Hypothetical Role of Long-Loop Reflex Pathways

We tested the hypothesis that blockade of N-methyl-d-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 ± 8 and 24 ± 6% of control ( n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 ± 22 to 129 ± 13% of control; n = 4) and vertebral nerves (from 253 ± 41 to 154 ± 20% of control; n = 7) and mean arterial pressure (from 39 ± 7 to 21 ± 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.

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Changes in Transmission in Some Reflex Pathways During Movement in Humans

Physiology ◽

10.1152/physiologyonline.1989.4.1.29 ◽

1989 ◽

Vol 4 (1) ◽

pp. 29-32

Author(s):

E Fournier ◽

P-D Emmanuel

Keyword(s):

Functional Role ◽

Voluntary Movement ◽

Spinal Pathways ◽

Reflex Pathways ◽

Spinal Circuitry ◽

Human Experiments

The gain of the monosynaptic stretch rerflex is controlled by many spinal pathways. Only human experiments allow the exploration of changes in transmission in these pathways during voluntary movement. Unexpected results have been obtained, which have led to new conceptions concerning the functional role of the spinal circuitry.

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Role of p75NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

AJP Renal Physiology ◽

10.1152/ajprenal.90501.2008 ◽

2008 ◽

Vol 295 (6) ◽

pp. F1778-F1789 ◽

Cited By ~ 41

Author(s):

Mary Beth Klinger ◽

Margaret A. Vizzard

Keyword(s):

Urinary Bladder ◽

Intravesical Instillation ◽

Bladder Function ◽

Neurotrophin Receptor ◽

P75 Neurotrophin Receptor ◽

Female Rat ◽

Rat Urinary Bladder ◽

Micturition Reflex ◽

Reflex Pathways

Previous studies demonstrated changes in urinary bladder neurotrophin content and upregulation of neurotrophin receptors, TrkA and the p75 neurotrophin receptor (p75NTR), in micturition reflex pathways after cyclophosphamide (CYP)-induced cystitis. p75NTR can bind nerve growth factor (NGF) and modulate NGF-TrkA binding and signaling. We examined p75NTR expression and the role of p75NTR in the micturition reflex in control and CYP-treated rats. p75NTR Immunoreactivity was present throughout the urinary bladder. CYP-induced cystitis (4 h, 48 h, chronic) increased ( P ≤ 0.05) p75NTR expression in whole urinary bladder as shown by Western blotting. The role of p75NTR in bladder function in control and CYP-treated rats was determined using conscious cystometry and immunoneutralization or PD90780, a compound known to specifically block NGF binding to p75NTR. An anti-p75NTR monoclonal antibody or PD90780 was infused intravesically and cystometric parameters were evaluated. Both methods of p75NTR blockade significantly ( P ≤ 0.05) decreased the intercontraction interval and void volume in control and CYP-treated rats. Intravesical infusion of PD90780 also significantly ( P ≤ 0.001) increased intravesical pressure and increased the number of nonvoiding contractions during the filling phase. Control intravesical infusions of isotype-matched IgG and vehicle were without effect. Intravesical instillation of PD90780 significantly ( P ≤ 0.01) reduced the volume threshold to elicit a micturition contraction in control rats (no inflammation) and CYP-treated in a closed urinary bladder system. These studies demonstrate 1) ubiquitous p75NTR expression in urinary bladder and increased expression with CYP-induced cystitis and 2) p75NTR blockade at the level of the urinary bladder produces bladder hyperreflexia in control and CYP-treated rats. The overall activity of the urinary bladder reflects the balance of NGF-p75NTR and NGF-TrkA signaling.

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Role of joint afferents in motor control exemplified by effects on reflex pathways from Ib afferents.

The Journal of Physiology ◽

10.1113/jphysiol.1978.sp012543 ◽

1978 ◽

Vol 284 (1) ◽

pp. 327-343 ◽

Cited By ~ 84

Author(s):

A Lundberg ◽

K Malmgren ◽

E D Schomburg

Keyword(s):

Motor Control ◽

Joint Afferents ◽

Reflex Pathways

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Rehabilitating the neurogenic bladder: The role of artificial neural reflex pathways in children with spina bifida

Current Urology Reports ◽

10.1007/s11934-006-0072-3 ◽

2006 ◽

Vol 7 (2) ◽

pp. 133-135

Author(s):

Sarah M. Lambert ◽

Kenneth I. Glassberg ◽

Richard C. Anderson

Keyword(s):

Spina Bifida ◽

Neurogenic Bladder ◽

Reflex Pathways ◽

Artificial Neural

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Role of L-DOPA in Spinal Nociceptive Reflex Activity: Higher Sensitivity of Aδ Versus C Fibre-Evoked Nociceptive Reflexes to L-DOPA

Physiological Research ◽

10.33549/physiolres.932104 ◽

2011 ◽

pp. 701-703

Author(s):

E. D. SCHOMBURG ◽

P. DIBAJ ◽

H. STEFFENS

Keyword(s):

Radiant Heat ◽

Reflex Activity ◽

Late Component ◽

Early Component ◽

Nociceptive Reflex ◽

Reflex Pathways ◽

Nociceptive Reflexes ◽

C Fibre ◽

Higher Sensitivity

The role of L-DOPA in spinal nociceptive reflex activity has been re-evaluated. In high spinal cats, with supraspinal loops being excluded, the onset of reflex facilitation induced by noxious radiant heat is delayed after injection of L-DOPA by 4 to 10 s, i.e. the early component of nociceptive reflex facilitation is blocked, while the late component persisted. Further investigations have shown that the early component of reflex facilitation induced by noxious radiant heat is mediated by Aδ-fibres and the late component by C-fibres. Therefore, it can be assumed that L-DOPA, like opioids, preferentially blocks the transmission in nociceptive reflex pathways from Aδ-fibres.

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TNF-α activates solitary nucleus neurons responsive to gastric distension

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2000.279.3.g582 ◽

2000 ◽

Vol 279 (3) ◽

pp. G582-G586 ◽

Cited By ~ 44

Author(s):

Gregory S. Emch ◽

Gerlinda E. Hermann ◽

Richard C. Rogers

Keyword(s):

Gastric Distension ◽

Gastric Stasis ◽

Disease States ◽

Reflex Pathways ◽

Tnf Α ◽

Vagal Reflex ◽

Factor Α ◽

A Site ◽

Necrosis Factor

Tumor necrosis factor-α (TNF-α) is liberated as part of the immune response to antigenic challenge, carcinogenesis, and radiation therapy. Previous studies have implicated elevated circulating levels of this cytokine in the gastric hypomotility associated with these disease states. Our earlier studies suggest that a site of action of TNF-α may be within the medullary dorsal vagal complex. In this study, we describe the role of TNF-α as a neuromodulator affecting neurons in the nucleus of the solitary tract that are involved in vago-vagal reflex control of gastric motility. The results presented herein suggest that TNF-α may induce a persistent gastric stasis by functioning as a hormone that modulates intrinsic vago-vagal reflex pathways during illness.

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Gastric emptying in rats: role of afferent neurons and cholecystokinin

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1990.258.4.g552 ◽

1990 ◽

Vol 258 (4) ◽

pp. G552-G556 ◽

Cited By ~ 16

Author(s):

E. R. Forster ◽

T. Green ◽

M. Elliot ◽

A. Bremner ◽

G. J. Dockray

Keyword(s):

Gastric Emptying ◽

Small Diameter ◽

Primary Afferents ◽

Delay Gastric Emptying ◽

Gastric Fistula ◽

Afferent Neurons ◽

Cholecystokinin Antagonist ◽

Reflex Pathways ◽

Intragastric Acid

Peptone, acid, and hyperosmolal saline delay gastric emptying in conscious gastric fistula rats. We have now studied the emptying of these solutions in animals pretreated with capsaicin to lesion small diameter primary afferents and in rats with both a gastric and duodenal cannula. In capsaicin-treated rats, hyperosmolal saline did not significantly inhibit gastric emptying, whereas the inhibitory action of acid and peptone was reversed but not abolished. In control rats, the action of peptone was inhibited by the selective cholecystokinin antagonist L364,718, but in capsaicin-treated rats, L364,718 enhanced the action of peptone in delaying gastric emptying. In rats with a duodenal cannula approximately 5 cm from the pylorus, intragastric peptone or hyperosmolal solutions only delayed emptying when the duodenal cannula was closed; in contrast, intragastric acid inhibited gastric emptying when the duodenal cannula was open or closed. The results suggest 1) that all three test meals delay emptying by mechanisms depending at least in part on afferent neurons; 2) peptone delays emptying by at least two mechanisms: one is mediated by cholecystokinin A-type receptors and afferent neurons, and the other requires neither these receptors nor small diameter afferents; and 3) acid, but not peptone or hyperosmolal saline, regulates emptying by an action localized to the stomach or proximal duodenum. The results suggest that there are several different reflex pathways by which liquid test meals act to delay gastric emptying.

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Endogenous opioids and electrolyte excretion after contralateral renal exclusion

AJP Renal Physiology ◽

10.1152/ajprenal.1983.244.4.f392 ◽

1983 ◽

Vol 244 (4) ◽

pp. F392-F398 ◽

Cited By ~ 2

Author(s):

J. Ribstein ◽

M. H. Humphreys

Keyword(s):

Renal Mass ◽

Opiate Receptors ◽

Opiate Receptor ◽

Endogenous Opioids ◽

Subcutaneous Implantation ◽

Electrolyte Excretion ◽

Contralateral Kidney ◽

Reflex Pathways ◽

Ureteral Occlusion

Acute reductions in functioning renal mass result in increases in both sodium (U Na V) and potassium (U K V) excretion by the contralateral kidney (CK). We studied the role of endogenous opioids in this response. In control experiments acute unilateral nephrectomy (AUN) increased U Na V from 1,788 +/- 1,125 (SD) to 3,939 +/- 1,819 and U K V from 1,385 +/- 561 to 2,254 +/- 832 neq/min by the CK (P less than 0.005 for both); similar results occurred in rats undergoing acute unilateral ureteral occlusion (UUO). These increases occurred without overall change in GFR or mean arterial pressure. In rats receiving a continuous infusion of the opiate-receptor antagonist naloxone (0.3 mg . kg-1 . h-1) neither AUN nor UUO produced significant alterations in U Na V or U K V by the CK; naloxone infusion by itself did not alter GFR or basal rates of cation excretion. A separate group of rats was made tolerant to morphine by subcutaneous implantation of pellets containing 75 mg morphine base. In these rats, AUN also failed to produce any increase in U Na V or U K V by the CK. The results suggest that acute reductions in functioning renal mass produced by either AUN or UUO stimulate cation excretion by the remaining kidney through reflex pathways that involve opiate receptors.

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