Responses of Collicular Fixation Neurons to Gaze Shift Perturbations in Head-Unrestrained Monkey Reveal Gaze Feedback Control
Responses of Collicular Fixation Neurons to Gaze Shift Perturbations in Head-Unrestrained Monkey Reveal Gaze Feedback Control
28
- 10.1007/bf00241115
- Jan 1, 1995
- Experimental Brain Research
80
- 10.1038/nn1027
- Mar 10, 2003
- Nature Neuroscience
33
- 10.1152/jn.2001.85.6.2639
- Jun 1, 2001
- Journal of neurophysiology
185
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- Nov 1, 1996
- Journal of Neurophysiology
111
- 10.1002/(sici)1096-9861(19991011)413:1<55::aid-cne3>3.0.co;2-k
- Aug 26, 1999
- The Journal of Comparative Neurology
282
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- May 1, 1997
- Journal of Neurophysiology
97
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- Journal of Neurophysiology
590
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391
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191
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- Dec 1, 1999
- Current Opinion in Neurobiology
- Research Article
19
- 10.1167/11.12.1
- Oct 6, 2011
- Journal of Vision
In primates, inspection of a visual scene is typically interrupted by frequent gaze shifts, occurring at an average rate of three to five times per second. Perceptually, these gaze shifts are accompanied by a compression of visual space toward the saccade target, which may be attributed to an oculomotor signal that transiently influences visual processing. While previous studies of compression have focused exclusively on saccadic eye movements made with the head artificially immobilized, many brain structures involved in saccade generation also encode combined eye-head gaze shifts. Thus, in order to understand the interaction between gaze motor and visual signals, we studied perception during eye-head gaze shifts and found a powerful compression of visual space that was spatially directed toward the intended gaze (and not the eye movement) target location. This perceptual compression was nearly constant in duration across gaze shift amplitudes, suggesting that the signal that triggers compression is largely independent of the size and kinematics of the gaze shift. The spatial pattern of results could be captured by a model that involves interactions, on a logarithmic map of visual space, between two loci of neural activity that encode the gaze shift vector and visual stimulus position relative to the fovea.
- Research Article
8
- 10.1109/tnsre.2013.2274284
- Aug 26, 2013
- IEEE Transactions on Neural Systems and Rehabilitation Engineering
We develop an adaptive controller for multi-joint, multi-muscle arm movements based on simplified spinal-like circuits found in the periphery, muscle synergies, and interpretations of gain-field projections from reach related neurons in the Superior Colliculus. The resulting innovation provides a highly robust sensory based controller that can be adapted to systems which require multi-muscle co-ordination. It provides human-like responses during perturbations elicited either internally or by the environment and for simple point-to-point reaching. We simulate limb motion and EMGs in Simulink using Virtual Muscle models and a variety of paradigms, including motion with external perturbations, and varying levels of antagonist muscle co-contractions. The results show that the system can exhibit smooth coordinated motions, without explicit kinematic or dynamic planning even in the presence of perturbations. In addition, we show by varying the level of muscle co-contractions from 0% to 40%, that the effects of external perturbations on joint trajectories can be reduced by up to 42%. The improved controller design is novel providing robust behavior during dynamic events and an automatic adaptive response from sensory-integration.
- Research Article
17
- 10.1016/j.mehy.2013.03.005
- Apr 6, 2013
- Medical Hypotheses
Brainspotting: Recruiting the midbrain for accessing and healing sensorimotor memories of traumatic activation
- Research Article
34
- 10.1523/jneurosci.5038-08.2009
- Jun 3, 2009
- The Journal of Neuroscience
The superior colliculus (SC) encodes a saccade via the spatial position of an ensemble of active neurons on its motor map. Downstream circuits control muscles with the temporal code of firing frequency and duration. The moving hill hypothesis resolves the SC-to-brainstem spatiotemporal transformation (STT) enigma by proposing feedback to the SC which "pushes" a hill of activity (height = frequency) caudorostrally such that its instantaneous position encodes the angular error [gaze-position error (GPE)] between gaze and target. This mechanism, proposed for cat but controversial in primate, has not been tested in the head-unrestrained monkey. We do this here. During large approximately 60 degrees control gaze shifts in the dark, a hill of activity began in the caudal SC and moved rostrally, but too sluggishly to encode veridical GPE. At gaze end the peak had not reached the rostral pole and only arrived there approximately 80 ms later. No moving hill accompanied approximately 20 degrees gaze shifts, in agreement with previous studies of head-fixed monkeys. To investigate feedback to the SC, we perturbed large gaze shifts producing initial and corrective gaze saccades separated by 50-800 ms of gaze immobility, the gaze plateau. Map activity was dramatically remodeled: the sluggishly moving hill stopped during the plateau, at the site encoding the corrective gaze saccade, thereby providing a tonic stationary spatially encoded memory signal of plateau GPE. A burst occurred before the corrective saccade. Feedback to map moves activity which encodes a low-pass filtered GPE signal, a process too slow to implement the STT but adequate for corrective gaze saccades.
- Research Article
42
- 10.1152/jn.00288.2011
- Jul 13, 2011
- Journal of Neurophysiology
Our perception of the positions of objects in our surroundings is surprisingly unaffected by movements of the eyes, head, and body. This suggests that the brain has a mechanism for maintaining perceptual stability, based either on the spatial relationships among visible objects or internal copies of its own motor commands. Strong evidence for the latter mechanism comes from the remapping of visual receptive fields that occurs around the time of a saccade. Remapping occurs when a single neuron responds to visual stimuli placed presaccadically in the spatial location that will be occupied by its receptive field after the completion of a saccade. Although evidence for remapping has been found in many brain areas, relatively little is known about how it interacts with sensory context. This interaction is important for understanding perceptual stability more generally, as the brain may rely on extraretinal signals or visual signals to different degrees in different contexts. Here, we have studied the interaction between visual stimulation and remapping by recording from single neurons in the superior colliculus of the macaque monkey, using several different visual stimulus conditions. We find that remapping responses are highly sensitive to low-level visual signals, with the overall luminance of the visual background exerting a particularly powerful influence. Specifically, although remapping was fairly common in complete darkness, such responses were usually decreased or abolished in the presence of modest background illumination. Thus the brain might make use of a strategy that emphasizes visual landmarks over extraretinal signals whenever the former are available.
- Research Article
25
- 10.1152/jn.00389.2012
- Aug 29, 2012
- Journal of Neurophysiology
Saccades are useful for directing the high-acuity fovea to visual targets that are of behavioral relevance. The selection of visual targets for eye movements involves the superior colliculus (SC), where many neurons respond to visual stimuli. Many of these neurons are also activated before and during saccades of specific directions and amplitudes. Although the role of the SC in controlling eye movements has been thoroughly examined, far less is known about the nature of the visual responses in this area. We have, therefore, recorded from neurons in the intermediate layers of the macaque SC, while using a sparse-noise mapping procedure to obtain a detailed characterization of the spatiotemporal structure of visual receptive fields. We find that SC responses to flashed visual stimuli start roughly 50 ms after the onset of the stimulus and last for on average ~70 ms. About 50% of these neurons are strongly suppressed by visual stimuli flashed at certain locations flanking the excitatory center, and the spatiotemporal pattern of suppression exerts a predictable influence on the timing of saccades. This suppression may, therefore, contribute to the filtering of distractor stimuli during target selection. We also find that saccades affect the processing of visual stimuli by SC neurons in a manner that is quite similar to the saccadic suppression and postsaccadic enhancement that has been observed in the cortex and in perception. However, in contrast to what has been observed in the cortex, decreased visual sensitivity was generally associated with increased firing rates, while increased sensitivity was associated with decreased firing rates. Overall, these results suggest that the processing of visual stimuli by SC receptive fields can influence oculomotor behavior and that oculomotor signals originating in the SC can shape perisaccadic visual perception.
- Research Article
45
- 10.1111/ejn.13093
- Dec 1, 2015
- European Journal of Neuroscience
We previously reported that visuomotor activity in the superior colliculus (SC)--a key midbrain structure for the generation of rapid eye movements--preferentially encodes target position relative to the eye (Te) during low-latency head-unrestrained gaze shifts (DeSouza et al., 2011). Here, we trained two monkeys to perform head-unrestrained gaze shifts after a variable post-stimulus delay (400-700 ms), to test whether temporally separated SC visual and motor responses show different spatial codes. Target positions, final gaze positions and various frames of reference (eye, head, and space) were dissociated through natural (untrained) trial-to-trial variations in behaviour. 3D eye and head orientations were recorded, and 2D response field data were fitted against multiple models by use of a statistical method reported previously (Keith et al., 2009). Of 60 neurons, 17 showed a visual response, 12 showed a motor response, and 31 showed both visual and motor responses. The combined visual response field population (n = 48) showed a significant preference for Te, which was also preferred in each visual subpopulation. In contrast, the motor response field population (n = 43) showed a preference for final (relative to initial) gaze position models, and the Te model was statistically eliminated in the motor-only population. There was also a significant shift of coding from the visual to motor response within visuomotor neurons. These data confirm that SC response fields are gaze-centred, and show a target-to-gaze transformation between visual and motor responses. Thus, visuomotor transformations can occur between, and even within, neurons within a single frame of reference and brain structure.
- Research Article
- 10.17827/aktd.1515245
- Sep 30, 2024
- Arşiv Kaynak Tarama Dergisi
Brainspotting, nörobiyolojik olarak uyumlu bir klinik ilişki çerçevesinde danışanın doğuştan gelen kendini gözlemleme ve kendini iyileştirme kapasitelerine erişen, David Grand tarafından keşfedilen ve geliştirilen nispeten yeni bir tür beyin-beden psikoterapötik yaklaşımıdır. Bu terapötik aracın çerçeve, protokol, beklenen etkiler ve etkinliğini açıklanmıştır. Bu çalışmanın amacı Brainspotting'in potansiyel uygulanabilirliğini incelemektir. Araştırmada veri toplama yolu olarak, "belge tarama- literatür tarama" yönteminden yararlanılmıştır. Brainspotting psikoterapisi, Travma Sonrası Stres Bozukluğu, duygusal düzensizlik, anksiyete ve/veya depresif sendromlar olmak üzere psiko-travmatik sendromlardan muzdarip hastaların yönetimini amaçlamaktadır. Bu yaklaşım, hipnoterapi ve EMDR'nin (Göz Hareketleriyle Duyarsızlaştırma ve Yeniden İşleme) özelliklerini birleştirir ve travmatik anıların psikolojik özümsenme süreçlerini teşvik edebilen göz pozisyonları kavramına dayanır. Brainspotting sayesinde danışanlar beynin esnekliğini deneyimler ve öz düzenleme yeteneğini geliştirebilir. Bu beyin değiştirici egzersiz, beynin farklı alanları arasındaki bağlantıları güçlendirebilir ve bir danışmanlık ilişkisinde konuşmalar yapma ve duygusal anıları görsel olarak yeniden işleme süreci yoluyla beyin yapısını değiştirebilir. Klinik psikolojide ve uygulamalı psikolojide psikoterapi yöntemi olarak kullanabilir.
- Research Article
2
- 10.1523/jneurosci.5073-08.2009
- Jan 21, 2009
- The Journal of neuroscience : the official journal of the Society for Neuroscience
The superior colliculus (SC) plays an essential role in the sensory-motor mechanisms that underlie saccadic eye movements. The superficial layers of the SC receive visual information from the retina and striate cortex, and the intermediate and deep layers send outputs to motor centers in the
- Preprint Article
- 10.1101/2021.04.25.441374
- Apr 26, 2021
Abstract To survive in unpredictable environments, animals must continuously evaluate their surroundings for behavioral targets, such as food and shelter, and direct their movements to acquire those targets. Although the ability to accurately select and acquire spatial targets depends on a shared network of brain regions, how these processes are linked by neural circuits remains unknown. The superior colliculus (SC) mediates the selection of spatial targets and remains active during orienting movements to acquire targets, which suggests the underexamined possibility that common SC circuits underlie both selection and acquisition processes. Here, we test the hypothesis that SC functional circuitry couples target selection and acquisition using adefault motor plangenerated by selection-related neuronal activity. Single-unit recordings from intermediate and deep layer SC neurons in male mice performing a spatial choice task demonstrated that choice-predictive neurons, including optogenetically identified GABAergic SC neurons whose activity was causally related to target selection, exhibit increased activity during movement to the target. By strategically recording from both rostral and caudal SC neurons, we also revealed an overall caudal-to-rostral shift in activity as targets were acquired. Finally, we used an attractor model to examine how target selection activity in the SC could generate a rostral shift in activity during target acquisition using only intrinsic SC circuitry. Overall, our results suggest a functional coupling between SC circuits that underlie target selection and acquisition, elucidating a key mechanism for goal-directed behavior.Significance StatementThe ability to quickly select and acquire spatial targets is essential to animal survival. Neural circuits underlying these processes are shared in an interconnected network of brain regions, however it is unclear how circuits link decision-making processes with motor commands to execute choices. Here, we examine single-unit activity in the superior colliculus (SC) as mice select and acquire spatial targets to test the hypothesis that choice-related activity promotes target acquisition by generating a default motor plan for orienting movements. By demonstrating that choice-predictive neurons increase their firing rates during movement and capturing the dynamics of SC activity with an attractor model of intrinsic SC circuitry, our results support a role for SC circuits in coupling target selection and acquisition.
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42
- 10.1016/j.neuron.2006.08.010
- Nov 1, 2006
- Neuron
Somatosensory-Motor Neuronal Activity in the Superior Colliculus of the Primate
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5
- 10.1152/jn.00665.2007
- Jun 20, 2007
- Journal of Neurophysiology
The superior colliculus (SC) is a multilayered structure in the mammalian midbrain. Even though the behavioral function of the SC has been studied for well over 30 yr, it continues to be a source of surprising new findings. Traditionally it has been assumed that the primate SC selects and generates
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112
- 10.1016/j.jaci.2009.08.048
- Dec 1, 2009
- Journal of Allergy and Clinical Immunology
Anatomy, pathology, and physiology of the tracheobronchial tree: Emphasis on the distal airways
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69
- 10.1074/jbc.m105823200
- Sep 4, 2001
- Journal of Biological Chemistry
Cholesterol and related sterols are known to modulate the physical properties of biological membranes and can affect the activities of membrane-bound protein complexes. Here, we report that an early step in protein translocation across the endoplasmic reticulum (ER) membrane is reversibly inhibited by cholesterol levels significantly lower than those found in the plasma membrane. By UV-induced chemical cross-linking we further show that high cholesterol levels prevent cross-linking between ribosome-nascent chain complexes and components of the Sec61 translocon, but have no effect on cross-linking to the signal recognition particle. The inhibiting effect on translocation is different between different sterols. Our data suggest that the protein translocation machinery may be sensitive to changes in cholesterol levels in the ER membrane.
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25
- 10.1038/sj.jid.5700189
- Apr 1, 2006
- Journal of Investigative Dermatology
Heavy Water Labeling of Keratin as a Non-Invasive Biomarker of Skin Turnover In Vivo in Rodents and Humans
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47
- 10.1016/j.cub.2013.03.050
- Apr 4, 2013
- Current Biology
Visual Crowding at a Distance during Predictive Remapping
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21
- 10.1074/jbc.m109.073908
- Jan 1, 2010
- Journal of Biological Chemistry
Norursodeoxycholic acid (norUDCA) exhibits efficient anti-cholestatic properties in an animal model of sclerosing cholangitis. norUDCA is eliminated as a C(23)-ester glucuronide (norUDCA-23G) in humans. The present study aimed at identifying the human UDP-glucuronosyltransferase (UGT) enzyme(s) involved in hepatic norUDCA glucuronidation and at evaluating the consequences of single nucleotide polymorphisms in the coding region of UGT genes on norUDCA-23G formation. The effects of norUDCA on the formation of the cholestatic lithocholic acid-glucuronide derivative and of rifampicin on hepatic norUDCA glucuronidation were also explored. In vitro glucuronidation assays were performed with microsomes from human tissues (liver and intestine) and HEK293 cells expressing human UGT enzymes and variant allozymes. UGT1A3 was identified as the major hepatic UGT enzyme catalyzing the formation of norUDCA-23G. Correlation studies using samples from a human liver bank (n = 16) indicated that the level of UGT1A3 protein is a strong determinant of in vitro norUDCA glucuronidation. Analyses of the norUDCA-conjugating activity by 11 UGT1A3 variant allozymes identified three phenotypes with high, low, and intermediate capacity. norUDCA is also identified as a competitive inhibitor for the hepatic formation of the pro-cholestatic lithocholic acid-glucuronide derivative, whereas norUDCA glucuronidation is weakly stimulated by rifampicin. This study identifies human UGT1A3 as the major enzyme for the hepatic norUDCA glucuronidation and supports that some coding polymorphisms affecting the conjugating activity of UGT1A3 in vitro may alter the pharmacokinetic properties of norUDCA in cholestasis treatment.
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211
- 10.1016/j.neuron.2010.06.004
- Jul 1, 2010
- Neuron
AMPA Receptor Synaptic Plasticity Induced by Psychostimulants: The Past, Present, and Therapeutic Future
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76
- 10.1074/jbc.m007666200
- Mar 1, 2001
- Journal of Biological Chemistry
We reported previously that freshly fractured silica (FFSi) induces activator protein-1 (AP-1) activation through extracellular signal-regulated protein kinases (ERKs) and p38 kinase pathways. In the present study, the biologic activities of FFSi and aged silica (ASi) were compared by measuring their effects on the AP-1 activation and phosphorylation of ERKs and p38 kinase. The roles of reactive oxygen species (ROS) in this silica-induced AP-1 activation were also investigated. We found that FFSi-induced AP-1 activation was four times higher than that of ASi in JB6 cells. FFSi also caused greater phosphorylation of ERKs and p38 kinase than ASi. FFSi generated more ROS than ASi when incubated with the cells as measured by electron spin resonance (ESR). Studies using ROS-sensitive dyes and oxygen consumption support the conclusion that ROS are generated by silica-treated cells. N-Acetylcysteine (an antioxidant) and polyvinyl pyridine-N-oxide (an agent that binds to Si-OH groups on silica surfaces) decreased AP-1 activation and phosphorylation of ERKs and p38 kinase. Catalase inhibited phosphorylation of ERKs and p38 kinase, as well as AP-1 activation induced by FFSi, suggesting the involvement of H(2)O(2) in the mechanism of silica-induced AP-1 activation. Sodium formate (an ( small middle dot)OH scavenger) had no influence on silica-induced MAPKs or AP-1 activation. Superoxide dismutase enhanced both AP-1 and MAPKs activation, indicating that H(2)O(2), but not O(2), may play a critical role in silica-induced AP-1 activation. These studies indicate that freshly ground silica is more biologically active than aged silica and that ROS, in particular H(2)O(2), play a significant role in silica-induced AP-1 activation.
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106
- 10.1016/j.neuron.2011.09.018
- Oct 1, 2011
- Neuron
Transcriptional Regulation of Neuronal Polarity and Morphogenesis in the Mammalian Brain
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6
- 10.1016/j.cub.2018.07.047
- Sep 1, 2018
- Current Biology
Superior Colliculus: A Vision for Orienting
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557
- 10.1016/j.neuron.2005.08.024
- Oct 1, 2005
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Math1 Expression Redefines the Rhombic Lip Derivatives and Reveals Novel Lineages within the Brainstem and Cerebellum
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44
- 10.1074/jbc.m506034200
- Jan 1, 2006
- Journal of Biological Chemistry
P-Rex1 is a specific guanine nucleotide exchange factor (GEF) for Rac, which is present in high abundance in brain and hematopoietic cells. P-Rex1 is dually regulated by phosphatidylinositol (3,4,5)-trisphosphate and the Gbetagamma subunits of heterotrimeric G proteins. We examined which of the multiple G protein alpha and betagamma subunits activate P-Rex1-mediated Rac guanine nucleotide exchange using pure, recombinant proteins reconstituted into synthetic lipid vesicles. AlF(-)(4) activated G(s),G(i),G(q),G(12), or G(13) alpha subunits were unable to activate P-Rex1. Gbetagamma dimers containing Gbeta(1-4) complexed with gamma(2) stimulated P-Rex1 activity with EC(50) values ranging from 10 to 20 nm. Gbeta(5)gamma(2) was not able to stimulate P-Rex1 GEF activity. Dimers containing the beta(1) subunit complexed with a panel of different Ggamma subunits varied in their ability to stimulate P-Rex1. The beta(1)gamma(3), beta(1)gamma(7), beta(1)gamma(10), and beta(1)gamma(13HA) dimers all activated P-Rex1 with EC(50) values ranging from 20 to 38 nm. Dimers composed of beta(1)gamma(12) had lower EC(50) values (approximately 112 nm). The farnesylated gamma(11) subunit is highly expressed in hematopoietic cells; surprisingly, dimers containing this subunit (beta(1)gamma(11)) were also less effective at activating P-Rex1. These findings suggest that the composition of the Gbetagamma dimer released by receptor activation may differentially activate P-Rex1.
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132
- 10.1074/jbc.272.28.17342
- Jul 1, 1997
- Journal of Biological Chemistry
Prolyl 4-hydroxylase (proline hydroxylase, EC 1.14.11.2) catalyzes the formation of 4-hydroxyproline in collagens. The vertebrate enzyme is an alpha2beta2 tetramer, the beta subunit of which is identical to protein disulfide-isomerase (PDI, EC 5.3.4.1). We report here on cloning of the recently discovered alpha(II) subunit from human sources. The mRNA for the alpha(II) subunit was found to be expressed in a variety of human tissues, and the presence of the corresponding polypeptide and the (alpha(II))2beta2 tetramer was demonstrated in cultured human WI-38 and HT-1080 cells. The type II tetramer was found to represent about 30% of the total prolyl 4-hydroxylase in these cells and about 5-15% in various chick embryo tissues. The results of coexpression in insect cells argued strongly against the formation of a mixed alpha(I)alpha(II)beta2 tetramer. PDI/beta polypeptide containing a histidine tag in its N terminus was found to form prolyl 4-hydroxylase tetramers as readily as the wild-type PDI/beta polypeptide, and histidine-tagged forms of prolyl 4-hydroxylase appear to offer an excellent source for a simple large scale purification of the recombinant enzyme. The properties of the purified human type II enzyme were very similar to those of the type I enzyme, but the Ki of the former for poly(L-proline) was about 200-1000 times that of the latter. In agreement with this, a minor difference, about 3-6-fold, was found between the two enzymes in the Km values for three peptide substrates. The existence of two forms of prolyl 4-hydroxylase in human cells raises the possibility that mutations in one enzyme form may not be lethal despite the central role of this enzyme in the synthesis of all collagens.
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138
- 10.1074/jbc.m801738200
- Sep 1, 2008
- Journal of Biological Chemistry
The calcium-sensing receptor (CaR) is a G-protein-coupled receptor that signals in response to extracellular calcium and regulates parathyroid hormone secretion. The CaR is also expressed on normal mammary epithelial cells (MMECs), where it has been shown to inhibit secretion of parathyroid hormone-related protein (PTHrP) and participate in the regulation of calcium and bone metabolism during lactation. In contrast to normal breast cells, the CaR has been reported to stimulate PTHrP production by breast cancer cells. In this study, we confirmed that the CaR inhibits PTHrP production by MMECs but stimulates PTHrP production by Comma-D cells (immortalized murine mammary cells) and MCF-7 human breast cancer cells. We found that changes in intracellular cAMP, but not phospholipase C or MAPK signaling, correlated with the opposing effects of the CaR on PTHrP production. Pharmacologic stimulation of cAMP accumulation increased PTHrP production by normal and transformed breast cells. Inhibition of protein kinase A activity mimicked the effects of CaR activation on inhibiting PTHrP secretion by MMECs and blocked the effects of the CaR on stimulating PTHrP production in Comma-D and MCF-7 cells. We found that the CaR coupled to Galphai in MMECs but coupled to Galphas in Comma-D and MCF-7 cells. Thus, the opposing effects of the CaR on PTHrP production are because of alternate G-protein coupling of the receptor in normal versus transformed breast cells. Because PTHrP contributes to hypercalcemia and bone metastases, switching of G-protein usage by the CaR may contribute to the pathogenesis of breast cancer.
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