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Biomedical subjects

Chao Qin

Publications and source records attributed to Chao Qin.

At least 37 records · Page 2Linked to original sources

Colonic inflammation increases Na+ currents in bladder sensory neurons.

The purpose of this study was to determine whether sensitization of pre-spinal afferents induced by colonic inflammation can affect the physiology of the urinary bladder. Tetrodotoxin-resistant (TTX-R) Na+ currents were examined in bladder sensory neurons after experimental colitis. Cell bodies of bladder dorsal root ganglia were retrogradely labeled and TTX-R Na+ currents were recorded in capsaicin-sensitive neurons. Colitis significantly enhanced response of bladder neurons to capsaicin by approximately 60% and the peak amplitude of TTX-R Na+ current by 51%. These results suggest that colonic inflammation leads to increased excitability of nociceptive bladder neurons.

Animals↗

c-Fos expression in rat brain stem and spinal cord in response to activation of cardiac ischemia-sensitive afferent neurons and electrostimulatory modulation.

The purpose of this study was to identify central neuronal sites activated by stimulation of cardiac ischemia-sensitive afferent neurons and determine whether electrical stimulation of left vagal afferent fibers modified the pattern of neuronal activation. Fos-like immunoreactivity (Fos-LI) was used as an index of neuronal activation in selected levels of cervical and thoracic spinal cord and brain stem. Adult Sprague-Dawley rats were anesthetized with urethane and underwent intrapericardial infusion of an "inflammatory exudate solution" (IES) containing algogenic substances that are released during ischemia (10 mM adenosine, bradykinin, prostaglandin E2, and 5-hydroxytryptamine) or occlusion of the left anterior descending coronary artery (CoAO) to activate cardiac ischemia-sensitive (nociceptive) afferent fibers. IES and CoAO increased Fos-LI above resting levels in dorsal horns in laminae I-V at C2 and T4 and in the caudal nucleus tractus solitarius. Dorsal rhizotomy virtually eliminated Fos-LI in the spinal cord as well as the brain stem. Neuromodulation of the ischemic signal by electrical stimulation of the central end of the left thoracic vagus excited neurons at the cervical and brain stem level but inhibited neurons at the thoracic spinal cord during IES or CoAO. These results suggest that stimulation of the left thoracic vagus excites descending inhibitory pathways. Inhibition at the thoracic spinal level that suppresses the ischemic (nociceptive) input signal may occur by a short-loop descending pathway via signals from cervical propriospinal circuits and/or a longer-loop descending pathway via signals from the nucleus tractus solitarius.

Animals↗

Esophagocardiac convergence onto thoracic spinal neurons: comparison of cervical and thoracic esophagus.

The aim of this study was to characterize thoracic spinal neurons receiving convergent inputs from the esophagus, heart and somatic receptive fields. Extracellular potentials of single T3-T4 spinal neurons were recorded in pentobarbital anesthetized male rats. Thoracic and cervical esophageal distensions (TED, CED) were produced by water inflation of a latex balloon. A catheter was placed in the pericardial sac to administer bradykinin or a mixture of algogenic chemicals. 96/311 (31%) neurons responded to both TED and intrapericardial chemicals (IC) and 48/177 (27%) neurons responded to both CED and IC. Long-lasting excitatory responses were more frequently encountered (P<0.05) in esophagocardiac spinal neurons responding to TED (T-ECSNs, 62/91) than in neurons responding to CED (C-ECSNs, 23/47). Ninety-one percent of T-ECSNs and 98% of C-ECSNs had somatic fields on chest, axilla and upper back areas. Esophagocardiac convergence on thoracic spinal neurons provided a spinal mechanism that might mediate viscerovisceral nociception and reflexes.

Animals↗

Syntheses, structures, and photoluminescence of a novel class of d10 metal complexes constructed from pyridine-3,4-dicarboxylic acid with different coordination architectures.

Two novel d(10) metal coordination polymers [Zn(PDB)](n)() (1) and [Cd(3)(PDB)(2)(OH)(2)(H(2)O)(2)](n)() (2) (H(2)PDB = pyridine-3,4-dicarboxylic acid) have been synthesized under hydrothermal conditions and characterized by elemental analysis, IR, TG analysis, and single-crystal X-ray diffraction. Crystal data for 1: C(7)H(3)NO(4)Zn, orthorhombic Pna2(1), a = 8.423(17) A, b = 6.574(13) A, c = 12.899(3) A, Z = 4. Crystal data for 2: C(14)H(12)N(2)O(12)Cd(3), monoclinic C2/c, a= 20.130(4) A, b = 6.692(13) A, c = 13.081(3) A, beta = 102.78(3) degrees, Z = 4. Both compounds exhibit novel three-dimensional frameworks. Compound 1 not only possesses a one-dimensional rectangular channel but also contains infinite double-stranded helical chains. Compound 2 has two different types of channels, one being built up from pyridine rings and [CdO(5)N] and [CdO(6)] building units and the other being constructed from pyridine rings and [CdO(5)N] building units. Furthermore, both compounds show strong photoluminescence properties at room temperature.

Journal Article↗

Viscerovisceral convergence of urinary bladder and colorectal inputs to lumbosacral spinal neurons in rats.

Extracellular potentials of single L6-S2 spinal neurons were recorded in pentobarbital anesthetized male rats. The urinary bladder was catheterized through the fundus and filled with warm saline for urinary bladder distension (UBD, 0.5-2.0 ml, 20 s). Colorectal distension (CRD) was produced by distending a latex balloon with air (20-80 mmHg, 20 s). Of 171 deeper neurons examined for responses to UBD and CRD, 49 (29%) neurons responded to both UBD and CRD; whereas 6/42 (14%) superficial neurons (depth < 0.3 mm) responded to both organs. Of 55 viscerovisceral convergent neurons, 25 (45%) neurons were excited by both UBD and CRD; the remainder exhibited multiple patterns of excitation and inhibition. In conclusion, responses of superficial and deeper lumbosacral spinal neurons to convergent inputs from urinary bladder and colon suggested that these neurons might contribute to the cross-talk that occurs between visceral organs.

Animals↗

Chemical activation of C1-C2 spinal neurons modulates intercostal and phrenic nerve activity in rats.

Chemical activation of upper cervical spinal neurons modulates activity of thoracic respiratory interneurons in rats. The aim of the present study was to examine the effects of chemical activation of C(1)-C(2) spinal neurons on thoracic spinal respiratory motor outflows. Electroneurograms of left phrenic (n = 23) and intercostal nerves (ICNs, n = 93) between T(3) and T(8) spinal segments were recorded from 36 decerebrated, vagotomized, paralyzed, and ventilated male rats. To activate upper cervical spinal neurons, glutamate pledgets (1 M, 1 min) were placed on the dorsal surface of the C(1)-C(2) spinal cord. Glutamate on C(1)-C(2) increased ICN tonic activity in 56/59 (95%) ICNs. The average maximal tonic activity of ICN was increased by 174% (n = 59). After spinal transection at rostral C(1), glutamate on C(1)-C(2) still increased ICN tonic activity in 33/35 ICNs. However, the effects of C(1)-C(2) glutamate on ICN phasic activity were highly variable, with observations of augmentation or suppression of both inspiratory and expiratory discharge. C(1)-C(2) glutamate augmented the average amplitude of phrenic burst by 20%, whereas the increases in amplitude of ICN inspiratory activity, when they occurred, averaged 120%. The burst rate of phrenic nerve discharge was decreased from 34.2 +/- 1.6 to 26.3 +/- 2.0 (mean +/- SE) breaths/min during C(1)-C(2) glutamate. These data suggested that upper cervical propriospinal neurons might play a role in descending modulation of thoracic respiratory and nonrespiratory motor activity.

Animals↗

Responses and afferent pathways of C1-C2 spinal neurons to cervical and thoracic esophageal stimulation in rats.

Because vagal and sympathetic inputs activate upper cervical spinal neurons, we hypothesized that stimulation of the esophagus would activate C(1)-C(2) neurons. This study examined responses of C(1)-C(2) spinal neurons to cervical and thoracic esophageal distension (CED, TED) and afferent pathways for CED and TED inputs to C(1)-C(2) spinal neurons. Extracellular potentials of single C(1)-C(2) spinal neurons were recorded in pentobarbital-anesthetized male rats. Graded CED or TED was produced by water inflation (0.1-0.5 ml) of a latex balloon. CED changed activity of 48/219 (22%) neurons; 34 were excited (E), 12 were inhibited (I), and 2 were E-I. CED elicited responses for 18/18 neurons tested after ipsilateral cervical vagotomy, for 12/14 neurons tested after bilateral vagotomy and for 9/11 neurons tested after bilateral vagotomy and C(6)-C(7) spinal cord transection. TED changed activity of 31/190 (16%) neurons (28E, 3 I). Ipsilateral cervical vagotomy abolished TED-evoked responses of 5/12 neurons. Bilateral vagotomy eliminated responses of 2/4 neurons tested, and C(6)-C(7) spinal transection plus bilateral vagotomy eliminated responses of 2/2 neurons. Thus inputs from CED to C(1)-C(2) neurons most likely entered upper cervical dorsal roots, whereas inputs from TED were dependent on vagal pathways and/or sympathetic afferent pathways that entered the thoracic dorsal roots. These results supported a concept that C(1)-C(2) spinal neurons play a role in integrating visceral information from cervical and thoracic esophagus.

Afferent Pathways↗

Afferent pathways and responses of T3-T4 spinal neurons to cervical and thoracic esophageal distensions in rats.

The purposes of this study were to (1) compare responses of T(3)-T(4) spinal neurons to thoracic and cervical esophageal distension (TED, CED) and (2) determine afferent pathways for esophageal input to these neurons. Extracellular potentials of single superficial and deeper T(3)-T(4) neurons were recorded in pentobarbital anesthetized male rats. Graded TED or CED was produced by water inflation (0.1-0.5 ml) of a latex balloon. TED changed activity of 121/432 (28%) neurons (114 were excited); CED activated 69/269 (26%) neurons (56 were excited). Of 151 neurons that were tested for responses to both TED and CED, 40 (26%) neurons responded to both TED and CED. Mean duration of excitatory responses in convergent neurons to TED was significantly longer than the duration of responses to CED (31.4+/-2.8 vs. 25.4+/-1.0 s, n=34, P<0.05). A total of 105 out of 121 (87%) and 66 out of 69 (96%) neurons responsive to TED and CED had somatic fields. Spinal transection at rostral C(1) and at C(7)-C(8) indicated that excitatory responses to TED resulted from activation of afferent input that entered thoracic spinal segments; whereas, excitatory responses to CED resulted from afferent inputs entering cervical or thoracic spinal segments. These data showed that the upper thoracic spinal cord received sensory information from the esophagus through cervical and/or thoracic spinal visceral afferent pathways.

Afferent Pathways↗

Hydrothermal synthesis and structure of a new helical chain constructed from only molybdenum-oxide building blocks.

The compound [NH(3)(CH(2))(2)NH(2)(CH(2))(2)NH(3)](2)[Mo(9)O(30)] was synthesized at 170 degrees C via hydrothermal techniques from the starting materials of Na(2)MoO(4).H(2)O, NH(2)(CH(2))(2)NH(CH(3))(2)NH(2), and H(2)O. The compound crystallizes in the space group C2/c of the monoclinic system with a = 21.308(4) A, b = 9.234(2) A, c = 19.195(4) A, beta = 120.27(3) degrees, V = 3261.9(11)A(3), Z = 4. Two novel and symmetrically related helices coexist in the centrosymmetric solid, in which the two kinds of helices appear in the left-handed and right-handed enantiomorphs, respectively. This is the first example of a helical chain structure consisting of only molybdenum-oxide building blocks. The central axis about each helical chain is a 2-fold screw axis.

Journal Article↗

Spinal neuronal responses to urinary bladder stimulation in rats with corticosterone or aldosterone onto the amygdala.

Elevating glucocorticoids in the amygdala produces colorectal hypersensitivity through activation of lumbosacral spinal neurons. The aim of this study was to determine if descending modulation from the amygdala affects spinal processing of input from urinary bladder afferents. Fischer-344 rats received cholesterol (inactive control)-, corticosterone-, or aldosterone-containing micropellets placed stereotaxically on the dorsal margin of the left and right amygdala (n = 10 for each group). Seven days after amygdaloid implantation, extracellular potentials of single L6-S1 spinal neurons were examined for the responses to graded (0.5-2.0 ml, 20 s) urinary bladder distension (UBD). Spontaneous activity of neurons with excitatory responses to UBD in aldosterone-implanted rats [11.0 +/- 1.7 (SE) imp/s], but not in corticosterone-implanted rats, was higher than in the cholesterol-implanted group (6.6 +/- 1.1 imp/s, P < 0.05). Noxious UBD (1.5 ml) produced a greater excitatory response (21.6 +/- 2.6 imp/s) in aldosterone-implanted rats compared with cholesterol- or corticosterone-implanted rats (15.1 +/- 1.5 and 13.6 +/- 1.4 imp/s; P < 0.05). In contrast, the duration of excitatory responses to UBD in corticosterone-implanted rats (38.5 +/- 3.4 imp/s) was significantly longer than those in the aldosterone or control groups (26.8 +/- 1.8 and 24.7 +/- 1.5 imp/s). Neurons with low thresholds for excitatory responses to UBD were seen more frequently in aldosterone-implanted rats than in corticosterone or cholesterol treated rats (74 vs. 44% and 39%, P < 0.05). No difference in somatic field properties of spinal neurons responsive or nonresponsive to UBD was found among the three groups. These findings suggest that both mineralocorticoid- and glucocorticoid-mediated mechanisms in the amygdala are involved in descending modulation to lumbosacral spinal neurons receiving inputs from the urinary bladder; and this mechanism may play a role in the activation and maintenance of primary central sensitization to noxious visceral stimuli.

Action Potentials↗

Effects of urinary bladder distension on activity of T3-T4 spinal neurons receiving cardiac and somatic noxious inputs in rats.

The aims of this study were to examine effects of urinary bladder distension (UBD) on T(3)-T(4) spinal neurons receiving cardiac and somatic noxious inputs and to determine the pathway involved in transmitting urinary bladder inputs to thoracic spinal segments. Extracellular potentials of single T(3)-T(4) neurons were recorded in pentobarbital anesthetized male rats. Either bradykinin solution (10(-5) M) or an allogenic mixture (adenosine 10(-3) M, bradykinin, histamine, serotonin, prostaglandin E2 10(-5) M each) was administered intrapericardially. UBD was produced by saline inflation (0.5-2.0 ml, 20 s). Of 487 neurons tested for responses to UBD, 70 were inhibited and 37 were excited. Seventy-six out of 336 neurons received convergent input from UBD and heart; 69/76 viscerovisceral convergent neurons had somatic fields. Spinal transection at rostral C(1) abolished UBD inhibition in 5/9 neurons; whereas transections at L(1)-L(2) abolished UBD inhibition in 3/3 cells tested. Results showed that T(3)-T(4) spinal neurons processing cardiac and somatic nociceptive information were primarily inhibited by input from the urinary bladder through either supraspinal structures or direct intraspinal pathways.

Action Potentials↗

New vanadium phosphate ([(phen)VIVO]2(VV2O5)(HPO4))n with chiral layer architecture.

A new layered vanadium phosphate ([(phen)V(IV)O](2)(V(V)(2)O(5))(HPO(4))n has been hydrothermally synthesized and structurally characterized by elemental analysis, IR, and single-crystal X-ray diffraction. This compound crystallized in the monoclinic space group P2/c with a = 9.979(2) A, b = 9.886(2) A, c = 15.298(3) A, beta = 102.86(3) degrees, V = 1471.3(5) A(3), and Z = 4. In the structure of this compound, two nitrogen atoms of 1,10-phen are directly coordinated to the vanadium skeleton. Interestingly, the crystal structure consists of two types of chiral layers, one left-handed and the other right-handed, which lead to a racemic solid-state compound. In each layer, there coexist three distinct rings, described as a 8-membered ring [V(2)(oct)P(2)O(4)], 12-membered ring [V(2)(omicron)(ct)V(2)(tet)P(2)O(6)], and 16-membered ring [V(2)(omicron)(ct)V(4)(tet)P(2)O(8)].

Journal Article↗

Responses and afferent pathways of C(1)-C(2) spinal neurons to gastric distension in rats.

Some evidence shows that the upper cervical spinal cord might play an important role in propriospinal processing as a sensory filter and modulator for visceral afferents. The aims of this study were to determine (1). the responses of C(1)-C(2) spinal neurons to gastric distension and (2). the relative contribution of vagal and spinal visceral afferent pathways for transmission of gastric input to the upper cervical spinal cord. Extracellular potentials of single C(1)-C(2) spinal neurons were recorded in pentobarbital anesthetized male rats. Graded gastric distension (20-80 mm Hg) was produced by air inflation of a latex balloon surgically placed in the stomach. Sixteen percent of the neurons (32/198) responded to gastric distension; 17 neurons were excited and 15 neurons were inhibited by gastric distension. Spontaneous activity of neurons with inhibitory responses was higher than those neurons with excitatory responses (18.1+/-2.7 vs. 3.8+/-1.7 impulses s(-1), p<0.001). Twenty-eight of thirty-two (87.5%) neurons responded to mechanical stimulation of somatic fields on head, neck, ears or shoulder. Most lesion sites of neurons with excitatory responses were found in laminae V, VII; however, neurons with inhibitory responses were in laminae III, IV. Bilateral cervical vagotomy abolished responses of 4/8 neurons tested. Spinal transection at C(6)-C(7) abolished responses of the other four neurons that still responded to gastric distension after bilateral vagotomy. Results of these data supported the concept that a group of C(1)-C(2) spinal neurons might play a role in processing sensory information from the stomach that travels in vagal and spinal visceral afferent fibers.

Afferent Pathways↗

Visceromotor and spinal neuronal responses to colorectal distension in rats with aldosterone onto the amygdala.

Stereotaxic delivery of corticosterone onto the amygdala produces colorectal hypersensitivity through activation of lumbosacral spinal neurons. Since corticosterone activates both the mineralocorticoid (MR) and glucocorticoid (GR) receptors, the aim of this study was to determine the importance of MRs in the regulation of colorectal hypersensitivity through the use of aldosterone that preferentially binds to MRs. Fischer-344 rats received either aldosterone (n = 18)- or cholesterol (control, n = 18)-containing micropellets bilaterally placed stereotaxically on the dorsal margin of the amygdala. After 1 wk, colorectal sensitivity to distension (30 mmHg) was measured in a subgroup of rats (n = 8/group). In other rats (n = 10/group), extracellular potentials of single L6-S1 spinal neurons in response to colorectal distension (CRD; 10-80 mmHg) were recorded. In aldosterone-implanted rats, CRD produced a greater visceromotor behavioral response compared with cholesterol controls (19 +/- 0.5 vs. 11.5 +/- 2.7; P < 0.01). A total of 68/182 (37%) and 56/167 (34%) of spinal neurons responded to noxious CRD in aldosterone-implanted and control groups, respectively. A total of 36/42 (86%) neurons excited by CRD had spontaneous activity in aldosterone-implanted groups compared with control (19/33, 58%, P < 0.01). Neurons with low thresholds for excitatory responses to CRD were seen more frequently in aldosterone-implanted rats than those in the control group (35/39 vs. 18/31, P < 0.05). Maximal excitatory responses of neurons to CRD in aldosterone-implanted rats were significantly greater (23.9 +/- 2.2 vs. 16.4 +/- 2.0 imp/s, P < 0.05), and the durations were longer (34.3 +/- 2.7 vs. 24.9 +/- 1.4 s, P < 0.05) than those in control group. Finally, a greater number of neurons had wide dynamic range responses to somatic stimulation in aldosterone-treated rats compared with cholesterol controls. Our findings suggest that, in the amygdala, MR receptor-mediated mechanisms are likely involved in descending pathways onto lumbosacral spinal neurons that induce colorectal hypersensitivity to luminal distension.

Aldosterone↗

Chemical activation of cardiac receptors affects activity of superficial and deeper T3-T4 spinal neurons in rats.

The purposes of this study were to examine responses of superficial (depth <300 microm) and deeper thoracic spinal neurons to chemical stimulation of cardiac afferents and effects of descending influences on these neurons. Extracellular potentials of single T(3)-T(4) neurons were recorded in pentobarbital anesthetized, paralyzed and ventilated male rats. A catheter was placed in the pericardial sac to administer 0.2 ml of a mixture of algogenic chemicals that contained adenosine (10(-3) M), bradykinin, histamine, serotonin, prostaglandin E(2) (10(-5) M). Fifteen of 55 (27%) superficial neurons responsive to intrapericardial chemicals were compared to 80/169 (47%) deeper neurons. All 15 superficial neurons that responded to cardiac afferents were excited (E), whereas 66 deeper neurons were excited, ten were inhibited and four showed excitation-inhibition. Spontaneous activity of superficial neurons with short-lasting excitatory responses was significantly lower than that of deeper neurons (P<0.05). Somatic receptive fields on chest, axilla, arm and upper back areas were found for 77/95 (81%) neurons that responded to intrapericardial chemicals. The proportion of somatic field properties and their sizes in superficial neurons were similar to deeper neurons. After cervical spinal transection, both spontaneous activity and responses to chemical stimulation of cardiac afferents significantly increased in six out of six neurons excited by intrapericardial injections. Results showed that chemical stimulation of cardiac afferents excited superficial T(3)-T(4) spinal neurons, whereas deeper neurons exhibited multiple patterns of responses. Some characteristics of subgroups of superficial neurons were quantitatively different from deeper neurons. Thoracic spinal neurons processing cardiac nociceptive information were under tonic descending inhibition.

Afferent Pathways↗