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PubMed1989

Central interleukin 1-elicited hyperinsulinemia is mediated by prostaglandins but not autonomics.

This laboratory previously reported that centrally administered interleukin 1 (IL-1) in fasted pentobarbital-anesthetized rats elicited significant hyperinsulinemic and febrile responses. In characterizing this putative central mechanism for the regulation of pancreatic insulin secretion, hyperinsulinemia and fever elicited by IL-1 injected intravenously (iv) or intracerebroventricularly (icv) was totally eliminated by prior cyclooxygenase inhibition with indomethacin, ibuprofen, or meclofenamate but not lipoxygenase inhibition with propyl gallate or leukotriene receptor antagonism with LY 171883. Furthermore, central administration of prostaglandin E2 at 10 and 100 ng doses consistently evoked hyperinsulinemic, hypercorticotropinemic, and febrile responses in anesthetized rats maintained on isothermal pads. beta-Adrenergic and vagus nerves to the pancreatic beta-cells seemed likely candidates to mediate the enhanced secretion of insulin elicited by IL-1 acting centrally. However, pretreatment of rats with hexamethonium, propanolol, atropine, or bilateral subdiaphragmatic vagotomy all failed to reduce hyperinsulinemia after IL-1 iv or icv. This evidence suggests that the central mechanism for enhanced pancreatic insulin secretion elicited by IL-1 may depend on a humoral rather than autonomic neural efferent pathway. Moreover, the hyperinsulinemia is mediated in part by prostaglandins just like the well-studied febrile response.

Acetophenones↗
PubMed1994

Role of peripheral capsaicin-sensitive neurons and CGRP in central vagally mediated gastroprotective effect of TRH.

We investigated in conscious rats the role of capsaicin-sensitive neurons and alpha-calcitonin gene-related peptide (CGRP), the form preferentially expressed in capsaicin sensory neurons, in mediating intracisternal thyrotropin-releasing hormone (TRH) analogue-induced vagal muscarinic gastroprotection against ethanol lesions. The TRH analogue RX-77368 (1.5 ng ic) reduced by 78 and 66% gastric hemorrhagic lesions induced by intragastric intubation of 60 and 80% ethanol, respectively. alpha-CGRP (1 nmol/kg iv) inhibited by 88% gastric lesions induced by 60% ethanol, and this peptide action was blocked by the CGRP antagonist, CGRP-(8-37) (128 nmol/kg iv). The protective effect of RX-77368 against 60% ethanol was completely abolished by the CGRP monoclonal antibody 4901 (4.8 mg/kg iv), CGRP-(8-37) (128 nmol/kg iv), and capsaicin pretreatment (125 mg/kg). Gastric lesions induced by 60% ethanol were not altered by the CGRP antagonist or antibody alone but were enhanced by capsaicin pretreatment. These results suggest that the gastroprotection induced by intracisternal TRH analogue involves an interaction between central vagal efferent pathways and splanchnic sensory afferent terminals containing CGRP.

Animals↗
PubMed1995

Central inhibitory action of peptide YY on gastric motility in rats.

Specific peptide YY (PYY) binding sites have recently been identified autoradiographically in the area postrema, nucleus of the solitary tract, and dorsal motor nucleus regions [collectively referred to as the dorsal vagal complex (DVC)] in rats. These medullary brain stem regions are responsible for vagovagal reflex control of gastric function, including gastric motility. We propose that PYY can modulate gastrointestinal functions, such as gastric motility, by interacting with PYY binding sites found in DVC. Furthermore, we predict that central PYY effects on gastric function are mediated by the vagus nerve. In the present study, urethan-anesthetized rats were used. PYY (20.0 and 2.0 fmol) injected directly into DVCs of the animals produced significant inhibition of gastric motility that was stimulated by centrally applied thyrotropin-releasing hormone (TRH). TRH is a well-accepted central stimulator of vagal efferent pathway to the stomach. Otherwise, an excitatory effect of PYY (2 pmol) on basal gastric motility was observed and considered as being pharmacological. The inhibitory effect of PYY was abolished completely by unilateral (the injection side) cervical vagotomy, suggesting that the inhibition was vagally dependent. These results support the view that physiological concentrations of PYY may inhibit proximal gut function as part of the "ileal brake" mechanism by acting directly on vagovagal control circuits in the dorsal medulla. However, extremely high doses of PYY may activate gastric function through pharmacological action at pancreatic polypeptide receptors in the DVC.

Animals↗
PubMed1995

Attenuation of the midbrain-evoked defense reaction by selective stimulation of medullary raphe neurons in rats.

In rats anesthetized with alfaxalone/alfadolone, electrical stimulation in the dorsal periaqueductal gray matter (PAG) evoked a cardiovascular defense reaction with increases in blood pressure, heart rate, femoral conductance, and respiratory activity but a decrease in renal conductance. These responses were attenuated significantly after microinjection of 200 nl 0.1 M DL-homocysteic acid (DLH) into nucleus raphe magnus (NRM, n = 12) or nucleus raphe obscurus (NRO, n = 22). The maximum reduction in the pressor response was similar after stimulation in NRM (-36.3%) and NRO (-37.3%). The reduction of the tachycardia, however, was greater after stimulation in NRM (-78.1%) compared with NRO (-34.6%). The maximum reduction in the PAG-evoked vasodilation of the hindlimb averaged -55.7% and -55.3% after stimulation of NRM and NRO, respectively, whereas the renal vasoconstriction was reduced by -66.4% and -79.0%. The PAG-evoked increase in respiratory amplitude was attenuated only after stimulation of NRO. It is concluded that neurons in NRM and NRO may be involved in modulating the level of excitability of neurons in the midbrain defense area and/or in its efferent pathway.

Animals↗
PubMed1999

Induction of endogenous tumor necrosis factor-alpha: suppression of centrally stimulated gastric motility.

Gastric stasis is frequently seen in conjunction with critical infectious illness, chronic inflammatory disorders, radiation sickness, and carcinogenesis. These conditions are associated with elevated circulating levels of the cytokine tumor necrosis factor-alpha (TNF-alpha). The present studies examined the relationship between endogenously produced TNF-alpha and the central neural mechanisms that augment gastric motility. Systemic lipopolysaccharide (LPS) was employed to induce TNF-alpha production in thiobutabarbital-anesthetized rats. Sixty minutes after intravenous LPS injection, gastric motility could not be stimulated by a potent centrally acting gastrokinetic stimulant, thyrotropin-releasing hormone (TRH). This failure to elicit gastric motility via central mechanisms coincided with high circulating levels of TNF-alpha. However, intravenous injections of bethanecol, a peripherally acting cholinergic agonist with direct gastrokinetic effects, were still able to elicit normal increases in gastric motility in the presence of TNF-alpha and LPS. Therefore, the inability to stimulate gastric motility via central TRH could not be attributed to the direct inhibitory effects of either LPS or TNF-alpha on the stomach. If the production of endogenous TNF-alpha was suppressed via the use of urethan as the anesthetic agent, then intravenous injections of LPS were no longer effective in suppressing gastric motility. Thus these effects on gastric motility are not directly attributable to LPS nor are they due to direct effects on the gastric smooth muscle. Our previous study demonstrated that microinjection of femtomole quantities of TNF-alpha in the brain stem dorsal vagal complex (DVC) can modulate gastric motility. This central TNF-alpha effect on gastric motility was dose dependent and required an intact vagal efferent pathway. The results from these two studies suggest that systemically produced TNF-alpha may gain access to the DVC to modulate gastric function.

Animals↗
PubMed1985

Reflex depression of cardiovascular function during lung inflation.

These experiments were intended 1) to determine the cardiovascular reflex response initiated by lung inflation and 2) to determine the autonomic neural mechanisms that mediate the reflex responses. To test only the reflex effects of lung inflation and eliminate the associated mechanical effects thereof, we isolated the left airway and left pulmonary artery of dogs and performed static inflations of the left lung. Left lung inflation (LLI) to 30 cmH2O caused left ventricular systolic pressure, heart rate, and hindlimb vascular resistance to fall 20, 31, and 15%, respectively. When the hearts were paced to eliminate Bowditch effects, LLI caused left ventricular contractility, which was measured as dP/dt at 30 mmHg developed pressure and as the maximal rate of shortening of the contractile element, to fall 23 and 20%, respectively, and cardiac output (stroke volume) to fall 31%. Transection of the left cervical vagus nerve, interrupting most afferent and some efferent pathways from the left lung, virtually eliminated subsequent cardiovascular responses to LLI. Hindlimb vasodilation was mediated by alpha-adrenergic activity, and the fall in left ventricular contractile state was caused by a reduction in beta-adrenergic activity. The reflex bradycardia was mediated by increased cholinergic and decreased beta-adrenergic activity. These data establish that reflex mechanisms exist whereby expansion of the lung can reflexly modulate heart rate, ventricular contractility, systemic vasomotor tone, cardiac output, and stroke volume independent of the direct mechanical influence of lung expansion on these circulatory phenomena.

Animals↗
PubMed1995

Diuretic effect of acute hypoxia in humans: relationship to hypoxic ventilatory responsiveness and renal hormones.

Acute hypoxia causes increased sodium and water excretion. Animal studies suggest that this renal response is largely driven by direct peripheral arterial chemoreceptor stimulation, independent of accompanying changes in ventilation and acid-base status. Whether the diuresis and natriuresis observed in humans made acutely hypoxic are caused by peripheral chemoreceptor stimulation is not known, but, if so, we hypothesized that people with a high ventilatory response to hypoxia (high peripheral chemosensitivity) should have greater diuresis and natriuresis than those with a low ventilatory response to hypoxia. The isocapnic hypoxic ventilatory response (HVR) of 16 subjects on a fixed sodium intake was measured, as were their urinary volume and sodium and bicarbonate losses during 6 h of breathing air (in a normobaric environmental chamber) and, on the subsequent day, 12% O2. The isocapnic HVR correlated positively with hypoxic diuresis (r = 0.87) and natriuresis (r = 0.76). In contrast, the isocapnic HVR did not correlate with bicarbonate excretion, despite the expected respiratory alkalosis of acute hypoxia. The magnitude of diuresis and natriuresis with hypoxia did not correlate with changes in circulating aldosterone, renin, atrial natriuretic peptide, vasopressin, or a digoxin-like immunoreactive substance. These findings are compatible with a role of the peripheral arterial chemoreceptors in mediating the renal response to hypoxia in humans. The efferent pathway remains unknown.

Acute Disease↗
PubMed2000

Bronchial vasodilation evoked by increased lower airway osmolarity in dogs.

Hyperosmotic saline solutions stimulate lower airway sensory nerves. To determine whether airway hyperosmolarity evokes neurally mediated changes in bronchial artery blood flow (Qbr), we measured the effect of injection of small volumes (1 ml) of hyperosmotic saline into a right lobar bronchus on Qbr of anesthetized, artificially ventilated dogs. In 14 dogs, hyperosmotic saline (1,200 and 2,400 mmol/l) increased Qbr by 58 +/- 12 (SE) and 118 +/- 12%, respectively, from a baseline of 8 +/- 2 ml/min. Qbr increased within 6-8 s of the injections, peaked at 20 s, and returned to control over 2-3 min. Isosmotic saline had minimal effects. In contrast, hyperosmotic saline decreased flow in an intercostal artery that did not supply the airways. The bronchial vasodilation was decreased by 72 +/- 11% after combined blockade of alpha-adrenoceptors and muscarinic cholinergic receptors and by 66 +/- 6% when the cervical vagus nerves were cooled to 0 degrees C. Blockade of H(1) and H(2) histamine receptors did not reduce the nonvagal response. We conclude that hyperosmolarity of the lower airways evokes bronchial vasodilation by both a centrally mediated reflex that includes cholinergic and adrenergic efferent pathways and by unidentified local mechanisms.

Aerosols↗
PubMed2006

Hippocampal sharp wave-ripples linked to slow oscillations in rat slow-wave sleep.

Slow oscillations originating in the prefrontal neocortex during slow-wave sleep (SWS) group neuronal network activity and thereby presumably support the consolidation of memories. Here, we investigated whether the grouping influence of slow oscillations extends to hippocampal sharp wave-ripple (SPW) activity thought to underlie memory replay processes during SWS. The prefrontal surface EEG and multiunit activity (MUA), along with hippocampal local field potentials (LFP) from CA1, were recorded in rats during sleep. Average spindle and ripple activity and event correlation histograms of SPWs were calculated, time-locked to half-waves of slow oscillations. Results confirm decreased prefrontal MUA and spindle activity during EEG slow oscillation negativity and increases in this activity during subsequent positivity. A remarkably close temporal link was revealed between slow oscillations and hippocampal activity, with ripple activity and SPWs being also distinctly decreased during negative half-waves and increased during slow oscillation positivity. Fine-grained analyses of temporal dynamics revealed for the slow oscillation a phase delay of approximately 90 ms with reference to up and down states of prefrontal MUA, and of only approximately 60 ms with reference to changes in SPWs, indicating that up and down states in prefrontal MUA precede corresponding changes in hippocampal SPWs by approximately 30 ms. Results support the notion that the depolarizing surface-positive phase of the slow oscillation and the associated up state of prefrontal excitation promotes hippocampal SPWs via efferent pathways. The preceding disfacilitation of hippocampal events temporally coupled to the negative slow oscillation half-wave appears to serve a synchronizing role in this neocorticohippocampal interplay.

Action Potentials↗
PubMed2002

Single-neuron analysis of human thalamus in patients with intention tremor and other clinical signs of cerebellar disease.

Tremor that occurs as a result of a cerebellar lesion, cerebellar tremor, is characteristically an intention tremor. Thalamic activity may be related to cerebellar tremor because transmission of some cerebellar efferent signals occurs via the thalamus and cortex to the periphery. We have now studied thalamic neuronal activity in a cerebellar relay nucleus (ventral intermediate-Vim) and a pallidal relay nucleus (ventralis oral posterior-Vop) during thalamotomy in patients with intention tremor and other clinical signs of cerebellar disease (tremor patients). The activity of single neurons and the simultaneous electromyographic (EMG) activity of the contralateral upper extremity in tremor patients performing a pointing task were analyzed by spectral cross-correlation analysis. EMG spectra during intention tremor often showed peaks of activity in the tremor-frequency range (1.9-5.8 Hz). There were significant differences in thalamic neuronal activity between tremor patients and controls. Neurons in Vim and Vop had significantly lower firing rates in tremor patients than in patients undergoing thalamic surgery for pain (pain controls). Other studies have shown that inputs to Vim from the cerebellum are transmitted through excitatory connections. Therefore the present results suggest that tremor in these tremor patients is associated with deafferentation of the thalamus from cerebellar efferent pathways. The thalamic X EMG cross-correlation functions were studied for cells located in Vim and Vop. Neuronal and EMG activity were as likely to be significantly correlated for cells in Vim as for those in Vop. Cells in Vim were more likely to have a phase lag relative to EMG than were cells in Vop. In monkeys, cells in the cerebellar relay nucleus of the thalamus, corresponding to Vim, are reported to lead movement during active oscillations at the wrist. In view of these monkey studies, the present results suggest that cells in Vim are deafferented and have a phase lag relative to tremor that is not found in normal active oscillations. The difference in phase of thalamic spike X EMG activity between Vim and Vop may contribute to tremor because lesions of pallidum or Vop are reported to relieve cerebellar tremor.

Action Potentials↗
PubMed2004

Suppression of visually and memory-guided saccades induced by electrical stimulation of the monkey frontal eye field. I. Suppression of ipsilateral saccades.

When a saccade occurs to an interesting object, visual fixation holds its image on the fovea and suppresses saccades to other objects. Electrical stimulation of the frontal eye field (FEF) has been reported to elicit saccades, and recently also to suppress saccades. This study was performed to characterize properties of the suppression of visually guided (Vsacs) and memory-guided saccades (Msacs) induced by electrical stimulation of the FEF in trained monkeys. For any given stimulation site, we determined the threshold for electrically evoked saccades (Esacs) at < or =50 microA and then examined suppressive effects of stimulation at the same site on Vsacs and Msacs. FEF stimulation suppressed the initiation of both Vsacs and Msacs during and about 50 ms after stimulation at stimulus intensities lower than those for eliciting Esacs, but did not affect the vector of these saccades. Suppression occurred for ipsiversive but not contraversive saccades, and more strongly for saccades with larger amplitudes and those with initial eye positions shifted more in the saccadic direction. The most effective stimulation timing for suppression was about 50 ms before saccade onset, which suggests that suppression occurred in the efferent pathway for generating Vsacs at the premotor rather than the motoneuronal level, most probably in the superior colliculus and/or the paramedian pontine reticular formation. Suppression sites of ipsilateral saccades were distributed over the classical FEF where saccade-related movement neurons were observed. The results suggest that the FEF may play roles in not only generating contraversive saccades but also maintaining visual fixation by suppressing ipsiversive saccades.

Animals↗
PubMed1975

Organization of cat striate cortex: a correlation of receptive-field properties with afferent and efferent connections.

The purposes of this study were 1) to relate the receptive-field characteristics of area 17 cells to their afferent and efferent connections, and 2) to obtain quantitative data from area 17 neurons for later comparison with area 18 cells. Intra- and extracellular recordings were obtained in paralyzed preparations which were anesthetized with nitrous oxide. The connectivities of the recorded cells were determined from responses to electrical stimulation of afferent and efferent pathways. In parallel to the classification of units as simple and complex cells, the receptive fields were grouped in four classes according to the spatial arrangement of on- and off-areas; class I, fields with exclusive on- or off-areas; class II, fields with spatially separate on- and off-areas; class III, fields with mixed on-off areas; class IV, fields which could not be mapped with stationary stimuli. The results from electrical stimulation suggest two major classes of cells: cells in the first group are driven mainly or exclusively by LGN afferents. They rarely receive additional excitation from intrinsic or callosal afferents and rarely possess corticofugal axons. Cells in the second group receive either converging inputs from LGN afferents and further intrinsic afferents or only from intrinsic afferents. They frequently received additional input from callosum and from recurrent collaterals of corticofugal axons. They project subcortically more often than cells in the first group. Cells in both groups can be driven either by X- or Y-type afferents. Cells in the first group have mainly class I and class II fields or simple fields, whereas the neurons in the second group have mainly class III and class IV fields or complex fields. Thus, simple and complex cells differ in their connectivity patterns, but the discriminative parameter is neither the selective connection to the X- or the Y-system nor, in a strict sense, the synaptic distance from subcortical input. From the combined consideration of receptive-field properties and connectivity patterns it is concluded that class I and class II cells or simple cells are concerned mainly with the primary analysis of subcortical activity, whereas class III and class IV cells or complex cells perform a correlative analysis between highly convergent activity from extrinsic and intrinsic afferents.

Animals↗
PubMed1983

Response to sudden torques about ankle in man: V effects of peripheral ischemia.

Sudden dorsiflexions and plantar flexions of the foot were imposed by a torque motor while blood flow to the lower leg was occluded by a sphygmomanometer cuff. Seated subjects were instructed to resist the torques and restore the foot to its original position as rapidly as possible. Measurements of the first two electromyographic (EMG) responses were made in the soleus (SOL) and anterior tibial (TA) muscles. These are the myotatic reflex at about 40 ms and the postmyotatic response at about 120 ms. In the anterior tibial muscle, the myotatic component often occurs at 60- to 90-ms latency and is continuous with the postmyotatic component. After about 20 min of ischemia, there is a rapid and eventually complete loss of the myotatic component of the response in the stretched muscle. Concurrent with the loss of the myotatic reflex there is usually a reduction of the postmyotatic component. The latency of postmyotatic component remains unchanged, even after the myotatic reflex is abolished. Voluntary restoration of the foot to its original position in opposition to the motor torque is delayed and slowed by the time that the myotatic reflex has vanished. By measuring electromyographic responses to visually triggered reactions, we demonstrate that the reduction of the postmyotatic response is not due to failure of the efferent pathway. On this basis we discuss the possible contributions made by myotatic mechanisms to the tasks of load compensation and maintenance of muscle tone. Hoffmann reflexes were evoked in similar experiments with stimulation of the posterior tibial nerve at the popliteal fossa, distal to the cuff. The maximal direct motor response and muscle twitch are unaffected by loss of the H-reflex. Myotatic and Hoffmann reflexes were both evoked with torque perturbations and with a stimulating electrode proximal to a below-the-knee cuff. In this case, the myotatic reflex failed while the maximal H-reflex was slightly facilitated. The loss of the myotatic reflex was accompanied by a modest reduction in the direct motor response to electrical stimulation and a somewhat greater reduction in the postmyotatic response to torque perturbation. The data are interpreted to support a dual role for the primary afferent pathway in the control of voluntary movements. It provides the fastest path for the activation of a stretched muscle to initiate a load-compensating contraction. It also provides a form of servo assistance in modulating descending control signals. The degree of this assistance is estimated. In this simple experimental paradigm, functional contributions of the reflex arc are demonstrated.

Ankle Joint↗
PubMed1990

Reflex activation of muscle spindles in human pretibial muscles during standing.

1. Experiments were performed in standing subjects to determine whether low-threshold cutaneous and muscle afferents from mechanoreceptors in the human foot reflexly influence fusimotor neurons innervating pretibial flexor muscles. Recordings were made from 30 identified muscle-spindle afferents, four tendon-organ afferents, and one alpha-motor axon innervating the pretibial flexor muscles. The subjects stood without support or vision on a force platform while trains of electrical stimuli (5 stimuli, 300 Hz) were delivered at nonpainful intensities to the sural nerve or to the posterior tibial nerve at the ankle. 2. Seventeen of the 30 spindle endings had no background discharge, and none was activated by the sural or posterior tibial stimuli. Five silent afferents were given a background discharge by sustained pressure on the relevant tendon, but with two the discharge was dominated by a tremor rhythm obscuring any reflex response to the stimuli. Based on peristimulus time histograms (PSTHs), the sural stimuli then produced increases in discharge of two of the remaining three endings at latencies of 84 and 90 ms. These effects could not be explained by muscle stretch and are presumed to have been fusimotor mediated. 3. When the subjects stood freely without support or vision, 13 muscle-spindle endings had a background discharge, but with three endings tremor developed at the ankle and dominated the spindle discharge. Sural stimuli affected the discharge of five of nine endings unaffected by tremor. With three of these endings, there were changes in discharge that could be explained by muscle stretch.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Surround inhibition among projection neurons is weak or nonexistent in the rat neostriatum.

1. Antidromic activation of striatal spiny projection neurons by substantia nigra stimulation in vivo did not evoke inhibitory postsynaptic potentials (IPSPs) in the antidromically activated neurons, or in neighboring spiny neurons. 2. More generalized activation of projection cells by stimulation of the efferent pathway in slices did not evoke IPSPs in spiny neurons. Inhibitory mechanisms were operative in these slices, as indicated by the presence of an IPSP component in the orthodromic response to local stimulation. 3. Dual intracellular recordings, obtained from cells located within 50-200 microns of each other in striatal slices also failed to demonstrate any inhibition among striatal spiny cells. Spikes triggered in one spiny neuron by current injection failed to produce any postsynaptic potential in nearby spiny cells at resting or depolarized membrane potentials. Excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of the cortex were not affected by spiking of neighboring cells. 4. It is impossible to rule out the presence of inhibition among striatal spiny neurons in all circumstances. However, the absence of demonstrable IPSPs in these experiments argue against the common view that mutual inhibition among spiny neurons is a central organizing principle of striatal function.

Animals↗
PubMed1996

Inhibition of bradykinin-induced synovial plasma extravasation produced by intrathecal nicotine is mediated by the hypothalamopituitary adrenal axis.

1. Bradykinin (BK)-induced plasma extravasation (PE) in the rat knee joint, which is dependent to a large extent on the sympathetic innervation of the synovium, is powerfully inhibited, dose dependently, by intrathecal administration of nicotine, especially after interruption of the impulse traffic in afferents of the abdominal vagus nerve. In this study we investigated in vagotomized animals possible efferent pathways that might mediate the inhibition produced by the intrathecally applied nicotine. We studied the role of the sympathetic supply to the knee joint, of the sympathoadrenal system, and of the hypothalamopituitary-adrenal (HPA) axis in the ability of intrathecal nicotine to inhibit BK-induced PE in the knee joint. The experimental interventions performed were as follows: recording activity in the lumbar sympathetic trunk; antagonizing the effect of epinephrine, released from the adrenal medulla; acute interruption of the lumbar sympathetic trunks; hypophysectomy; and blockade of the glucocorticoid receptors. We employed acutely vagotomized animals because in these animals nicotine-induced inhibition is enhanced. 2. We found that hypophysectomy or blockade of the glucocorticoid receptors markedly attenuated the inhibition of BK-induced PE produced by intrathecal nicotine. 3. Intrathecal nicotine did not affect activity in the sympathetic chain. 4. Acute interruption of the lumbar sympathetic chain, which leaves the sympathetic terminals in the synovium intact but abolishes activity in the sympathetic postganglionic neurons, did not change the inhibition of BK-induced PE produced by intrathecal nicotine. 5. Blockade of the beta 2 adrenoceptors in the knee joint, preventing in this way potential effects of epinephrine released by the adrenal medulla, did not affect the inhibition of BK-induced PE produced by intrathecal nicotine. 6. The results of the present experiments strongly support the hypothesis that the powerful suppression of BK-induced PE in the knee joint generated by intrathecal nicotine is mediated via the HPA axis and not via activity in sympathetic neurons innervating the knee joint or the adrenal medulla. Future studies are needed to determine in which functional contexts this pathway is active in the control of PE in the synovia and of other aspects of inflammation.

Adrenal Glands↗
PubMed1996

Temporal processing of aortic nerve evoked activity in the nucleus of the solitary tract.

1. Temporal processing of heterogenous afferent signals by nucleus of the solitary tract (NTS) neurons has been previously characterized. Experiments were performed in 26 pentobarbital-sodium-anesthetized male Sprague-Dawley rats to characterize the temporal processing of evoked activity in NTS neurons with the use of the aortic nerve, which contains exclusively arterial baroreceptor afferent fibers. 2. Extracellular single-cell activity was examined in the NTS during electrical stimulation of the aortic nerve with the use of a conditioning-test paradigm. 3. Results were obtained from 49 neurons, 22 of which were characterized as receiving monosynaptic input from aortic nerve afferents. The average number of evoked potentials per aortic nerve stimulation was 1.1 +/- 0.1 (SE) for the monosynaptic neurons and 1.2 +/- 0.2 for the polysynaptic neurons. Spontaneous activity averaged 3.7 +/- 0.7 Hz. No neuron exhibited an obvious pulse-rhythmic discharge. The average peak onset latency for monosynaptic cells of 17 +/- 2 ms (range 3-31 ms) was significantly (P < 0.05) shorter than the average of 26 +/- 1 ms (range 13-38 ms) for the polysynaptic cells. The average onset latency variability was also less in monosynaptic compared with polysynaptic cells (4 +/- 1 ms vs. 8 +/- 1 ms; P < 0.05). 4. Neurons characterized as receiving a monosynaptic input from the aortic afferents generally did not exhibit time-dependent inhibition. Significant inhibition was observed only at a conditioning-test interval of 50 ms, when the average test response was 79 +/- 8% of control. In contrast, the average response following a 50-ms conditioning-test interval for neurons receiving polysynaptic input from the aortic nerve was only 32 +/- 8% of control. Significant inhibition was observed at conditioning-test intervals of up to 200 ms. 5. At a conditioning-test interval of 50 ms, only 5 of 22 monosynaptic neurons were inhibited by > 50%. Mean arterial pressure during the conditioning-test procedure was significantly lower for these neurons than for the 17 cells that were inhibited by < 50%. This suggests that the level of activity in convergent afferent input might influence the magnitude of time-dependent inhibition. 6. There was an essentially linear recovery from time-dependent inhibition evident in polysynaptic neurons that were tested at all conditioning-test intervals, suggesting a single mechanism of variable duration. Results reported here are consistent with current theory that time-dependent inhibition is mediated by disfacilitation. 7. The results demonstrate that NTS neurons receiving monosynaptic input from the aortic depressor nerve infrequently exhibit time-dependent inhibition. This could allow for the original, unmodified afferent information to be dispersed to subsequent neurons. In contrast, neurons receiving polysynaptic input undergo time-dependent inhibition similar to that which has been reported for other afferent inputs. This could allow for differential degrees of fidelity in the transfer of the afferent information to specific efferent pathways. Therefore the temporal pattern of firing in individual baroreceptor afferents could play a critical role in the function of the arterial baroreflex and therefore in the regulation of blood pressure.

Afferent Pathways↗
PubMed1998

Innervation pattern of different cartilaginous tissues in the rat.

BACKGROUND: The innervation of skeletal tissues by sensory nerves is poorly understood - especially of nerve fibres which reach into the bony and cartilaginous tissue. METHODS: Samples of rat cartilaginous tissues from different locations (knee joint, vertebral column, temporomandibular joint) were fixed by perfusion and decalcified. The distribution of protein gene product (PGP) 9.5-, calcitonin gene-related peptide (CGRP)- and tachykinin (TK)-immunoreactive axons was analysed using fluorescence immunohistochemistry. RESULTS: Nerve fibres were detected in the outer regions of the hyaline cartilage of the knee joint, in the hyaline cartilage of the vertebral body, in the fibrocartilage of the intervertebral disc and menisci, and in the articular disc of the temporomandibular joint. Predominantly, they were found to be CGRP-immunoreactive. CONCLUSION: The neuropeptidergic innervation of the hyaline cartilage in different locations and the presence of nerve fibres in the fibrocartilage might indicate that in addition to the classical neuronal afferent and efferent pathway these fibres may also mediate trophic actions like tissue adaptation and repair.

Animals↗