Systems Neuroscience
Birthdays of retinal amacrine cell subtypes are systematically related to their molecular identity and soma position.
Publication Date: 2009 Nov 13 PMID: 19918927
Authors: Voinescu, P. E. - Kay, J. N. - Sanes, J. R.
Journal: J Comp Neurol
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Authors: Voinescu, P. E. - Kay, J. N. - Sanes, J. R.
Journal: J Comp Neurol
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Changes in synaptic populations in the spinal dorsal horn following a dorsal rhizotomy in the monkey.
Publication Date: 2010 Jan 1 PMID: 19882723
Authors: Darian-Smith, C. - Hopkins, S. - Ralston, H. J. 3rd
Journal: J Comp Neurol
Studies in monkeys have shown substantial neuronal reorganization and behavioral recovery during the months following a cervical dorsal root lesion (DRL; Darian-Smith [2004] J. Comp. Neurol. 470:134-150; Darian-Smith and Ciferri [2005] J. Comp. Neurol. 491:27-45, [2006] J. Comp. Neurol. 498:552-565). The goal of the present study was to identify ultrastructural synaptic changes post-DRL within the dorsal horn (DH). Two monkeys received a unilateral DRL, as described previously (Darian-Smith and Brown [2000] Nat. Neurosci. 3:476-481), which removed cutaneous and proprioceptive input from the thumb, index finger, and middle finger. Six weeks before terminating the experiment at 4 post-DRL months, hand representation was mapped electrophysiologically within the somatosensory cortex, and anterograde tracers were injected into reactivated cortex to label corticospinal terminals. Sections were collected through the spinal lesion zone. Corticospinal terminals and inhibitory profiles were visualized by using preembedding immunohistochemistry and postembedding gamma-aminobutyric acid (GABA) immunostaining, respectively. Synaptic elements were systematically counted through the superficial DH and included synaptic profiles with round vesicles (R), pleomorphic flattened vesicles (F; presumed inhibitory synapses), similar synapses immunolabeled for GABA (F-GABA), primary afferent synapses (C-type), synapses with dense-cored vesicles (D, mostly primary afferents), and presynaptic dendrites of interneurons (PSD). Synapse types were compared bilaterally via ANOVAs. As expected, we found a significant drop in C-type profiles on the lesioned side ( approximately 16% of contralateral), and R profiles did not differ bilaterally. More surprising was a significant increase in the number of F profiles ( approximately 170% of contralateral) and F-GABA profiles ( approximately 315% of contralateral) on the side of the lesion. Our results demonstrate a striking increase in the inhibitory circuitry within the deafferented DH.
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Authors: Darian-Smith, C. - Hopkins, S. - Ralston, H. J. 3rd
Journal: J Comp Neurol
Studies in monkeys have shown substantial neuronal reorganization and behavioral recovery during the months following a cervical dorsal root lesion (DRL; Darian-Smith [2004] J. Comp. Neurol. 470:134-150; Darian-Smith and Ciferri [2005] J. Comp. Neurol. 491:27-45, [2006] J. Comp. Neurol. 498:552-565). The goal of the present study was to identify ultrastructural synaptic changes post-DRL within the dorsal horn (DH). Two monkeys received a unilateral DRL, as described previously (Darian-Smith and Brown [2000] Nat. Neurosci. 3:476-481), which removed cutaneous and proprioceptive input from the thumb, index finger, and middle finger. Six weeks before terminating the experiment at 4 post-DRL months, hand representation was mapped electrophysiologically within the somatosensory cortex, and anterograde tracers were injected into reactivated cortex to label corticospinal terminals. Sections were collected through the spinal lesion zone. Corticospinal terminals and inhibitory profiles were visualized by using preembedding immunohistochemistry and postembedding gamma-aminobutyric acid (GABA) immunostaining, respectively. Synaptic elements were systematically counted through the superficial DH and included synaptic profiles with round vesicles (R), pleomorphic flattened vesicles (F; presumed inhibitory synapses), similar synapses immunolabeled for GABA (F-GABA), primary afferent synapses (C-type), synapses with dense-cored vesicles (D, mostly primary afferents), and presynaptic dendrites of interneurons (PSD). Synapse types were compared bilaterally via ANOVAs. As expected, we found a significant drop in C-type profiles on the lesioned side ( approximately 16% of contralateral), and R profiles did not differ bilaterally. More surprising was a significant increase in the number of F profiles ( approximately 170% of contralateral) and F-GABA profiles ( approximately 315% of contralateral) on the side of the lesion. Our results demonstrate a striking increase in the inhibitory circuitry within the deafferented DH.
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Distribution of prolactin-responsive neurons in the mouse forebrain.
Publication Date: 2010 Jan 1 PMID: 19882722
Authors: Brown, R. S. - Kokay, I. C. - Herbison, A. E. - Grattan, D. R.
Journal: J Comp Neurol
Prolactin has numerous biological actions in the brain, and transgenic mice are increasingly being used to investigate these actions. The present study aimed to provide a detailed mapping of the prolactin-responsive neurons in the female mouse forebrain by describing the distribution of prolactin receptor mRNA by in situ hybridization, and measuring prolactin-induced phosphorylation of signal transducer and activation of transcription 5 (pSTAT5) by immunohistochemistry. For in situ hybridization, a probe designed to detect both long and short receptor isoforms showed mRNA expression in a heterogeneous manner within the forebrain. Strong expression was observed in the rostral hypothalamus, particularly in periventricular regions, as well as in the arcuate and ventromedial nuclei of the mediobasal hypothalamus. There was also significant expression in some nonhypothalamic regions, notably high expression in the choroid plexus, and lower levels of expression in the medial amygdala, bed nucleus of the stria terminalis, and lateral septum. Prolactin-induced pSTAT5, detected by immunohistochemistry, provided a functional index of prolactin receptor activation in neurons. Prolactin-induced pSTAT5 was only observed in areas containing prolactin receptor mRNA, and was particularly prominent in the rostral and mediobasal hypothalamus. Most other areas that contained prolactin receptor mRNA also showed positive signal for prolactin-induced pSTAT5. The major exceptions were paraventricular nucleus and median preoptic nucleus, in which prolactin receptor mRNA was observed, but no induction of pSTAT5 by prolactin. The data provide key neuroanatomical information facilitating the use of the mouse model for furthering our understanding of prolactin actions in the brain.
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Authors: Brown, R. S. - Kokay, I. C. - Herbison, A. E. - Grattan, D. R.
Journal: J Comp Neurol
Prolactin has numerous biological actions in the brain, and transgenic mice are increasingly being used to investigate these actions. The present study aimed to provide a detailed mapping of the prolactin-responsive neurons in the female mouse forebrain by describing the distribution of prolactin receptor mRNA by in situ hybridization, and measuring prolactin-induced phosphorylation of signal transducer and activation of transcription 5 (pSTAT5) by immunohistochemistry. For in situ hybridization, a probe designed to detect both long and short receptor isoforms showed mRNA expression in a heterogeneous manner within the forebrain. Strong expression was observed in the rostral hypothalamus, particularly in periventricular regions, as well as in the arcuate and ventromedial nuclei of the mediobasal hypothalamus. There was also significant expression in some nonhypothalamic regions, notably high expression in the choroid plexus, and lower levels of expression in the medial amygdala, bed nucleus of the stria terminalis, and lateral septum. Prolactin-induced pSTAT5, detected by immunohistochemistry, provided a functional index of prolactin receptor activation in neurons. Prolactin-induced pSTAT5 was only observed in areas containing prolactin receptor mRNA, and was particularly prominent in the rostral and mediobasal hypothalamus. Most other areas that contained prolactin receptor mRNA also showed positive signal for prolactin-induced pSTAT5. The major exceptions were paraventricular nucleus and median preoptic nucleus, in which prolactin receptor mRNA was observed, but no induction of pSTAT5 by prolactin. The data provide key neuroanatomical information facilitating the use of the mouse model for furthering our understanding of prolactin actions in the brain.
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Quantitative study of the developmental changes in calcium-permeable AMPA receptor-expressing neurons in the rat somatosensory cortex.
Publication Date: 2010 Jan 1 PMID: 19882721
Authors: Hsu, C. I. - Wang, T. C. - Hou, S. Y. - Chin, T. Y. - Chang, Y. C.
Journal: J Comp Neurol
The distribution of cells expressing calcium-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (CP-AMPARs) in the somatosensory cortex of rats at different developmental stages was studied using a kainate-stimulated Co(2+)-labeling assay in a quantitative manner. The applicability of this assay for identifying CP-AMPAR-expressing cells was first verified using cultured rat cortical neurons by means of fluorescence Ca(2+) imaging and pharmacological tools. Cells positively identified by the Co(2+)-labelinig assay resided primarily in the marginal zone and subplate of young fetuses and became more widely distributed throughout the cortex as the fetus matured. The majority, >80%, of these Co(2+)-positive cells were neurons, exhibiting immunoreactivity with the neuronal marker NeuN. The proportion of neurons that were Co(2+)-positive increased from approximately 25% to approximately 60% as the rat fetus grew into adulthood. In contrast, less than 20% of nonneuronal cells were Co(2+)-positive. Of the Co(2+)-positive neurons, 15%-31% exhibited GABA immunoreactivity and nonpyramidal-shaped cell bodies; these were presumably GABAergic neurons. Most of the remaining non-GABAergic/Co(2+)-positive neurons had pyramidal-shaped cell bodies and were presumably excitatory principle neurons. Around 70% of GABAergic neurons in the cortex were Co(2+)-positive. Furthermore, in the cortex of neonatal rats the Co(2+)-positive neurons were found to be more susceptible to kainate toxicity than the Co(2+)-negative cells. The Co(2+)-positive neurons in the subplate of neonatal rats were more vulnerable to kainate toxicity than their counterparts in the remaining cortical areas. Together, the widespread distribution and distinct susceptibility to excitotoxicity of CP-AMPAR-expressing neurons suggest that they play various important roles in the development and physiology of the rat cerebral cortex.
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Authors: Hsu, C. I. - Wang, T. C. - Hou, S. Y. - Chin, T. Y. - Chang, Y. C.
Journal: J Comp Neurol
The distribution of cells expressing calcium-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (CP-AMPARs) in the somatosensory cortex of rats at different developmental stages was studied using a kainate-stimulated Co(2+)-labeling assay in a quantitative manner. The applicability of this assay for identifying CP-AMPAR-expressing cells was first verified using cultured rat cortical neurons by means of fluorescence Ca(2+) imaging and pharmacological tools. Cells positively identified by the Co(2+)-labelinig assay resided primarily in the marginal zone and subplate of young fetuses and became more widely distributed throughout the cortex as the fetus matured. The majority, >80%, of these Co(2+)-positive cells were neurons, exhibiting immunoreactivity with the neuronal marker NeuN. The proportion of neurons that were Co(2+)-positive increased from approximately 25% to approximately 60% as the rat fetus grew into adulthood. In contrast, less than 20% of nonneuronal cells were Co(2+)-positive. Of the Co(2+)-positive neurons, 15%-31% exhibited GABA immunoreactivity and nonpyramidal-shaped cell bodies; these were presumably GABAergic neurons. Most of the remaining non-GABAergic/Co(2+)-positive neurons had pyramidal-shaped cell bodies and were presumably excitatory principle neurons. Around 70% of GABAergic neurons in the cortex were Co(2+)-positive. Furthermore, in the cortex of neonatal rats the Co(2+)-positive neurons were found to be more susceptible to kainate toxicity than the Co(2+)-negative cells. The Co(2+)-positive neurons in the subplate of neonatal rats were more vulnerable to kainate toxicity than their counterparts in the remaining cortical areas. Together, the widespread distribution and distinct susceptibility to excitotoxicity of CP-AMPAR-expressing neurons suggest that they play various important roles in the development and physiology of the rat cerebral cortex.
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Depression of Ca(2+)/calmodulin-dependent protein kinase II in dorsal root ganglion neurons after spinal nerve ligation.
Publication Date: 2010 Jan 1 PMID: 19882720
Authors: Kojundzic, S. L. - Puljak, L. - Hogan, Q. - Sapunar, D.
Journal: J Comp Neurol
The enzyme calcium/calmodulin-dependent protein kinase II (CaMKII) is associated with memory and its alpha isoform is critical for development of activity-induced synaptic changes. Therefore, we hypothesized that CaMKII is involved in altered function of dorsal root ganglion (DRG) neurons after neuronal injury. To test this hypothesis, Sprague-Dawley rats were made hyperalgesic by L5 and L6 spinal nerve ligation (SNL), and changes in total phosphorylated and unphosphorylated CaMKII (tCaMKII) and phosphorylated form of its alpha isoform (pCaMKIIalpha) were analyzed using immunochemistry in different subpopulations of DRG. SNL did not induce any changes in tCaMKII between experimental groups, while the overall percentage of pCaMKIIalpha-positive neurons in injured L5 DRG SNL (24.8%) decreased significantly when compared to control (41.7%). SNL did not change the percentage of pCaMKIIalpha/N52 colabeled neurons but decreased the percentage of N52-negative nonmyelinated neurons that expressed pCaMKIIalpha from 27% in control animals to 11% after axotomy. We also observed a significant decrease in the percentage of small nonpeptidergic neurons labeled with IB4 (37.6% in control vs. 4.0% in L5 SNL DRG), as well as a decrease in the percentage of pCaMKIIalpha/IB4 colabeled neurons in injured L5 DRGs (27% in control vs. 1% in L5 DRG of SNL group). Our results show that reduction in pCaMKIIalpha levels following peripheral injury is due to the loss of IB4-positive neurons. These results indicate that diminished afferent activity after axotomy may lead to decreased phosphorylation of CaMKIIalpha.
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Authors: Kojundzic, S. L. - Puljak, L. - Hogan, Q. - Sapunar, D.
Journal: J Comp Neurol
The enzyme calcium/calmodulin-dependent protein kinase II (CaMKII) is associated with memory and its alpha isoform is critical for development of activity-induced synaptic changes. Therefore, we hypothesized that CaMKII is involved in altered function of dorsal root ganglion (DRG) neurons after neuronal injury. To test this hypothesis, Sprague-Dawley rats were made hyperalgesic by L5 and L6 spinal nerve ligation (SNL), and changes in total phosphorylated and unphosphorylated CaMKII (tCaMKII) and phosphorylated form of its alpha isoform (pCaMKIIalpha) were analyzed using immunochemistry in different subpopulations of DRG. SNL did not induce any changes in tCaMKII between experimental groups, while the overall percentage of pCaMKIIalpha-positive neurons in injured L5 DRG SNL (24.8%) decreased significantly when compared to control (41.7%). SNL did not change the percentage of pCaMKIIalpha/N52 colabeled neurons but decreased the percentage of N52-negative nonmyelinated neurons that expressed pCaMKIIalpha from 27% in control animals to 11% after axotomy. We also observed a significant decrease in the percentage of small nonpeptidergic neurons labeled with IB4 (37.6% in control vs. 4.0% in L5 SNL DRG), as well as a decrease in the percentage of pCaMKIIalpha/IB4 colabeled neurons in injured L5 DRGs (27% in control vs. 1% in L5 DRG of SNL group). Our results show that reduction in pCaMKIIalpha levels following peripheral injury is due to the loss of IB4-positive neurons. These results indicate that diminished afferent activity after axotomy may lead to decreased phosphorylation of CaMKIIalpha.
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Angiotensin type-1 receptor inhibition is neuroprotective to amacrine cells in a rat model of retinopathy of prematurity.
Publication Date: 2010 Jan 1 PMID: 19882719
Authors: Downie, L. E. - Hatzopoulos, K. M. - Pianta, M. J. - Vingrys, A. J. - Wilkinson-Berka, J. L. - Kalloniatis, M. - Fletcher, E. L.
Journal: J Comp Neurol
Retinopathy of prematurity (ROP) is characterized by deficits in the scotopic pathway, although the cellular locus for these deficits is not clear. Here we examined neurochemical and cellular changes that develop during oxygen-induced retinopathy, a model of ROP. In addition, we examined whether treatment with the angiotensin II type-1 receptor inhibitor, valsartan, prevented these changes. Newborn Sprague-Dawley rats were exposed from postnatal day (P) 0 to 11 to 80%:20% O(2) (22:2 hr/day) and then room air until P18. Valsartan (40 mg/kg/day) was administered from P12-P18. Pattern recognition analysis of overlapping amino acid profiles was used to provide a statistically robust and spatially complete classification of neural elements for each experimental condition. Classification yielded 12 neuronal theme classes in controls and nine classes following ROP. ROP was associated with a reduction in the number of amacrine and bipolar cell theme classes. The reduction in theme classes was confirmed as true neuronal loss by quantifying anatomical changes and using an apoptotic marker. ROP was associated with shifts in amino acid levels across all neuronal populations except for horizontal cells. A reduction in the density of glycine-immunoreactive amacrine cells, and particularly parvalbumin-immunoreactive AII amacrine cells, was observed following ROP. Valsartan treatment during ROP prevented loss of theme classes and loss of AII amacrine cells. This study suggests that deficits in scotopic vision during ROP may be associated with loss of AII amacrine cells. In addition, this study highlights the potential of AT(1)R blockade in preventing neuronal anomalies in this condition.
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Authors: Downie, L. E. - Hatzopoulos, K. M. - Pianta, M. J. - Vingrys, A. J. - Wilkinson-Berka, J. L. - Kalloniatis, M. - Fletcher, E. L.
Journal: J Comp Neurol
Retinopathy of prematurity (ROP) is characterized by deficits in the scotopic pathway, although the cellular locus for these deficits is not clear. Here we examined neurochemical and cellular changes that develop during oxygen-induced retinopathy, a model of ROP. In addition, we examined whether treatment with the angiotensin II type-1 receptor inhibitor, valsartan, prevented these changes. Newborn Sprague-Dawley rats were exposed from postnatal day (P) 0 to 11 to 80%:20% O(2) (22:2 hr/day) and then room air until P18. Valsartan (40 mg/kg/day) was administered from P12-P18. Pattern recognition analysis of overlapping amino acid profiles was used to provide a statistically robust and spatially complete classification of neural elements for each experimental condition. Classification yielded 12 neuronal theme classes in controls and nine classes following ROP. ROP was associated with a reduction in the number of amacrine and bipolar cell theme classes. The reduction in theme classes was confirmed as true neuronal loss by quantifying anatomical changes and using an apoptotic marker. ROP was associated with shifts in amino acid levels across all neuronal populations except for horizontal cells. A reduction in the density of glycine-immunoreactive amacrine cells, and particularly parvalbumin-immunoreactive AII amacrine cells, was observed following ROP. Valsartan treatment during ROP prevented loss of theme classes and loss of AII amacrine cells. This study suggests that deficits in scotopic vision during ROP may be associated with loss of AII amacrine cells. In addition, this study highlights the potential of AT(1)R blockade in preventing neuronal anomalies in this condition.
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Neuroprotection of midbrain dopaminergic cells in MPTP-treated mice after near-infrared light treatment.
Publication Date: 2010 Jan 1 PMID: 19882716
Authors: Shaw, V. E. - Spana, S. - Ashkan, K. - Benabid, A. L. - Stone, J. - Baker, G. E. - Mitrofanis, J.
Journal: J Comp Neurol
This study explores whether near-infrared (NIr) light treatment neuroprotects dopaminergic cells in the substantia nigra pars compacta (SNc) and the zona incerta-hypothalamus (ZI-Hyp) from degeneration in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. BALB/c albino mice were divided into four groups: 1) Saline, 2) Saline-NIr, 3) MPTP, 4) MPTP-NIr. The injections were intraperitoneal and they were followed immediately by NIr light treatment (or not). Two doses of MPTP, mild (50 mg/kg) and strong (100 mg/kg), were used. Mice were perfused transcardially with aldehyde fixative 6 days after their MPTP treatment. Brains were processed for tyrosine hydroxylase (TH) immunochemistry. The number of TH(+) cells was estimated using the optical fractionator method. Our major finding was that in the SNc there were significantly more dopaminergic cells in the MPTP-NIr compared to the MPTP group (35%-45%). By contrast, in the ZI-Hyp there was no significant difference in the numbers of cells in these two groups. In addition, our results indicated that survival in the two regions after MPTP insult was dose-dependent. In the stronger MPTP regime, the magnitude of loss was similar in the two regions ( approximately 60%), while in the milder regime cell loss was greater in the SNc (45%) than ZI-Hyp ( approximately 30%). In summary, our results indicate that NIr light treatment offers neuroprotection against MPTP toxicity for dopaminergic cells in the SNc, but not in the ZI-Hyp.
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Authors: Shaw, V. E. - Spana, S. - Ashkan, K. - Benabid, A. L. - Stone, J. - Baker, G. E. - Mitrofanis, J.
Journal: J Comp Neurol
This study explores whether near-infrared (NIr) light treatment neuroprotects dopaminergic cells in the substantia nigra pars compacta (SNc) and the zona incerta-hypothalamus (ZI-Hyp) from degeneration in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. BALB/c albino mice were divided into four groups: 1) Saline, 2) Saline-NIr, 3) MPTP, 4) MPTP-NIr. The injections were intraperitoneal and they were followed immediately by NIr light treatment (or not). Two doses of MPTP, mild (50 mg/kg) and strong (100 mg/kg), were used. Mice were perfused transcardially with aldehyde fixative 6 days after their MPTP treatment. Brains were processed for tyrosine hydroxylase (TH) immunochemistry. The number of TH(+) cells was estimated using the optical fractionator method. Our major finding was that in the SNc there were significantly more dopaminergic cells in the MPTP-NIr compared to the MPTP group (35%-45%). By contrast, in the ZI-Hyp there was no significant difference in the numbers of cells in these two groups. In addition, our results indicated that survival in the two regions after MPTP insult was dose-dependent. In the stronger MPTP regime, the magnitude of loss was similar in the two regions ( approximately 60%), while in the milder regime cell loss was greater in the SNc (45%) than ZI-Hyp ( approximately 30%). In summary, our results indicate that NIr light treatment offers neuroprotection against MPTP toxicity for dopaminergic cells in the SNc, but not in the ZI-Hyp.
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Melanocortin-4 receptor expression in a vago-vagal circuitry involved in postprandial functions.
Publication Date: 2010 Jan 1 PMID: 19882715
Authors: Gautron, L. - Lee, C. - Funahashi, H. - Friedman, J. - Lee, S. - Elmquist, J.
Journal: J Comp Neurol
Vagal afferents regulate energy balance by providing a link between the brain and postprandial signals originating from the gut. In the current study, we investigated melanocortin-4 receptor (MC4R) expression in the nodose ganglion, where the cell bodies of vagal sensory afferents reside. By using a line of mice expressing green fluorescent protein (GFP) under the control of the MC4R promoter, we found GFP expression in approximately one-third of nodose ganglion neurons. By using immunohistochemistry combined with in situ hybridization, we also demonstrated that approximately 20% of GFP-positive neurons coexpressed cholecystokinin receptor A. In addition, we found that the GFP is transported to peripheral tissues by both vagal sensory afferents and motor efferents, which allowed us to assess the sites innervated by MC4R-GFP neurons. GFP-positive efferents that co-expressed choline acetyltransferase specifically terminated in the hepatic artery and the myenteric plexus of the stomach and duodenum. In contrast, GFP-positive afferents that did not express cholinergic or sympathetic markers terminated in the submucosal plexus and mucosa of the duodenum. Retrograde tracing experiments confirmed the innervation of the duodenum by GFP-positive neurons located in the nodose ganglion. Our findings support the hypothesis that MC4R signaling in vagal afferents may modulate the activity of fibers sensitive to satiety signals such as cholecystokinin, and that MC4R signaling in vagal efferents may contribute to the control of the liver and gastrointestinal tract.
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Authors: Gautron, L. - Lee, C. - Funahashi, H. - Friedman, J. - Lee, S. - Elmquist, J.
Journal: J Comp Neurol
Vagal afferents regulate energy balance by providing a link between the brain and postprandial signals originating from the gut. In the current study, we investigated melanocortin-4 receptor (MC4R) expression in the nodose ganglion, where the cell bodies of vagal sensory afferents reside. By using a line of mice expressing green fluorescent protein (GFP) under the control of the MC4R promoter, we found GFP expression in approximately one-third of nodose ganglion neurons. By using immunohistochemistry combined with in situ hybridization, we also demonstrated that approximately 20% of GFP-positive neurons coexpressed cholecystokinin receptor A. In addition, we found that the GFP is transported to peripheral tissues by both vagal sensory afferents and motor efferents, which allowed us to assess the sites innervated by MC4R-GFP neurons. GFP-positive efferents that co-expressed choline acetyltransferase specifically terminated in the hepatic artery and the myenteric plexus of the stomach and duodenum. In contrast, GFP-positive afferents that did not express cholinergic or sympathetic markers terminated in the submucosal plexus and mucosa of the duodenum. Retrograde tracing experiments confirmed the innervation of the duodenum by GFP-positive neurons located in the nodose ganglion. Our findings support the hypothesis that MC4R signaling in vagal afferents may modulate the activity of fibers sensitive to satiety signals such as cholecystokinin, and that MC4R signaling in vagal efferents may contribute to the control of the liver and gastrointestinal tract.
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Organization of the posterior parietal cortex in galagos: I. Functional zones identified by microstimulation.
Publication Date: 2009 Dec 20 PMID: 19852065
Authors: Stepniewska, I. - Fang, P. C. - Kaas, J. H.
Journal: J Comp Neurol
We used half-second trains of intracortical microstimulation to study the functional organization of the posterior parietal cortex (PPC) in prosimian galagos. These trains of current pulses evoked meaningful behaviors from the anterior, but not posterior, half of PPC. Stimulation of dorsal PPC caused contralateral forelimb movements, including defensive, hand-to-mouth, and reaching movements. Defensive and hand-to-mouth movement territories overlapped, although hand-to-mouth movements were usually evoked from more rostrolateral sites than defensive movements. Reaching movement sites were typically more caudal than defensive or hand-to-mouth movement sites. Stimulation of the most medial PPC sites evoked complex movements of forelimbs and hindlimbs. Ventral PPC commonly represented defensive face movements. Similar defensive movements, with the addition of widely opening the mouth to expose the teeth, were elicited from a small area in front of the PPC defensive face zone. Sometimes defensive face movements occurred with forelimb movements. Thus, subregions of PPC relate to different ethologically relevant categories of behavior. Most movements were initiated within 33-100 msec after stimulus onset. Face, eye blink, and ear movements were generally less delayed than forelimb movements. The present results in galagos, together with those obtained from macaque monkeys by Graziano and coworkers (Graziano et al. [2002a] Neuron 34:841-851; Cooke et al., [2003] Proc. Natl. Acad. Sci. U.S.A. 100:6163-6168), suggest that the functional involvement of the PPC in specific types of sensorimotor behavior evolved early in the course of primate evolution and that networks for complex movements involving motor and posterior parietal areas are characteristic of all primate brains.
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Authors: Stepniewska, I. - Fang, P. C. - Kaas, J. H.
Journal: J Comp Neurol
We used half-second trains of intracortical microstimulation to study the functional organization of the posterior parietal cortex (PPC) in prosimian galagos. These trains of current pulses evoked meaningful behaviors from the anterior, but not posterior, half of PPC. Stimulation of dorsal PPC caused contralateral forelimb movements, including defensive, hand-to-mouth, and reaching movements. Defensive and hand-to-mouth movement territories overlapped, although hand-to-mouth movements were usually evoked from more rostrolateral sites than defensive movements. Reaching movement sites were typically more caudal than defensive or hand-to-mouth movement sites. Stimulation of the most medial PPC sites evoked complex movements of forelimbs and hindlimbs. Ventral PPC commonly represented defensive face movements. Similar defensive movements, with the addition of widely opening the mouth to expose the teeth, were elicited from a small area in front of the PPC defensive face zone. Sometimes defensive face movements occurred with forelimb movements. Thus, subregions of PPC relate to different ethologically relevant categories of behavior. Most movements were initiated within 33-100 msec after stimulus onset. Face, eye blink, and ear movements were generally less delayed than forelimb movements. The present results in galagos, together with those obtained from macaque monkeys by Graziano and coworkers (Graziano et al. [2002a] Neuron 34:841-851; Cooke et al., [2003] Proc. Natl. Acad. Sci. U.S.A. 100:6163-6168), suggest that the functional involvement of the PPC in specific types of sensorimotor behavior evolved early in the course of primate evolution and that networks for complex movements involving motor and posterior parietal areas are characteristic of all primate brains.
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Expression of the diabetes-associated gene TCF7L2 in adult mouse brain.
Publication Date: 2009 Dec 20 PMID: 19845015
Authors: Lee, S. - Lee, C. E. - Elias, C. F. - Elmquist, J. K.
Journal: J Comp Neurol
Polymorphisms of the gene TCF7L2 (transcription factor 7-like 2) are strongly associated with the development and progression of type 2 diabetes. TCF7L2 is important in the development of peripheral organs such as adipocytes, pancreas, and the intestine. However, very little is known about its expression elsewhere. In this study we used in situ hybridization histochemistry to show that TCF7L2 has a unique expression pattern in the mouse brain. TCF7L2 is expressed in two distinct populations. First, it is highly expressed in thalamic and tectal structures. Additionally, TCF7L2 mRNA is expressed at moderate to low levels in specific cells of the hypothalamus, preoptic nucleus, and circumventricular organs. Collectively, these patterns of expression suggest that TCF7L2 has distinct functions within the brain, with a general role in the development and maintenance of thalamic and midbrain neurons, and then a distinct role in autonomic homeostasis.
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Authors: Lee, S. - Lee, C. E. - Elias, C. F. - Elmquist, J. K.
Journal: J Comp Neurol
Polymorphisms of the gene TCF7L2 (transcription factor 7-like 2) are strongly associated with the development and progression of type 2 diabetes. TCF7L2 is important in the development of peripheral organs such as adipocytes, pancreas, and the intestine. However, very little is known about its expression elsewhere. In this study we used in situ hybridization histochemistry to show that TCF7L2 has a unique expression pattern in the mouse brain. TCF7L2 is expressed in two distinct populations. First, it is highly expressed in thalamic and tectal structures. Additionally, TCF7L2 mRNA is expressed at moderate to low levels in specific cells of the hypothalamus, preoptic nucleus, and circumventricular organs. Collectively, these patterns of expression suggest that TCF7L2 has distinct functions within the brain, with a general role in the development and maintenance of thalamic and midbrain neurons, and then a distinct role in autonomic homeostasis.
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From Wikipedia,
Systems neuroscience is a subdiscipline of neuroscience which studies the function of neural circuits and systems, most commonly in awake, behaving intact organisms. It is an umbrella term, encompassing a number of areas of study concerned with how nerve cells behave when connected together to form neural networks: vision, for example, or voluntary movement. At this level of analysis, neuroscientists study how different neural circuits analyze sensory information, form perceptions of the external worlds, make decisions, and execute movements. Researchers concerned with systems neuroscience focus on the vast space that exists between molecular and cellular approaches to the brain and the study of high-level mental functions such as language, memory, and self-awareness (which are the purview of behavioral and cognitive neuroscience). Few neuroscientists identify themselves primarily as doing "systems neuroscience": usually they give a more specific description, such as "behavioral neuroscience" or "cognitive neurophysiology". The term is used most commonly in an educational framework: a common sequence of graduate school neuroscience courses consists of cellular/molecular neuroscience for the first semester, then systems neuroscience for the second semester. It is also sometimes used to distinguish a subdivision within a neuroscience department at an academic institution.
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