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PubMed1989

TRH analog YM-14673 improves outcome following traumatic brain and spinal cord injury in rats: dose-response studies.

YM-14673 is a thyrotropin-releasing hormone (TRH) analog that has a modification of the N-terminal (pyroglutamyl) moiety of the tripeptide. It is longer acting than TRH and has substantially greater potency with regard to central facilitatory activity. In the present studies, the effect of YM-14673 was examined in rats following standardized traumatic brain or spinal cord injury. Pentobarbital-anesthetized animals were subjected to fluid-percussion-induced brain trauma to the parietal cortex or impact trauma to the thoracic spinal cord. After injury animals were randomly assigned to treatment with i.v. YM-14673 at varying doses--0.1 mg/kg (low), 1.0 mg/kg (moderate), or 10 mg/kg (high)--or equal volume physiological saline. Treatment with YM-14673 improved chronic neurological recovery after trauma in both injury models; optimal beneficial effects were found at a dose of 1.0 mg/kg. These findings confirm previous observations that TRH or TRH analogs may improve outcome after traumatic brain and spinal cord injury and are consistent with the hypothesis that TRH analogs preserving the C-terminus are effective in CNS trauma.

Animals↗
PubMed1989

Magnesium protects against neurological deficit after brain injury.

The biochemical factors that mediate secondary or delayed damage to the central nervous system (CNS) remain speculative. We have recently demonstrated that brain injury in rats causes a rapid decline in brain intracellular free magnesium (Mg2+) and total magnesium concentrations that is significantly correlated with the severity of injury. In order to further investigate the relationship between Mg2+ and brain injury, we examined the effect of Mg2+ treatment on posttraumatic neurological outcome following fluid-percussion brain injury (2.0 atm) in rats. Since administration of ATP-MgCl2 has been shown to be beneficial in a variety of models of organ ischemia, we also examined the efficacy of ATP-MgCl2 or ATP alone in the treatment of experimental brain injury. Animals treated with low (12.5 mumol) or high (125 mumol) dose MgCl2 at 30 min postinjury showed a significant dose-dependent improvement in neurological function when compared to saline-treated controls. Treatment with ATP-MgCl2 (12.5 mumol) or ATP alone (12.5 mumol) caused no significant improvement in chronic neurological outcome. MgCl2-treated animals showed no change in postinjury mean arterial blood pressure (MAP), whereas animals treated with either ATP-MgCl2 or ATP alone showed a transient but significant fall in MAP (P less than 0.01) during the drug-infusion period. Our results suggest that postinjury treatment with MgCl2 is effective in limiting the extent of neurological dysfunction following experimental traumatic brain injury in the rat.

Adenosine Triphosphate↗
PubMed1989

The effects of morphine and traumatic brain injury on central cholinergic neurons.

This study examined the effects of morphine and fluid percussion traumatic brain injury (TBI) on the activity of cholinergic neurons in specific areas of the rat brain 12 min after injury. Acetylcholine (ACh) turnover, used as an index of cholinergic neuronal activity, was determined using gas chromatography-mass spectrometry. Although morphine administration alone in general did not significantly affect ACh content and turnover in specific brain areas, morphine administered prior to TBI either prevented injury-induced changes in ACh turnover (dorsal pontine tegmentum) or actually reduced the rate constant for ACh utilization (kACh) and the turnover rate of ACh (TRACh) following injury (thalamus, amygdala, cingulate/frontal cortex, and hippocampus). Thus, the protective effects of morphine against enduring behavioral deficits following TBI may involve the inhibition of central cholinergic neurons.

Acetylcholine↗
PubMed1990

Excitatory amino acid receptor subtype binding following traumatic brain injury.

Sprague-Dawley rats were subjected to a moderate level (2.2 atm) of traumatic brain injury (TBI) using fluid percussion. Injured animals were allowed post-trauma survival periods of 5 min, 3 and 24 h. Regional glutamate receptor subtype binding was assessed with quantitative autoradiography in each group for N-methyl-D-aspartate (NMDA), quisqualate and kainate receptor subpopulations at approximately the -3.8 bregma level and compared to a sham control group. [3H]glutamate binding to the NMDA receptor was significantly (P less than 0.05) decreased at 3 h post-TBI in the hippocampal CA1 stratum radiatum, the molecular layers of the dentate gyri and the outer (layers 1-3) and inner (layers 5 and 6) overlying neocortex. NMDA receptor binding was significantly reduced in layers 5 and 6 of the neocortex at all post-trauma survival times but no further differences were seen in the hippocampi. No significant changes were observed with [3H]AMPA binding to quisqualate receptors and [3H]KA binding was significantly reduced only in layers 5 and 6 of the neocortex at 24 h after TBI. These data further confirm the pathological involvement of the NMDA receptor complex in brain regions selectively vulnerable to moderate levels of TBI in this model.

Animals↗
PubMed1991

Dynamic changes in local cerebral glucose utilization following cerebral conclusion in rats: evidence of a hyper- and subsequent hypometabolic state.

Following cerebral concussion, in which there is no evidence of direct morphological damage, cells are exposed to an increase in extracellular potassium as well as an accumulation of calcium. This concussion-induced ionic flux most likely alters the cellular energy demands thereby modifying metabolic processes. To investigate the metabolic changes after cerebral concussion, local cerebral metabolic rates for glucose (lCMRglc) utilizing [14C]2-deoxy-D-glucose were studied in rats (n = 98; 250-300 g) immediately, 30 min, 6 h, 1, 2, 3, 5 and 10 days following a unilateral frontoparietal fluid percussion (F-P) injury (3.7-4.3 atm). Compared to sham controls, animals exhibited bilateral hypermetabolism immediately following brain injury. However, this effect was more pronounced in structures ipsilateral to the site of F-P and was especially marked for the cerebral cortex (46.6-30.1% higher than control) and hippocampus (90.1-84.4% higher than control). By 30 min post-trauma many ipsilateral regions still showed evidence of hypermetabolism, although their lCMRglc had subsided. Beginning as early as 6 h following injury many regions within the ipsilateral cortex and hippocampus went into a state of metabolic depression (16.4-33.7% of control) which lasted for as long as 5 days. These results indicate that, although not mechanically damaged from the insult, cells exposed to concussive injury dramatically alter their metabolic functioning. This period of post-concussive metabolic dysfunction may delineate a period of time, following injury, during which cells are functionally compromised.

Animals↗
PubMed1991

Diffuse prolonged depression of cerebral oxidative metabolism following concussive brain injury in the rat: a cytochrome oxidase histochemistry study.

Utilizing a lateral fluid percussion injury as a model of cerebral concussion, rats were studied histochemically measuring the degree of cytochrome oxidase activity present within different structures at different times following injury. After concussion, the cerebral cortex ipsilateral to the site of injury exhibited a diffuse decrease in its level of chromotome oxidase (CO) activity beginning at as soon as one day and lasting for up to 10 days after the insult. The ipsilateral dorsal hippocampus also exhibited an injury-induced decrease in CO activity, however, it was not as severe as in the cortex. These results indicate that oxidative metabolism is depressed primarily within the cerebral cortex and hippocampus for several days following a cerebral concussion. We propose that this period of metabolic depression may delineate a period of time during which the injured brain is unable to function normally and thus would be vulnerable to a second insult.

Animals↗
PubMed1992

Postinjury scopolamine administration in experimental traumatic brain injury.

A single bolus dose of scopolamine (1.0 mg/kg) or saline (equal volume) was injected (i.p.) at 15, 30 or 60 min after fluid percussion traumatic brain injury in the rat. Scopolamine administered at 15 min postinjury significantly reduced beam walking deficits and body weight loss assessed for 5 days after injury. Scopolamine treatment at 30 or 60 min postinjury had no effect on behavioral outcome assessed for 5 days after injury. Plasma concentrations of scopolamine were measured with a radioreceptor assay. The plasma half-life for scopolamine was 21.6 min in injured rats and 17.3 min in normal rats (P less than 0.05). These results, along with evidence from previous studies, suggest that a brief period of excessive neuronal excitation can produce relatively long-lasting behavioral deficits. The temporal effectiveness of receptor antagonist intervention in this process appears to be brief.

Animals↗
PubMed1992

Blockade of acute hypertensive response does not prevent changes in behavior or in CSF acetylcholine (ACH) content following traumatic brain injury (TBI).

There is evidence that the blood-brain barrier (BBB) is breached following traumatic brain injury (TBI), allowing the unregulated entry of circulating neuroactive substances into the central nervous system. As the traumatic episode is typically associated with an acute hypertensive event, which in itself may alter BBB status, the effects of the blockade of TBI-associated hypertension on injury-associated behavioral and cerebrospinal fluid (CSF) neurochemical changes were assessed in rats. Animals were injected with either saline or hexamethonium 15 min prior to a moderate fluid percussion injury while under light methoxyflurane anesthesia. This dose of hexamethonium was demonstrated to block the hypertensive response to TBI. Pretreatment with hexamethonium prevented neither acute nor more enduring behavioral deficits observed after TBI. Hexamethonium did not prevent TBI-associated increases in CSF acetylcholine (ACh) content in separate group of rats sampled 12 min following TBI. Furthermore, histological inspection indicated that hexamethonium did not prevent TBI-induced disruption of the BBB, as assessed by intravascular horseradish peroxidase (HRP). Thus, blockade of the hypertensive response to TBI does not afford behavioral protection nor does it prevent changes in the BBB or CSF ACh content following TBI. TBI is in itself sufficient to modify behavior, neurochemistry and BBB function in the absence of hypertension.

Acetylcholine↗
PubMed1992

Post-traumatic selective stimulation of glycolysis.

Ventilated, chloralose anesthetized cats were subjected to 3.2 atmosphere fluid percussion injury and compared with sham operated controls. In both groups, global cerebral blood flow (CBF), cerebral metabolic rate of oxygen utilization (CMRO2), cerebral metabolic rate of glucose utilization (CMRG1), and 31P magnetic resonance spectroscopy (MRS) determinations of tissue pH (pHi) phosphocreatine (PCr), and inorganic phosphate (Pi) were measured before and 5, 15, 30, and 60 min post-trauma. Following trauma, pH decreased slightly 30 min following trauma and gradually returned to normal. CMRO2, CBF, and arterial pO2 remained at control values throughout the experiment while CMRG1 increased 243% at 5 min post-injury then rapidly returned to control values. This combination of acidosis and increased glucose utilization indicates that trauma causes a transient isolated increase in cerebral glycolysis and may be important to consider when investigating the etiology of post traumatic acidosis.

Animals↗
PubMed1992

Enduring suppression of hippocampal long-term potentiation following traumatic brain injury in rat.

This study investigated changes in synaptic responses (population spike and population EPSP) of CA1 pyramidal cells of the rat hippocampus to stimulation of the Schaffer collateral/commissural pathways 2-3 h after traumatic brain injury (TBI). TBI was induced by a fluid percussion pulse delivered to the parietal epidural space resulting in loss of righting responses for 4.90-8.98 min. Prior to tetanic stimulation, changes observed after the injury included: (1) decreases in population spikes threshold but not EPSP thresholds; (2) decreases in maximal amplitude of population spikes as well as EPSPs. TBI also suppressed long-term potentiation (LTP), as evidenced by reductions in post-tetanic increases in population spikes as well as EPSPs. Since LTP may reflect processes involved in memory formation, the observed suppression of LTP may be an electrophysiological correlate of enduring memory deficits previously demonstrated in the same injury model.

Animals↗
PubMed1993

Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study.

In order to determine the extent and duration of calcium (Ca2+) flux following a lateral fluid percussion brain injury in the rat, 45Ca autoradiography was used to study animals immediately, 6, 24 and 96 h after the insult. In addition, cell suspension studies were conducted to determine the extent of cellular flux of 45Ca. Optical density and/or scintillation counting was utilized to provide a relative measure of 45Ca accumulation within 20 different structures. The results indicated that in animals who exhibited no gross morphological damage, 45Ca accumulation following injury was exhibited primarily within the ipsilateral cerebral cortex, dorsal hippocampus and striatum. This accumulation continued for several days returning to control levels by the 4th day after injury. In animals who sustained morphological damage, the contusion site exhibited a marked accumulation of 45Ca which did not resolve spontaneously over the course of 4 days. We conclude from this work that Ca2+ flux is a major component of this experimental model of traumatic injury. Furthermore, that depending on the extent of cell damage, the accumulation of Ca2+ is regionally different. Finally, that even in an injury which by itself does not produce gross morphological tissue damage, accumulation of Ca2+ can continue for at least 48 h.

Animals↗
PubMed1993

The nootropic compound BMY-21502 improves spatial learning ability in brain injured rats.

Although long-lasting cognitive dysfunction often follows clinical traumatic brain injury (TBI), few pharmacologic regimens have been developed to treat post-traumatic cognitive deficits. We have previously shown that, in the rat, experimental lateral fluid-percussion (FP) brain injury induces a profound impairment in retrograde memory. In the present study, we characterized alterations in the ability of rats to learn a novel task following lateral FP brain injury and examined the potential modulatory effects of the nootropic cognitive enhancer BMY-21502 on post-injury learning. Male Sprague-Dawley rats were subjected to lateral (parasagittal) FP brain injury of moderate severity (2.4 atm) or sham surgery (no injury). On days 7 and 8 post-injury, animals were tested in a Morris water maze for their ability to learn to navigate to a submerged, invisible platform using external visual cues. BMY-21502 (10 mg/kg) or vehicle was administered 30 min prior to the first trial on both days. A highly significant (P < 0.001) impairment in post-injury learning was observed in vehicle-treated brain-injured animals compared with vehicle-treated sham animals. Injured animals treated with BMY-21502 at one week post-injury showed significantly (P < 0.05) improvement in post-injury learning ability compared to injured animals treated with vehicle. Paradoxically, in uninjured control animals BMY-21502 treatment appeared to worsen learning scores. The results of this study indicate that BMY-21502 may be useful for attenuating the dysfunction in learning ability that occurs following TBI.

Animals↗
PubMed1993

Combined scopolamine and morphine treatment of traumatic brain injury in the rat.

Previous studies have indicated that either scopolamine (1.0 mg/kg) or morphine (10.0 mg/kg) administered to rats prior to or soon after moderate fluid percussion traumatic brain injury (TBI) reduces behavioral deficits associated with injury. In this study, a series of experiments examined the effects of a combination of these drugs, as well as each drug individually, on behavioral outcome, brain temperature, and systemic physiological responses to TBI. Experiment I: a single systemic bolus injection of scopolamine (n = 10), morphine (n = 11), scopolamine plus morphine (n = 11), or saline (n = 10) was administered to rats 15 min prior to TBI. Animals were assessed on beam-walking behavioral performance for 5 days after injury. Scopolamine alone or morphine alone significantly reduced (P < 0.05) deficits produced by injury. Treatment with a combination of scopolamine and morphine provided greater protection on beam-walking behavioral measures than either drug alone. Experiment II: morphine raised brain temperature in uninjured rats (n = 5) to a mean of 39.3 degrees C +/- 0.3 by 60 min post-injection. Neither scopolamine (n = 5) nor scopolamine plus morphine (n = 5) altered brain temperature. Experiment III: scopolamine (n = 7) significantly raised heart rate for 5 min after injury. Saline (n = 8), morphine (n = 9) and scopolamine plus morphine (n = 7) significantly lowered heart rate after injury. All four groups had similar hypertensive responses to TBI which peaked at 10 s after injury. The results confirm that pharmacological blockade of muscarinic receptors or stimulation of mu opioid receptors reduces functional deficits associated with TBI.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Estrogen improves biochemical and neurologic outcome following traumatic brain injury in male rats, but not in females.

Phosphorus magnetic resonance spectroscopy was used in conjunction with neurologic motor function tests to assess the effects of estrogen on biochemical and neurologic outcome following traumatic brain injury in male and female rats. Male (n = 18) and female (n = 18) rats were randomly assigned into three groups, and 4 h prior to injury received either 17 beta-estradiol (144 micrograms/kg intraperitoneally), equal volume vehicle (30% ethanol in saline), or no treatment. Traumatic brain injury was induced at 2.8 atm using a fluid percussion injury device, and animals monitored for 4 h using phosphorus magnetic resonance spectroscopy to determine brain intracellular pH, free magnesium concentration and cytosolic phosphorylation potential. Males treated with estrogen demonstrated a significant improvement in free magnesium concentration, and slightly improved values of cytosolic phosphorylation potential after trauma when compared to controls. There was also a significant improvement in post-traumatic motor function at 1 week after trauma. In contrast, estrogen treatment in females lowered cytosolic phosphorylation potential after trauma, but did not affect free magnesium concentration after trauma. Mortality in all female groups was significantly worse than in males. We conclude that estrogen is protective in males, but exacerbates brain injury in females through effects mediated by estrogen receptor binding.

Animals↗
PubMed1995

Neuroprotective effects of 619C89, a use-dependent sodium channel blocker, in rat traumatic brain injury.

Release of the excitatory amino acid (EAA) neurotransmitter glutamate has been implicated in secondary tissue damage following central nervous system (CNS) trauma and ischemia. The present study evaluated the neuroprotective actions of 619C89, a sodium channel blocker that inhibits ischemia-induced glutamate release, on traumatic brain injury (TBI) in rats using a lateral fluid percussion model. Various motor-related behavioral outcomes were used to evaluate neurologic function. Glial fibrillary acidic protein (GFAP) immunostaining and Cresyl violet staining were used to assess the histological changes. Treatment with 619C89, at a dose of 30 mg/kg administered intravenously 15 min before brain injury, significantly attenuated behavioral deficits at 24 h and 1 week. At 2 weeks, neuronal loss in the CA1 and CA3 pyramidal cell layers of the hippocampus was significantly decreased by 619C89 administration. Treatment with this compound also significantly attenuated increases in GFAP-immunoreactivity in both ipsilateral and contralateral CA1 regions. The present results suggest a potential therapeutic role for sodium channel blockade and/or glutamate release inhibition in the treatment of TBI.

Animals↗
PubMed1995

Lactate accumulation following concussive brain injury: the role of ionic fluxes induced by excitatory amino acids.

During the first few minutes following traumatic brain injury, cells are exposed to an indiscriminate release of glutamate from nerve terminals resulting in a massive ionic flux (e.g., K+ efflux) via stimulation of excitatory amino acid (EAA)-coupled ion channels. The present study was undertaken to elucidate the causal relationship between these ionic shifts and lactate accumulation in the injured brain, by examining the effects of ouabain (an inhibitor of Na+/K+-ATPase), Ba2+ (an inhibitor or non-energy-dependent glial K+ uptake) and kynurenic acid (KYN; a broad-spectrum EAA antagonist) on lactate accumulation. Two microdialysis probes were placed bilaterally in the rat parietal cortex. One was perfused with a test drug (1.0 mM ouabain, 2.0 mM Ba2+ or 10 mM KYN) and the other with Ringer's solution (control) for 30 min prior to injury. Following a 2.2-2.7 atm fluid-percussion injury, lactate levels in the dialysate increased (up to 116.6% above baseline) for the first 16 min and returned to baseline levels within 20 min after injury. This lactate accumulation was attenuated by preinjury administration of ouabain and KYN and was prolonged by Ba2+ administration. These findings indicate that lactate accumulations following concussive brain injury is a result of increased glycolysis which supports ion-pumping mechanisms, thereby, restoring the ionic balance which was disrupted by stimulation of EAA-coupled ion channels.

Animals↗
PubMed1994

Traumatic injury induces interleukin-6 production by human astrocytes.

The brain is being evaluated as a de novo source of cytokines. Because recent evidence indicates that interleukin-6 (IL-6) may influence blood-brain barrier function and vascular permeability, we have sought to determine whether mechanical injury can directly induce in situ cerebral IL-6 production. Adult human astrocyte cultures were subjected to mechanical injury by the in vitro method of fluid percussion barotrauma, developed in our laboratory. Serial supernatant samples were collected for 8 h and evaluated for IL-6 activity using a proliferation assay employing the dependent B cell hybridoma cell line, B9. At optimum injury, the IL-6 level became significantly (P < 0.0001, analysis of variance) elevated from baseline 2 h after trauma and continued to increase over the observation period. Our study shows that following mechanical injury human astrocytes produce IL-6, which may contribute to post-traumatic cerebrovascular dysfunction. Elucidating the precise role of intracerebral cytokines is essential to our understanding of the mechanism responsible for post-traumatic cerebrovascular dysfunction.

Astrocytes↗
PubMed1994

Traumatic brain injury causes a decrease in M2 muscarinic cholinergic receptor binding in the rat brain.

Numerous studies indicate that an acute, excessive activation of muscarinic acetylcholine receptors (mAChR) contributes to the pathophysiological sequela of TBI. The present study examined the effect of moderate fluid percussion traumatic brain injury (TBI) on binding to M1 and M2 mAChR subtypes in the hippocampal formation and adjacent cortex using quantitative autoradiography. Injured animals along with concurrent controls were sacrificed by in situ freezing at 3 h or 24 h following TBI. Slide-mounted tissue sections were incubated in either [3H]pirenzepine (23 nM) for M1 or [3H]AFDX384 (9 nM) for M2 mAChR subtype labeling. Binding of [3H]pirenzepine to the M1 mAChR subtype was not significantly altered by TBI when compared to sham-injured animals. [3H]AFDX384 binding to the M2 mAChR subtype was significantly decreased at 24 h in hippocampal CA2-3 region and dorsal blade of the dentate gyrus (P < 0.05). The differences observed between M1 and M2 subtypes suggests that these muscarinic subtypes may differentially contribute to the pathophysiology of TBI.

Animals↗