regions, for example, prefrontal and piriform cortexes, lateral amygdaloid nucleus, and thalamic nucleus (Harkin, Kelly, & Leonard, 2003; Song & Leonard, 2005). However, the exact nature of glutamatergic dysregulation seems to be much more complex, because some studies have shown increased NMDA density in the prefrontal cortex (Webster et al, 2000) and amygdala (Nakanishi et al, 1990). Furthermore, novelty-induced cortical glutamate release in the OBX model is believed to be responsible for some of the typical depressive-like phenotypes, especially irritability, hyperactivity in an unknown environment, and maladaptation to stress (Ho et al, 2000).…”

Mapping resting-state brain networks in conscious animals

“…For example, connections from the PFC to cingulate cortex and NAcc have been implicated in emotional processing (Hajos et al, 1998). While connections to the thalamus and cortical regions might be related to the modulatory function of the PFC on the thalamo-cortical input (Anderson and DeVito, 1987), connections to the olfactory bulb might be related to the finding that olfactory bulbectomy alters NMDA receptor levels in the rat PFC (Webster et al, 2000). In terms of the connections between the PFC and hippocampus, there are substantial evidences showing that the hippocampus projects densely to the medial PFC (Swanson, 1981; Ferino et al, 1987; Jay et al, 1989; Jay and Witter, 1991; Carr and Sesack, 1996; Ishikawa and Nakamura, 2003).…”

Brain NMDA Receptors in Schizophrenia and Depression

“…Chronic corticosterone administration, which emulates the endocrine response to stress, increased GRIN2A and GRIN2B mRNAs, which mediated the deleterious effects on the hippocampus [208]. Further, the olfactory bulbectomy model of depression reduces NMDA receptor binding in the prefrontal cortex and amygdala [209,210]. On the other hand, in the frontal cortex, BDNF deficiency, which occurs under chronic stress and is one of the leading causes of depression, also increased the density of GRIN1, GRIN2A and GRIN2B genes in the early stages of development [211].…”

Differential characteristics of ketamine self-administration in the olfactory bulbectomy model of depression in male rats.

“…Lower NMDA receptor density was also found in several brain regions, for example, prefrontal and piriform cortexes, lateral amygdaloid nucleus, and thalamic nucleus (Harkin, Kelly, & Leonard, 2003; Song & Leonard, 2005). However, the exact nature of glutamatergic dysregulation seems to be much more complex, because some studies have shown increased NMDA density in the prefrontal cortex (Webster et al, 2000) and amygdala (Nakanishi et al, 1990). Furthermore, novelty-induced cortical glutamate release in the OBX model is believed to be responsible for some of the typical depressive-like phenotypes, especially irritability, hyperactivity in an unknown environment, and maladaptation to stress (Ho et al, 2000).…”

Mapping resting-state brain networks in conscious animals

“…For example, connections from the PFC to cingulate cortex and NAcc have been implicated in emotional processing (Hajos et al, 1998). While connections to the thalamus and cortical regions might be related to the modulatory function of the PFC on the thalamo-cortical input (Anderson and DeVito, 1987), connections to the olfactory bulb might be related to the finding that olfactory bulbectomy alters NMDA receptor levels in the rat PFC (Webster et al, 2000). In terms of the connections between the PFC and hippocampus, there are substantial evidences showing that the hippocampus projects densely to the medial PFC (Swanson, 1981; Ferino et al, 1987; Jay et al, 1989; Jay and Witter, 1991; Carr and Sesack, 1996; Ishikawa and Nakamura, 2003).…”

Brain NMDA Receptors in Schizophrenia and Depression

“…Chronic corticosterone administration, which emulates the endocrine response to stress, increased GRIN2A and GRIN2B mRNAs, which mediated the deleterious effects on the hippocampus [208]. Further, the olfactory bulbectomy model of depression reduces NMDA receptor binding in the prefrontal cortex and amygdala [209,210]. On the other hand, in the frontal cortex, BDNF deficiency, which occurs under chronic stress and is one of the leading causes of depression, also increased the density of GRIN1, GRIN2A and GRIN2B genes in the early stages of development [211].…”