scholarly journals Glucose is an adequate energy substrate for the depolarizing action of GABA and glycine in the neonatal rat spinal cord in vitro

2012 ◽  
Vol 107 (11) ◽  
pp. 3107-3115 ◽  
Author(s):  
Rémi Bos ◽  
Laurent Vinay
Keyword(s):  
Spinal Cord ◽  
Energy Supply ◽  
Reversal Potential ◽  
Neonatal Rat ◽  
Lumbar Spinal Cord ◽  
Primary Afferent ◽  
Artificial Cerebrospinal Fluid ◽  
High Concentrations ◽  
Lumbar Spinal

In vitro studies have repeatedly demonstrated that the neurotransmitters γ-aminobutyric acid (GABA) and glycine depolarize immature neurons in many areas of the CNS, including the spinal cord. This widely accepted phenomenon was recently challenged by experiments showing that the depolarizing action of GABA on neonatal hippocampus and neocortex in vitro was prevented by adding energy substrates (ES), such as the ketone body metabolite dl-β-hydroxybutyric acid (DL-BHB), lactate, or pyruvate to the artificial cerebrospinal fluid (ACSF). It was suggested that GABA-induced depolarizations in vitro might be an artifact due to inadequate energy supply when glucose is the sole energy source, consistent with the energy metabolism of neonatal rat brain being largely dependent on ESs other than glucose. Here we examined the effects of these ESs (DL-BHB, lactate, pyruvate) on inhibitory postsynaptic potentials (IPSPs) recorded from neonatal rat lumbar spinal cord motoneurons (MNs), in vitro. We report that supplementing the ACSF with physiologic concentrations of DL-BHB, lactate, or pyruvate does not alter the reversal potential of IPSPs ( EIPSP). Only high concentrations of pyruvate hyperpolarized EIPSP. In addition, the depolarizing action of GABA on primary afferent terminals was not affected by supplementing the ACSF with ES at physiologic concentrations. We conclude that depolarizing IPSPs in immature MNs and the primary afferent depolarizations are not caused by inadequate energy supply. Glucose at its standard concentration appears to be an adequate ES for the neonatal spinal cord in vitro.

Small-caliber afferent inputs produce a heterosynaptic facilitation of the synaptic responses evoked by primary afferent A-fibers in the neonatal rat spinal cord in vitro

1993 ◽  
Vol 69 (6) ◽  
pp. 2116-2128 ◽  
Author(s):  
S. W. Thompson ◽  
C. J. Woolf ◽  
L. G. Sivilotti
Keyword(s):  
Spinal Cord ◽  
Dorsal Root ◽  
Fiber Strength ◽  
Conditioning Stimulus ◽  
Neonatal Rat ◽  
Primary Afferent ◽  
Synaptic Potentials ◽  
C Fiber ◽  
Afferent Inputs

1. The effect of brief primary afferent inputs on the amplitude and duration of the synaptic potentials evoked in ventral horn (VH) neurons by the activation of other unconditioned primary afferents was studied by current-clamp intracellular recording in the neonatal rat hemisected spinal cord in vitro. Low-frequency (1 Hz) trains of stimulation were applied to a lumbar dorsal root (Conditioning root) for 20-30 s. Test excitatory synaptic potentials (EPSPs) were evoked by single electrical shocks applied to an adjacent Test dorsal root. 2. Test and Conditioning inputs were generated at stimulation strengths sufficient to activate A beta-, A delta- and C-afferent fibers successively. At A delta- and C-fiber strength the EPSPs lasted for 4-6 s, and, during the repetitive Conditioning inputs, these summated to produce a progressively incrementing cumulative depolarization that slowly decayed back to the control Vm over tens of seconds. 3. Dorsal root conditioning produced heterosynaptic facilitation, defined as an enhancement of Test EPSPs above their DC matched controls, in 7 out of 20 neurons. To facilitate the unconditioned afferent input, the intensity of conditioning stimulation had to exceed the threshold for the activation of thin myelinated (A delta) afferents: conditioning at A beta-fiber strength had no effect, whereas A delta- and C-fiber strength conditioning were equally effective. 4. Heterosynaptic facilitation of only A beta- or A delta-fiber-evoked Test EPSPs was observed, no enhancement of C-fiber strength Test EPSPs could be demonstrated. The facilitation manifested as increases in the EPSP peak amplitude, area or the number of action potentials evoked. 5. Conditioning trials that produced heterosynaptic facilitation generated cumulative depolarizations larger than those produced by ineffective conditioning trials (9.1 +/- 3.1 vs. 3.3 +/- 0.5 mV after 20 s conditioning at resting Vm, mean +/- SE, n = 6 and 13, respectively; P < 0.05). The slope of the Vm trajectory during the summation of the conditioning EPSPs was higher in trials resulting in heterosynaptic facilitation, at 0.31 +/- 0.10 mV/s in neurons with heterosynaptic facilitation and 0.06 +/- 0.02 mV/s in cells without heterosynaptic facilitation (P < 0.05). 5. Four of the 20 VH neurons in our sample responded to A delta/C-fiber conditioning with action-potential windup: all 4 also displayed heterosynaptic facilitation. 6. Heterosynaptic facilitation decayed after the completion of the conditioning stimulus with a time course that was parallel to but not superimposable on that of the slow Vm depolarization evoked by the conditioning.(ABSTRACT TRUNCATED AT 400 WORDS)

Concussive head injury producing suppression of sensory transmission within the lumbar spinal cord in cats

1985 ◽  
Vol 63 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Yoichi Katayama ◽  
James D. Glisson ◽  
Donald P. Becker ◽  
Ronald L. Hayes
Keyword(s):  
Spinal Cord ◽  
Head Injury ◽  
Dorsal Root ◽  
Lumbar Spinal Cord ◽  
Primary Afferent ◽  
Sensory Transmission ◽  
General Response ◽  
Lumbar Spinal ◽  
Dorsal Root Potentials ◽  
Root Stimulation

✓ This study examines the effects of concussive levels of a fluid-percussion head injury on sensory transmission within the lumbar spinal cord of the cat. Primary afferent depolarization (PAD) was suppressed for 2 to 5 minutes following injury, as assessed by dorsal root potentials and augmentation of antidromic dorsal root potentials, both evoked by stimulation of adjacent dorsal roots. Polysynaptic reflex discharges in ventral root potentials evoked by dorsal root stimulation were also profoundly suppressed during this same period, even when spontaneous and monosynaptic reflex discharges were facilitated. Changes in PAD produced by injury were abolished by spinal cord transection, but were not affected by midpontine transection. These findings suggest that concussive head injury can produce suppression of segmental sensory transmission by neurally mediated processes involving the bulbar brain stem. Recordings of dorsal root resting potentials, antidromic dorsal root potentials, and reductions of antidromic dorsal root potentials induced by tetanic root stimulation indicated that depressed segmental sensory function produced by injury was due to suppression of postsynaptic interneuronal transmission rather than to excitability changes in primary afferent fibers. Somatosensory cortical potentials evoked by dorsal root stimulation were profoundly depressed at the same time as segmental sensory transmission was suppressed, suggesting that suppressed segmental sensory transmission may also contribute to suppression of ascending sensory transmission. It is hypothesized that transmission failure of interneuronal systems in the initial period following insult may be a general response occurring in wide areas of the central nervous system, and not restricted to areas to which mechanical stress is directly applied. This response pattern may result from indiscriminate activation of interconnected excitatory and inhibitory elements of interneuronal systems.

scholarly journals Berberine alleviates visceral hypersensitivity in rats by altering gut microbiome and suppressing spinal microglial activation

2021 ◽  
Author(s):  
Jin-dong Zhang ◽  
Jiao Liu ◽  
Shi-wei Zhu ◽  
Yuan Fang ◽  
Ben Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Gut Microbiome ◽  
Microglial Activation ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Visceral Hypersensitivity ◽  
Lumbar Spinal Cord ◽  
Microbial Composition ◽  
Lumbar Spinal

AbstractAccumulating evidence shows that agents targeting gut dysbiosis are effective for improving symptoms of irritable bowel syndrome (IBS). However, the potential mechanisms remain unclear. In this study we investigated the effects of berberine on the microbiota-gut-brain axis in two rat models of visceral hypersensitivity, i.e., specific pathogen-free SD rats subjected to chronic water avoidance stress (WAS) and treated with berberine (200 mg· kg−1 ·d−1, ig, for 10 days) as well as germ-free (GF) rats subjected to fecal microbiota transplantation (FMT) from a patient with IBS (designated IBS-FMT) and treated with berberine (200 mg· kg−1 ·d−1, ig, for 2 weeks). Before the rats were sacrificed, visceral sensation and depressive behaviors were evaluated. Then colonic tryptase was measured and microglial activation in the dorsal lumbar spinal cord was assessed. The fecal microbiota was profiled using 16S rRNA sequencing, and short chain fatty acids (SCFAs) were measured. We showed that berberine treatment significantly alleviated chronic WAS-induced visceral hypersensitivity and activation of colonic mast cells and microglia in the dorsal lumbar spinal cord. Transfer of fecal samples from berberine-treated stressed donors to GF rats protected against acute WAS. FMT from a patient with IBS induced visceral hypersensitivity and pro-inflammatory phenotype in microglia, while berberine treatment reversed the microglial activation and altered microbial composition and function and SCFA profiles in stools of IBS-FMT rats. We demonstrated that berberine did not directly influence LPS-induced microglial activation in vitro. In both models, several SCFA-producing genera were enriched by berberine treatment, and positively correlated to the morphological parameters of microglia. In conclusion, activation of microglia in the dorsal lumbar spinal cord was involved in the pathogenesis of IBS caused by dysregulation of the microbiota–gut–brain axis, and the berberine-altered gut microbiome mediated the modulatory effects of the agent on microglial activation and visceral hypersensitivity, providing a potential option for the treatment of IBS.

5-HT Modulation of Multiple Inward Rectifiers in Motoneurons in Intact Preparations of the Neonatal Rat Spinal Cord

2001 ◽  
Vol 85 (2) ◽  
pp. 580-593 ◽  
Author(s):  
Ole Kjaerulff ◽  
Ole Kiehn
Keyword(s):  
Spinal Cord ◽  
Neonatal Rat ◽  
Inward Rectification ◽  
Lumbar Spinal Cord ◽  
Slow Time ◽  
Biophysical Parameters ◽  
Time Constants ◽  
Low Concentrations ◽  
Order Of Magnitude ◽  
Lumbar Spinal

This study introduces novel aspects of inward rectification in neonatal rat spinal motoneurons (MNs) and its modulation by serotonin (5-HT). Whole cell tight-seal recordings were made from MNs in an isolated lumbar spinal cord preparation from rats 1–2 days of age. In voltage clamp, hyperpolarizing step commands were generated from holding potentials of −50 to −40 mV. Discordant with previous reports involving slice preparations, fast inward rectification was commonly expressed and in 44% of the MNs co-existed with a slow inward rectification related to activation of I h. The fast inward rectification is likely caused by an I Kir. Thus it appeared around E K and was sensitive to low concentrations (100–300 μM) of Ba2+ but not to ZD 7288, which blocked I h. Both I Kir and I h were inhibited by Cs2+ (0.3–1.5 mM). Extracellular addition of 5-HT (10 μM) reduced the instantaneous conductance, most strongly at membrane potentials above E K. Low [Ba2+] prevented the 5-HT–induced instantaneous conductance reduction below, but not that above, E K. This suggests that 5-HT inhibits I Kir, but also other instantaneous conductances. The biophysical parameters of I h were evaluated before and under 5-HT. The maximal I h conductance, G max, was 12 nS, much higher than observed in slice preparations. G maxwas unaffected by 5-HT. In contrast, 5-HT caused a 7-mV depolarizing shift in the activation curve of I h. Double-exponential fits were generally needed to describe I h activation. The fast and slow time constants obtained by these fits differed by an order of magnitude. Both time constants were accelerated by 5-HT, the slow time constant to the largest extent. We conclude that spinal neonatal MNs possess multiple forms of inward rectification. I h may be carried by two spatially segregated channel populations, which differ in kinetics and sensitivity to 5-HT. 5-HT increases MN excitability in several ways, including inhibition of a barium-insensitive leak conductance, inhibition of I Kir, and enhancement of I h. The quantitative characterization of these effects should be useful for further studies seeking to understand how neuromodulation prepares vertebrate MNs for concerted behaviors such as locomotor activity.

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