The medial sural cutaneous nerve (MSCN) and peroneal communicating nerve (PCN) conjoin in the calf area to form the sural nerve (SN). In previous anatomic studies, there was unresolved debate as to the main contributor to the sural nerve, and the relative contributions of MSCN and PCN had not been studied. The purpose of this study is to determine their relative neurophysiologic contributions to the SN by nerve conduction study (NCS). A total of 47 healthy subjects (25 males and 22 females, mean age 29.6+/-10.4 yrs, range 20-59 yrs) participated in the study. This study employed the orthodromic nerve conduction technique: stimulation at the ankle and recording at the mid calf (SN); specifically, we preformed stimulation at the mid calf (MSCN, PCN) and recording at 14cm proximal to the middle of the popliteal fossa (MSCN) and fibular head (PCN). The onset and peak latencies (ms) were SN 2.3+/-0.2 and 3.0+/-0.2; MSCN 2.1+/-0.2 and 2.8+/-0.2; and PCN 2.1+/-0.2 and 2.8+/-0.2. The peak-to-peak amplitudes (micro) and areas (nVsec) of the SN, MSCN, and PCN were 9.7+/-3.9, 7.0+/-4.7, and 5.0+/-3.2; and 7.2+/-2.9, 5.7+/-3.4, and 4.0+/-2.4, respectively. The side-to-side difference was not statistically significant. The main contributor to the SN was found to be the MSCN. The relative contribution ratio of the MSCN to the PCN was 1.37:1 by amplitude and 1.42:1 by area. However, in 32.9% of the subjects, the contribution of the PCN was greater than that of the MSCN.
Sural Nerve/*anatomy & histology/*physiology ; Peroneal Nerve/*anatomy & histology/*physiology ; Neural Conduction/*physiology ; Middle Aged ; Male ; Humans ; Female ; Adult

Measurement of motor nerve conduction velocity(MNCV) of the median and peroneal nerves was performed in 79 normal fullterm newborn infants and children up through the age of 329 weeks. They were divided into eight groups by age. The following study was undertaken to obtain the mean +/- S.D. and the regression equation of Y (MNCV) on X (age). The MNCV values of each group were compared with those of normal adults.
Child ; Child, Preschool ; Human ; Infant ; Infant, Newborn ; Median Nerve/physiology ; Motor Neurons/physiology* ; Nerve Fibers/physiology ; Neural Conduction* ; Peroneal Nerve/physiology

AIMTo explore whether dorsomedial hypothalamic nucleus (DMH) is involved in the cardiovascular responses induced by habenular nucleus (Hb) stimulation and inhibitory effect of deep peroneal nerve (DPN) stimulation on above responses or not and to analysis transmitter mechanism.

METHODSExperiments were performed on white male rabbits anesthetised with chloralose and urethan. Experimental data were collected by means of stimulating Hb and DPN, recording arterial blood pressure and ectal electrocardiogram (EECG) and microinjecting transmitter blocker.

RESULTSProminent pressor and ischemic EECG segment changes were elicited by Hb stimulation (P < 0.01) Microinjecting kynurenic acid into ipsilateral DMH had partial blocking effect on pressor and ischemic EECG-ST segment changes induced by Hb stimulation (P < 0.01). Stimulation of bilateral DPN prominently inhibited the pressor and ischemic EECG-ST changes induced by Hb stimulation (P < 0.01, P < 0.05). Microinjecting naloxone into ipsilateral DMH decreased the inhibitory effect of DPN stimulation on above cardiovascular responses elicited by Hb stimulation (P < 0.01, P < 0.05).

CONCLUSIONGlutamic acid receptor in DMH is involved in pressor and ischemic changes induced by Hb stimulation. DMH and opiate peptide receptors in DMH are involved in the inhibitory effect of DPN stimulation on pressor and ischemic changes induced by Hb stimulation.

Animals ; Cardiovascular System ; Dorsomedial Hypothalamic Nucleus ; physiology ; Electric Stimulation ; Electrocardiography ; Habenula ; physiology ; Heart Rate ; Male ; Peroneal Nerve ; physiology ; Rabbits

Animals ; Area Postrema ; physiology ; Blood Pressure ; Electric Stimulation ; Electrocardiography ; Male ; Neurotransmitter Agents ; Peroneal Nerve ; physiology ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the inhibitory effect of the deep peroneal nerve (DPN) on the cardiovascular responses induced by excitation of the paraventricular nucleus of hypothalamus (PVN) and the role of central nucleus of amygdala (CeA) in this effect.

METHODSCeA was injected by L-glutamate or Kainic acid (KA). The femoral arterial pressure, mean arterial pressure (MAP), electrocardiogram (ECG) and heart rate (HR) of SD rats were recorded while PVN or DPN was electrically stimulated.

RESULTSIt showed that MAP increased when PVN was activated by electrical stimulation. Stimulating contralateral DPN inhibited this pressor response. Ten minutes after microinjection of KA(0.02 mol/L, 100 nl) into ipsilateral CeA, MAP increased for (13.8 +/- 3.2) mmHg when PVN was stimulated. Microinjection of KA into CeA could not only reduce the pressor response elicited by stimulation of PVN for (6.6 +/- 1.6) mmHg (P < 0.05), but also the inhibitory effect of DPN from 51.5% to 32.0% .

CONCLUSIONThe results suggest that central nucleus of amygdala partly mediate the central pressor response induced by stimulation of PVN. The neurons in central nucleus of amygdala are involved in the inhibitory effect of DPN on the above pressor response.

Afferent Pathways ; Amygdala ; physiology ; Animals ; Blood Pressure ; Central Nervous System ; physiology ; Hypothalamus ; physiology ; Paraventricular Hypothalamic Nucleus ; physiology ; Peroneal Nerve ; physiology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the role of the dorsal column (DC) in the inhibitory effect of somatic afferent inputs on the central pressor response.

METHODSThe femoral arterial pressure, mean arterial pressure (MAP), electrocardiogram (ECG) and heart rate (HR) of the male SD rats were recorded when the hypothalamic paraventricular nucleus (PVN) was electrically stimulated with or without destruction of DC. The inhibitory effect of the deep peroneal nerve (DPN) on the pressor response induced by stimulation of PVN was observed 20 min or 5 d after ipsilateral DC destruction.

RESULTSStimulating DPN inhibited the pressor response elicited by electrical stimulation of PVN with an inhibitory rate of 43.29%. Twenty minutes after destroying the right DC, stimulation of the right or left DPN could inhibit the pressor response with an inhibitory rate of 38.64% and 39.97%, respectively (P>0.05); five days later the inhibitory rates remained as 33.87% and 36.86% respectively (P>0.05). The pain responses of both hindlimbs in the rats with the right DC destroyed showed no significant difference compared with the intact rats.

CONCLUSIONDC is not involved in the inhibitory effect of DPN on the pressor response induced by PVN stimulation.

Afferent Pathways ; physiology ; Animals ; Blood Pressure ; physiology ; Electric Stimulation ; Male ; Paraventricular Hypothalamic Nucleus ; physiology ; Peroneal Nerve ; physiology ; Pressoreceptors ; physiology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; physiology ; Spinothalamic Tracts ; physiology

OBJECTIVETo assess the inhibitory modulation of blood pressure by stimulation of the deep peroneal nerve (DPN) and to determine the involvement of nociceptive fibers in the modulation.

METHODSAll the animals were divided into six groups (A-F). The rats in groups A and B received no pretreatment. The rats in groups C and D received subcutaneous injection of capsaicin or control vehicle, respectively, near the DPN for 2 days. Those in groups E and F had the DPN exposed to capsaicin or control vehicle, respectively, for 20 min. Subsequently, pressor responses were induced by stimulation of paraventricular nucleus (PVN) either electrically (groups A and C C-F) or chemically via injection of glutamate (group B). After two stable pressor responses (baseline), all groups were subject to 5-min DPN stimulation followed by PVN stimulation for 10 s. Arterial blood pressure, heart rate, and electrocardiogram were recorded. The pressor response was calculated as the difference in the mean arterial pressure (MAP) before and after PVN stimulation, and changes from baseline in pressor response after DPN stimulation were compared between the groups.

RESULTSIncreases of MAP of 22.88±2.18 mm Hg and 20.32±5.25 mm Hg were induced by electrical (group A) or chemical (group B) stimulation of the PVN, respectively. These pressor responses were inhibited by stimulation of the DPN, and the MAP was reduced to 12.00±2.10 mm Hg in group A (n=6, P<0.01) and 7.00±2.85 mm Hg in group B (n=6, P<0.01). Subcutaneous injection of capsaicin (125 mg/kg) near the DPN in group C (n=7) had no effect on the inhibitory effect of DPN stimulation compared with the group D (n=9), and neither did blockade of nociceptive fibers with capsaicin in group E (n=6) compared with group F (n=8).

CONCLUSIONStimulation of the DPN mimicking acupuncture has an inhibitory effect on the pressor response, and the effect is mediated by capsaicin-insensitive afferent fibers in the DPN.

Acupuncture Therapy ; Anesthesia ; Animals ; Blood Pressure ; drug effects ; Capsaicin ; administration & dosage ; pharmacology ; Electric Stimulation ; Injections, Subcutaneous ; Male ; Paraventricular Hypothalamic Nucleus ; cytology ; drug effects ; Peroneal Nerve ; drug effects ; physiology ; Pressoreceptors ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the role of nitric oxide in the inhibitory effect of somatic afferent input on the pressor response caused by electrical stimulation of the paraventricular nucleus of the hypothalamus (PVN).

METHODSSD rats anesthetized by urethane were used in the study. Bipolar stainless stimulating electrode was inserted into PVN for electrical stimulation. Multi-barreled micropipettes were used for microinjection of L-NAME or normal saline into the lateral ventricle or amygdala. Deep peroneal nerve (DPN) was stimulated with electrical current pulses of 0.4 mA with duration of 0.5 ms at 4 Hz for 5 min. PVN was stimulated by electrical current pulses of 0.3 mA with duration of 0.5 ms at 80 Hz for 10 sec.

RESULTElectrical stimulation of PVN increased mean arterial pressure. Stimulation of DPN significantly inhibited the pressor response induced by stimulation of PVN (P<0.01), with the inhibitory percentage of 43.27%. Microinjection of L-NAME (0.5 mol/L,10 microl) into the lateral ventricle of brain attenuated the inhibitory effect of DPN. The inhibitory percentage decreased from 47.73% to 12.49% (P<0.05). Microinjection of L-NAME (2 mol/L,100 nl) into amygdala reduced the inhibitory effect of DPN. The inhibitory percentage of stimulating DPN on the pressor response decreased from 50.71% to 25.30% (P<0.05).

CONCLUSIONNitric oxide in the brain and amygdala are involved in the inhibitory effect of somatic afferent input on central pressor response.

Afferent Pathways ; drug effects ; physiology ; Amygdala ; drug effects ; physiology ; Animals ; Blood Pressure ; physiology ; Electric Stimulation ; Enzyme Inhibitors ; pharmacology ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide ; antagonists & inhibitors ; physiology ; Nitric Oxide Synthase ; antagonists & inhibitors ; Paraventricular Hypothalamic Nucleus ; drug effects ; physiology ; Peroneal Nerve ; physiology ; Pressoreceptors ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the ability of aqueous extract of Hericium erinaceus mushroom in the treatment of nerve injury following peroneal nerve crush in Sprague-Dawley rats.

METHODSAqueous extract of Hericium erinaceus was given by daily oral administration following peroneal nerve crush injury in Sprague-Dawley rats. The expression of protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) signaling pathways; and c-Jun and c-Fos genes were studied in dorsal root ganglia (DRG) whereas the activity of protein synthesis was assessed in peroneal nerves by immunohistochemical method.

RESULTSPeripheral nerve injury leads to changes at the axonal site of injury and remotely located DRG containing cell bodies of sensory afferent neurons. Immunofluorescence studies showed that DRG neurons ipsilateral to the crush injury in rats of treated groups expressed higher immunoreactivities for Akt, MAPK, c-Jun and c-Fos as compared with negative control group (P <0.05). The intensity of nuclear ribonucleoprotein in the distal segments of crushed nerves of treated groups was significantly higher than in the negative control group (P <0.05).

CONCLUSIONH. erinaceus is capable of promoting peripheral nerve regeneration after injury. Potential signaling pathways include Akt, MAPK, c-Jun, and c-Fos, and protein synthesis have been shown to be involved in its action.

Agaricales ; chemistry ; Animals ; Axons ; pathology ; Female ; Ganglia, Spinal ; metabolism ; Glucans ; analysis ; MAP Kinase Signaling System ; Nerve Crush ; Nerve Regeneration ; physiology ; Peripheral Nerves ; enzymology ; physiology ; Peroneal Nerve ; physiology ; Protein Biosynthesis ; Proto-Oncogene Proteins c-akt ; metabolism ; Proto-Oncogene Proteins c-fos ; genetics ; metabolism ; Proto-Oncogene Proteins c-jun ; genetics ; metabolism ; Rats, Sprague-Dawley