Effect of corticosteroid hormones on electrical activity in rat hippocampus.

Pyramidal neurons in the rat CA1 hippocampal area contain both mineralocorticoid (MR) and glucocorticoid receptors (GR) which bind the endogenous adrenal steroid corticosterone with differential affinity. With intracellular electrophysiological recording techniques we have investigated how corticosterone affects the membrane properties of these cells. We observed that low doses (1 nM) of corticosterone or aldosterone can, through MR, reduce the spike frequency accommodation and afterhyperpolarization (AHP) evoked by a short depolarizing current in pyramidal neurons. As the accommodation/AHP can be considered as an intrinsic mechanism of CA1 neurons to attenuate transmission of excitatory input, the MR-mediated action might potentially enhance cellular excitability in the CA1 area. Higher doses of corticosterone or selective glucocorticoids were able to reverse the MR-mediated effect on accommodation/AHP, eventually increasing particularly the amplitude of the AHP. GR-mediated events may thus potentially suppress excitability in the hippocampal CA1 area. Not only current- but also transmitter-induced membrane effects were affected by the steroids. Firstly, GR-ligands were able to suppress a temporary noradrenaline-evoked decrease in accommodation/AHP. Secondly, membrane hyperpolarizations induced by serotonin were reduced by MR-agonists. We propose that cellular excitability in the hippocampus is at least partly under control of coordinative, antagonistic MR- and GR-mediated effects on electrical activity.     

Effects of dexamethasone on the electrical activity of spinal neurons in rats with the transected sciatic nerve

Effects of the glucocorticoid hormone dexamethasone on the reflex discharges in the lumbar ventral roots and background activity (BA) of single neurons in the dorsal laminae of spinal grey were studied in rats after transection of the sciatic nerve. Administration of the hormone during early post-traumatic period (up to seven days) evoked no significant changes in the amplitude of increased (due to the postdenervation hyperreflexia) monosynaptic discharges on the side of nerve transection. At the same time, the monosynaptic discharges grew by 150–170% on the intact side. During later post-transection periods (up to 35 days), when ventral root reflex discharges were suppressed, dexamethasone facilitated reflex transmission via the polysynaptic segmental pathways on both the operated and intact sides. Nonetheless, the monosynaptic component of reflex discharges on the injured side did not recover. Dexamethasone treatment resulted in an increase in the number of BA-generating interneurons within the superficial dorsal horn laminae, and in a decrease in the proportion of units generating bursting activity (possibly of pathological nature).Neirofiziologiya/Neurophysiology, Vol. 27, No. 1, pp. 26–31, January–February, 1995.     

Changes within maturing neurons limit axonal regeneration in the developing spinal cord

Embryonic birds and mammals display a remarkable ability to regenerate axons after spinal injury, but then lose this ability during a discrete developmental transition. To explain this transition, previous research has emphasized the emergence of myelin and other inhibitory factors in the environment of the spinal cord. However, research in other CNS tracts suggests an important role for neuron-intrinsic limitations to axon regeneration. Here we re-examine this issue quantitatively in the hindbrain-spinal projection of the embryonic chick. Using heterochronic cocultures we show that maturation of the spinal cord environment causes a 55% reduction in axon regeneration, while maturation of hindbrain neurons causes a 90% reduction. We further show that young neurons transplanted in vivo into older spinal cord can regenerate axons into myelinated white matter, while older axons regenerate poorly and have reduced growth cone motility on a variety of growth-permissive ligands in vitro, including laminin, L1, and N-cadherin. Finally, we use video analysis of living growth cones to directly document an age-dependent decline in the motility of brainstem axons. These data show that developmental changes in both the spinal cord environment and in brainstem neurons can reduce regeneration, but that the effect of the environment is only partial, while changes in neurons by themselves cause a nearly complete reduction in regeneration. We conclude that maturational events within neurons are a primary cause for the failure of axon regeneration in the spinal cord.     

Effects of hydrocortisone on electrical activity of the cat spinal cord

The effect of the corticosteroid hormone hydrocortisone on electrical activity in the lumbosacral portion of the spinal cord was studied in acute experiments on cats anesthetized with urethane and chloralose and immobilized with succinylcholine. The amplitude of mono- and polysynaptic discharges arising in the ventral roots in response to stimulation of various afferents of the animal's hind limb was increased by a statistically significant degree after intravenous injection of the hormone. The potentiating action of the hormone was strongest and most stable with respect to early and late postsynaptic potentials of the spinal cord. The dorsal cord potentials were not significantly changed by hydrocortisone. Spontaneous unit activity in the intermediate nucleus of the spinal cord rose sharply after administration of hydrocortisone. Before the action of the hormone the mean frequency of spontaneous discharges of 46 neurons was 7.91/sec, rising to 20/sec after the injection. The number of neurons with a high spontaneous firing rate also was increased. Prolonged extracellular recording of the spontaneous activity of the same neuron before and after administration of hydrocortisone also revealed a marked increase in the frequency of its discharges. The results are evidence of the activating effect of hydrocortisone on spinal interneuronal activity.     

Increased number of neurons in the cervical spinal cord of aged female rats

In the brain, specific signaling pathways localized in highly organized regions called niches allow the persistence of a pool of stem and progenitor cells that generate new neurons in adulthood. Much less is known about the spinal cord where a sustained adult neurogenesis is not observed. Moreover, there is scarce information concerning cell proliferation in the adult mammalian spinal cord and virtually none in aging animals or humans. We performed a comparative morphometric and immunofluorescence study of the entire cervical region (C1-C8) in young (5 mo.) and aged (30 mo.) female rats. Serum prolactin (PRL), a neurogenic hormone, was also measured. Gross anatomy showed a significant age-related increase in size of all of the cervical segments. Morphometric analysis of cresyl violet stained segments also showed a significant increase in the area occupied by the gray matter of some cervical segments of aged rats. The most interesting finding was that both the total area occupied by neurons and the number of neurons increased significantly with age, the latter increase ranging from 16% (C6) to 34% (C2). Taking the total number of cervical neurons the age-related increase ranged from 19% (C6) to 51% (C3), C3 being the segment that grew most in length in the aged animals. Some bromodeoxyuridine positive-neuron specific enolase negative (BrdU(+)-NSE(-)) cells were observed and, occasionally, double positive (BrdU(+)-NSE(+)) cells were detected in some cervical segments of both young and aged rats groups. As expected, serum PRL increased markedly with age. We propose that in the cervical spinal cord of female rats, both maturation of pre-existing neuroblasts and/or possible neurogenesis occur during the entire life span, in a process in which PRL may play a role.     

Changes in the levels of activity of spinal neurons after long-lasting vibrational stimulation of the shin muscles in rats

Vibrational stimulation of the tendon of the mm.gastrocnemius+soleus (100 sec^–1) in rats anesthetized with chloral hydrate (400 mg/kg) resulted in the appearance of considerable Fos immunoreactivity in the lumbar spinal cord (L1-L6), as compared with that in intact animals. Total densities of Fos-immunopositive (Fos-ip) neurons in each of the examined segments were higher than 40 units per 40-μm-thick slice; the respective index reached the maximum at the L4 level (78.9 ± 2.3 cells). Most Fos-ip neurons were localized in laminae 4 to 7 of the gray matter, both ipsi- and contralaterally with respect to the side of stimulation (28.5 ± 0.6 and 28.4 ± 0.6, respectively). Single Fos-ip motoneurons were found bilaterally in the ventral horn motor nuclei. Thus, activation of muscle spindle receptors induced by vibrational stimulation applied to the Achilles tendon induces noticeable bilateral c-fos expression in spinal neuronal networks related to transmission of proprioceptive muscle-born impulsation.     

The effects of hyposmolality on spinal cord activity

The consequences of decreases in osmotic pressure were investigated using the isolated, hemisected frog spinal cord. The lateral column evoked ventral root response (LC-VRR) was depressed by a decrease in osmolality secondary to a decrease in the Na⁺ concentration in the bathing medium. This depression resulted from neither a depression of motoneuronal excitability nor a depression of central axonal conduction but rather from an increased excitability of lateral column terminals. The depression of the LC-VRR and augmentation of the lateral column terminal excitability were reversed by picrotoxin (10-⁴ M). Results are discussed in terms of the possible roles of endogenous gamma-aminobutyric acid (GABA) and extracellular K⁺ in the effect produced by the hyposmotic (low Na⁺) media.     

急性脊髓损伤后大鼠电刺激运动诱发电位的变化

目的：比较不同程度脊髓损伤（SCI）与运动诱发电位（MEP）变化之间的关系,探索MEP检查在SCI早期诊断及预后中的价值。方法：27只雄性SD大鼠以改良Allen‘s打击法致伤T8－T9脊髓,按打击冲量随机分为空白对照组（n=5),SCI A组（50gcf,n=8),SCI B组（70gcf,n=8)和SCI C组（100gcf,n=6),采用单极经皮层电刺激,分别于损伤前、伤后即刻、15min、30min、1h、3h和6h连续观察scMEP变化,并计算脊髓出血坏死区域占脊髓横截面积的比率。结果：对照组MEP无显著改变,SCI A组和SCI B组动物MEP早成份波幅立即减低或消失,以后有所恢复,晚成份波消失后未再出现。SCI C组动物除2只大鼠SCI后MEP仍有所恢复外,其余动物再未出现MEP波。脊髓损伤随打击冲量增大而增加,与伤后1h scMEP最大波幅呈显著相关（r=-0.821)。结论：SCI后scMEP的变化程度与打击冲量和脊髓病理损伤面积相关,提示scMEP可以作为一种脊髓功能检测的客观指标。     

Synaptic processes in spinal cord interneurons under rubrospinal effects

Synaptic processes of the spinal cord interneurons under rubrospinal effects have been investigated. A recording was made of 156 interneurons from the different parts of the gray matter, 111 of the interneurons were activated by descending effects from the red nucleus and 47 were not activated. Sixty nine interneurons of the first group responded only to rubrospinal impulsation and 42 neurons were also activated by afferent volleys. Interneurons activated only by the rubrospinal tract were located in the most lateral part of the VII Rexed's gray matter layer; the majority of interneurons activated by both rubrospinal and peripheral afferent volleys were located in the nucleus propius of the dorsal horn and the Cajal intermediate nucleus. The mean latencies of EPSP's and action potentials in interneurons activated only by a rubrospinal tract were 64±0.2 and 9.5±0.62 msec, respectively. The mean latency of EPSP's in motoneurons of flexor muscles was 10.3±0.62 msec and of IPSP's in motoneurons of extensor muscles, it was 11.5±1.28 msec. It is assumed that rubrospinal impulsation evokes excitatory PSP's in the motoneurons via the disynaptic pathway with the participation of special interneurons located in the lateral part of the VII layer. Inhibitory and late excitatory responses are, apparently, evoked via additional interneurons.A. A. Bogomolets Institute of Physiology of the Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 1, No. 2, pp. 158–166, September–October, 1969.     

Effect of local depression of inhibition on electrical activity of the spinal cord

The dorsal cord, dorsal root, and focal potentials in response to peripheral nerve stimulation were investigated in rats with local depression of inhibition in the left or right half of the lumbar segments produced by the action of tetanus toxin. The investigation was carried out at the stage of poisoning when excitation of the neuron population with disturbed inhibition caused generalized excitation of spinal and bulbar motoneurons. Experiments on spinal animals showed that if a cutaneous nerve is stimulated on the side affected by the toxin these responses have a greater amplitude and a much longer duration than those evoked by stimulation of the opposite nerve or responses in healthy rats. The maximal increase in amplitude and duration of the negative component of the focal potential corresponding to the time of the increased P wave of the dorsal cord potential was found in the ventral quadrant on the side affected by the toxin. Besides evoked focal potentials, spontaneous rhythmic negative waves also were recorded in this area. The mechanisms of spread of seizure activity from the focus of depressed inhibition are discussed and the structures generating spreading seizure activity are identified.     

Human spinal GABA neurons alleviate spasticity and improve locomotion in rats with spinal cord injury

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