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At least 811 records · Page 45Linked to original sources
PubMed1991

Synaptic effects in lumbar alpha-motoneurones evoked from group II muscle afferents via two different interneuronal pathways in the cat.

Conditioning of monosynaptic reflexes was used to investigate group II excitation from quadriceps (Q) and sartorius (Sart) in posterior biceps-semitendinosus (PBSt) motoneurones and different lesions were made to analyze the interneuronal pathways. The purpose of the investigation was to find if the excitation from group II Q and Sart afferents, which enter the spinal cord in L4-L6, is relayed to motoneurones by interneurones located in these segments and/or in the same segments (L7-S1) as the PBSt motoneurones. In some experiments a transection of the dorsal column in L6, which interrupts the group II input from Sart and Q to interneurones in the L7-S1 segments, resulted in a marked decrease (by about 2/3) of group II excitation from these nerves. In other experiments the same lesion did not reduce the group II effect. In the latter cases the effect could be abolished by a second lesion of the lateral funiculus (LF) in L5-L6. It is postulated that potent effects from Q and Sart group II afferents can be evoked by interneurones located in L7-S1, i.e. in the same segments as the PBSt motoneurones (L7-S1), and/or via interneurones in more rostral segments. The axons of the more rostrally located group II interneurones appear to descend mainly in the middle part of the LF.

Animals↗
PubMed1996

GABA metabolism controls inhibition efficacy in the mammalian CNS.

The effects of changes in gamma-aminobutyric acid (GABA) metabolism or inhibitory processes was studied in the perforant path-dentate gyrus synapses in rat cortico-hippocampal slices, and in the monosynaptic-reflex circuit in isolated newborn, rat spinal cord. GABA metabolism was modulated by pharmacological block of either the anabolic enzyme glutamate decarboxylase (GAD) or the catabolic enzyme GABA transaminase (GABA-T). The results support the notion that GABA concentration determines the efficacy of inhibition in these regions of the central nervous system (CNS).

3-Mercaptopropionic Acid↗
PubMed1991

Substance P-evoked release of acetylcholine from isolated spinal cord of the newborn rat.

Isolated spinal cords of newborn rats were perfused with artificial cerebrospinal fluid and the release of endogenous acetylcholine was measured using high-performance liquid chromatography with an electrochemical detection system. Application of high-K+ (90 mM) medium evoked about an eight-fold increase in the acetylcholine release, and the K(+)-evoked release was Ca2+ dependent. Veratridine (20 microM) also evoked about a four-fold increase in the acetylcholine release, and this increase was suppressed by 0.2 microM tetrodotoxin. Application of substance P at 0.3-3 microM evoked a concentration-dependent release of acetylcholine. The substance P-evoked acetylcholine release was Ca2+ dependent and abolished by tetrodotoxin. Neurokinin A, neurokinin B, acetyl-Arg6-septide and senktide (3 microM each) also evoked a release of acetylcholine. Electrophysiological experiments using isolated spinal cords of newborn rats showed that bath application of substance P induced a depolarization of motoneurons, which was enhanced by edrophonium. This enhancement of substance P-induced depolarization by edrophonium disappeared in a low-Ca2+ medium or in the presence of atropine and dihydro-beta-erythroidine. In the presence of edrophonium and dihydro-beta-erythroidine, substance P induced an inhibition of monosynaptic reflex, and this inhibition was abolished by atropine. These results suggest that substance P and other tachykinins induce a release of acetylcholine from the newborn rat spinal cord by exciting cholinergic neurons.

Acetylcholine↗
PubMed1992

Supersensitivity of spinal dopaminergic receptors in rat after chronic haloperidol.

In order to examine the effect of chronic neuroleptics on spinal dopaminergic system, rats were treated with haloperidol (0.5 mg/kg IP) for 21 days and the monosynaptic mass reflex (MMR) as well as dopamine (DA) metabolism were investigated. MMR, recorded from ventral root L6 following supramaximal stimulation to ipsilateral dorsal root L6 in spinalized rats, were found to be unaffected following chronic haloperidol treatment when compared to control. Apomorphine (0.1 mg/kg IV) caused 10-20% depression of MMR in control animals which was augmented to 40-50% in chronically haloperidol-treated animals suggesting an upregulation of DA receptors in the spinal cord. DA content of lumbar region of the spinal cord was unaffected whereas its major metabolite, homovanillic acid, was significantly reduced in chronic haloperidol-treated animals. This decreased utilization of DA may compensate the upregulation of DA receptors to maintain the physiological homeostasis of the spinal dopaminergic system.

Animals↗
PubMed1994

Cotransmitter-mediated locus coeruleus action on motoneurons.

This article reviews evidence for a direct noradrenergic projection from the dorsolateral pontine tegmentum (DLPT) to spinal motoneurons. The existence of this direct pathway was first inferred by the observation that antidromically evoked responses occur in single cells in the locus coeruleus (LC), a region within the DLPT, following electrical stimulation of the ventral horn of the lumbar spinal cord of the cat. We subsequently confirmed that there is a direct noradrenergic pathway from the LC and adjacent regions of the DLPT to the lumbar ventral horn using anatomical studies that combined retrograde tracing with immunohistochemical identification of neurotransmitters. These anatomical studies further revealed that many of the noradrenergic neurons in the LC and adjacent regions of the DLPT of the cat that send projections to the spinal cord ventral horn also contain colocalized glutamate (Glu) or enkephalin (ENK). Recent studies from our laboratory suggest that Glu and ENK may function as cotransmitters with norepinephrine (NE) in the descending pathway from the DLPT. Electrical stimulation of the LC evokes a depolarizing response in spinal motoneurons that is only partially blocked by alpha 1 adrenergic antagonists. In addition, NE mimicks only the slowly developing and not the fast component of LC-evoked depolarization. Furthermore, the depolarization evoked by LC stimulation is accompanied by a decrease in membrane resistance, whereas that evoked by NE is accompanied by an increased resistance. That Glu may be a second neurotransmitter involved in LC excitation of motoneurons is supported by our observation that the excitatory response evoked in spinal cord ventral roots by electrical stimulation of the LC is attenuated by a non-N-methyl-D-aspartate glutamatergic antagonist. ENK may participate as a cotransmitter with NE to mediate LC effects on lumbar monosynaptic reflex (MSR) amplitude. Electrical stimulation of the LC has a biphasic effect on MSR amplitude, facilitation followed by inhibition. Adrenergic antagonists block only the facilitator effect of LC stimulation on MSR amplitude, whereas the ENK antagonist naloxone reverses the inhibition. The chemical heterogeneity of the cat DLPT system and the differential responses of motoneurons to the individual cotransmitters help to explain the diversity of postsynaptic potentials that occur following LC stimuli.

Animals↗
PubMed1992

A metabotropic L-glutamate receptor agonist: pharmacological difference between rat central neurones and crayfish neuromuscular junctions.

1. 2S,3S,4S-2-(carboxycyclopropyl)glycine (L-CCG-I), a conformationally restricted glutamate analogue, is a potent metabotropic L-glutamate receptor agonist in the mammalian central nervous system. 2. Depolarizing actions of L-CCG-I and trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD) in the newborn rat spinal motoneurone are temperature-sensitive, and are not depressed by 3-[(+/-)-2-carboxypiperazin-4-yl] propyl-1-phosphonic acid (CPP) and/or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). 3. L-CCG-I and trans-ACPD induced oscillatory responses in Xenopus oocytes injected with rat brain mRNA. Oocytes with oscillatory responses to L-CCG-I and trans-ACPD showed reversal potential of about -20 mV, which was very close to the equilibrium potential of chloride ions. 4. In rat hippocampal synaptoneurosomes, L-CCG-I stimulated phosphoinositide hydrolysis in a concentration dependent manner. L-CCG-I was less potent than quisqualate but more potent than trans-ACPD. 5. At low concentrations, L-CCG-I did not cause any depolarization of newborn rat spinal motoneurones, but reduced substantially amplitudes of monosynaptic reflexes. 6. At the crayfish neuromuscular junction L-CCG-I, acting presynaptically, reduced the amplitude of excitatory junctional potentials. This action was prevented by application of picrotoxin but not pertussis toxin. The actions of trans-ACPD differ from those of either L-CCG-I or ibotenate at the crayfish neuromuscular junction. 7. L-CCG-I has a potential to provide further useful information on metabotropic L-glutamate receptor function.

Amino Acids, Dicarboxylic↗
PubMed2006

Differential motor and electrophysiological outcome in rats with mid-thoracic or high lumbar incomplete spinal cord injuries.

We have investigated the motor changes in rats subjected to a moderate photochemical injury on mid-thoracic (T8) or high lumbar (L2) spinal cord segments. Fourteen days after surgery, L2 injured animals presented gross locomotor deficits (scored 10+/-2.8 in the BBB scale), decreased amplitude of motor-evoked potentials (MEPs) recorded on tibialis anterior (TA) and plantar (PL) muscles (24% and 6% of the preoperative mean values, respectively), reduced M wave amplitudes (75%, 62%), and also facilitated monosynaptic reflexes evidenced by an increase of the H/M amplitude ratio (158% and 563%). On the other hand, T8 injured animals had only slight deficits in locomotion (18+/-0.6 in the BBB scale), a minimal reduction in MEP amplitudes (78% and 71% in TA and PL muscles), normal M wave amplitudes, and a milder increase of the H/M ratio in the TA muscle (191%) but less pronounced in the PL muscle (172%). The percentage of spared tissue at the site of injury was similar in both experimental groups (L2: 79% and T8: 82%). Taken together, these results indicate that lumbar spinal injuries have more severe consequences on hindlimb motor output than injuries exerted on thoracic segments. The causes of this anatomical difference may be attributed to damage inflicted on the central pattern generator of locomotion resulting in dysfunction of lumbar motoneurons and altered spinal reflexes modulation.

Animals↗
PubMed2003

Involvement of the GABAergic system for Ptychodiscus brevis toxin-induced depression of synaptic transmission elicited in isolated spinal cord from neonatal rats.

The involvement of inhibitory transmitters for Ptychodiscus brevis toxin (PbTx)-induced depression of spinal synaptic transmission in neonatal rats was investigated. Stimulation of a dorsal root evoked monosynaptic reflex (MSR) and polysynaptic reflex (PSR) potentials in the segmental ventral root. The PbTx depressed the reflexes in a concentration-dependent manner and the depression was blocked by GABA(A) antagonist, bicuculline (1 microM). GABA also produced depression of the reflexes in a concentration-dependent manner. Simultaneous application of submaximal concentrations of PbTx (28 microM) and GABA (30 microM) enhanced the depression (>75%). In contrast, PbTx alone (28 microM) depressed the MSR and the PSR by 33 and 47%, respectively, and GABA (30 microM) alone depressed the reflexes by 30%. The N-methyl-D-aspartate receptor antagonist, DL-2-amino-5-phosphono-pentanoic acid (10 microM), blocked the PbTx-induced depression of MSR and also the enhancement of GABA response by PbTx. A glycine receptor antagonist, strychnine (1 microM), failed to block the depression by the toxin up to 28 microM; however, the depression was attenuated significantly at 84 microM of the toxin. The results indicate that PbTx depressed the spinal reflexes via GABA(A) receptors. Furthermore, the potentiation of GABAergic action by PbTx requires the N-methyl-D-aspartate dependent mechanism.

Animals↗
PubMed1991

Locus coeruleus control of spinal motor output.

Using electrophysiological techniques, we investigated the functional properties of the coeruleospinal system for regulating the somatomotor outflow at lumbar cord levels. Many of the fast-conducting, antidromically activated coeruleospinal units were shown to exhibit the alpha 2-receptor response common to noradrenergic locus coeruleus (LC) neurons. Electrically activating the coeruleospinal system potentiated the lumbar monosynaptic reflex and depolarized hindlimb flexor and extensor motoneurons via an alpha 1-receptor mechanism. The latter synaptically induced membrane depolarization was mimicked by norepinephrine applied iontophoretically to motoneurons. That LC inhibited Renshaw cell activity and induced a positive dorsal root potential at the lumbar cord also reinforced LC's action on motor excitation. We conclude that LC augments the somatomotor output, at least in part, via an alpha 1-adrenoceptor-mediated excitation of ventral horn motoneurons. Such process is being strengthened by LC's suppression of the recurrent inhibition pathway as well as by its presynaptic facilitation of afferent impulse transmission at the spinal cord level.

Action Potentials↗
PubMed2003

Deprenyl blocks the aglycemia-induced depression of the synaptic transmission but not the ischemia-induced depression in neonatal rat spinal cord in vitro.

The protective action of R-(-)-deprenyl against the aglycemia (glucose-free) and the ischemia (glucose-free and O2-free)-induced changes in the synaptic transmission was investigated. The in vitro "glucose-free and O2-free" condition mimics in vivo ischemia where there is a deficiency of O2 and energy substrate, hence the term ischemia was used. The monosynaptic reflex (MSR) and polysynaptic reflex (PSR) potentials were elicited in the ventral root by stimulating the corresponding dorsal root in an isolated spinal cord from the neonatal rat. Aglycemia and ischemia depressed the spinal reflexes in a time-dependent manner and abolished them within 30 min. The 50% depression of the reflexes (T-50) occurred around 25 min for aglycemia and 15 min for ischemia. Creatine phosphate, an energy supplement, attenuated the aglycemia- and ischemia-induced depression of the reflexes. The T-50 values for both the reflexes were around 40 and 25 min for aglycemia and ischemia, respectively. Deprenyl (10 microM) blocked the aglycemia-induced depression completely but failed to block the ischemia-induced depression. The present results indicate that aglycemia and ischemia abolished the synaptic transmission simultaneously and energy supplementation partially attenuated the depression. The protective effects of deprenyl against aglycemia may not be due to its MAO-B action and suggest for the involvement of non-MAO-B mechanisms.

Action Potentials↗
PubMed1998

The effect of FMRF-amide-like peptides on electrical activity in isolated mammalian spinal cord.

FMRFamide and seven FMRFamide-like peptides were manually synthesized on solid phase and their effects tested upon the amplitude of the dorsal root-ventral root monosynaptic reflex (MSR) and dorsal horn field potentials (FP) in an isolated preparation of rat spinal cord. FLFQPQRFamide (NPFF) and AGEGLSSPFWSLAAPQRFamide (NPAF) both depressed a fast component of the FP with similar potencies. FMRFamide also inhibited the FP but its potency was much lower. NPFF and NPAF potentiated the amplitude of the MSR while FMRFamide had no effect. PQRFamide, PFRFamide, FFRFamide, DPQRFamide and Fmoc-FLFQPQRFamide were also examined on the MSR. PQRFamide and PFRFamide potentiated the MSR whereas FFRFamide and DPQRFamide caused a small depression at high concentrations. The increase in amplitude of the MSR induced by NPFF was completely abolished when the N-terminal was left protected with an Fmoc-group. The results suggest that PFRFamide and PQRFamide may act as agonists of NPFF and NPAF whereas the other peptides did not show such activity.

Amino Acid Sequence↗
PubMed2003

Which stages of processing are speeded by a warning signal?

This article reviews psychophysiological and behavioral studies that attempt to identify which stages of processing are speeded by a neutral warning signal (WS), that is to say, one that conveys no information about the nature of the imperative stimulus or the required response. Experiments involving the lateralized readiness potential (LRP) provide evidence against the widely held view that warning effects on reaction time (RT) are due to facilitation of low-level motor processes. Studies of modality-specific evoked potentials similarly rule out a locus within sensory-perceptual processing. It is concluded that the speeding of RT by a neutral WS is most likely due to nonspecific motor priming within an early phase of response selection. In addition, fast-guess responses, in which subjects choose a response without fully analyzing the stimulus, are assumed to contribute to warning effects.

Animals↗
PubMed2002

Facilitation of the spinal H-reflex by auditory stimulation in dyslexic adults.

Dyslexic subjects show a variety of mild sensory and motor deficits that have been assumed to reflect dysfunction of the large-diameter 'magnocells' in different parts of the brain. Hearing as a warning sense relies on rapidly-conducting fibers, and on the basis of the magnocellular deficit theory, we wondered whether auditory alerting would be weakened in dyslexic adults. We quantified the strength of sound-induced spinal facilitation in seven dyslexic and eight normal-reading adults by measuring the amplitudes of H-reflex, a monosynaptic spinal reflex, after loud binaural sounds. The audiospinal facilitation was of similar strength in dyslexic and control adults, indicating normal auditory alerting via cerebrospinal pathways. The slightly prolonged facilitation in dyslexics agrees with the dyslexics' general sluggishness of sensorimotor processing.

Acoustic Stimulation↗
PubMedDate not supplied

Motor conduction velocity and the Hoffman reflex in diabetes.

The motor conduction velocity (MCV) and various parameters of the Hoffman reflex were studied in 55 diabetics compared to a control population of the same age. In the diabetics there were statistically significant alterations of the MCV, the Hmax/Mmax ratio and the H index, which are closely connected. These changes were more precise when there were clinical signs of neuropathy (absence of the Achilles reflex) but they still existed in the absence of signs. The older the diabetics, the more the electro-physiological parameters were altered. However, the H index is abnormal earlier than the Hmax-Mmax ratio or the MCV. Changes in the excitability cycle to double shock involve mainly phase IV of secondary facilitation and may be related to central disturbances.

Adult↗
PubMed1984

[Tendon areflexia in congenital myopathies accompanied by atrophy of type I fibers. Electrophysiologic study].

A predominance and/or an atrophy of type I fibers and a loss of deep tendon reflexes are often observed in different types of congenital myopathy. Various data indicate that both findings can be linked: dysfunction of the myotatic reflex can induce predominant involvement of type I fibers. In order to specify the mechanism of the loss of tendon reflex, an investigation of the Hoffmann reflex (H reflex) was performed in one case of centronuclear myopathy and in one case of congenital type fiber disproportion with type I hypertrophy. The Achilles tendon reflex was absent but the H reflex showed normal recruitment amplitude and latency. The Jendrassik maneuver reinforced the H reflex. These results indicate the involvement of muscle spindles or impairment of the fusimotor system. Nuclear bag intrafusal fibers have common characteristics with type I extrafusal fibers. Both types of fibers could be involved simultaneously in congenital myopathies, thus explaining the loss of tendon reflex.

Child↗