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PubMed1995

Differential recovery of volitional motor function, lateralized cognitive function, dopamine agonist-induced rotation and dopaminergic parameters in monkeys made hemi-parkinsonian by intracarotid MPTP infusion.

There is still controversy regarding the frequency and extent of spontaneous functional recovery in primate models of parkinsonism, perhaps in part stemming from the variety of ways in which recovery has been assessed. The present study examined functional recovery in monkeys made unilaterally parkinsonian by intracarotid infusion of MPTP. Monkeys were evaluated prior to lesioning and for at least 1 year after lesioning on a battery of tests including a rating of spontaneous behaviors, a learned reaction time/movement time task, tests of lateralized neglect or inattention (i.e. lateralized reward retrieval task, extinction with double simultaneous stimulation, and response to a target moving from one hemispace to the other), and rotational asymmetry in response to a dopamine agonist. Some animals also received 6-[18F]Fluoro-L-Dopa (F-DOPA) position emission tomography (PET) scans before MPTP, when symptomatic, and when showing signs of functional recovery. These animals were sacrificed for post mortem neurochemical assessment following the last PET scan. Results showed that estimates of functional recovery in hemi-parkinsonian monkeys may depend upon the behavioral assay used. Even in behavioral tasks that were sensitive to recovery effects, the degree of functional recovery shown by an animal on one such task did not predict recovery on another. This may in part be due to the inherent difficulty in designing behavioral tests to assess basal ganglia functioning, when there is no consensus concerning which aspects of behavior the normal basal ganglia actually control.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMedDate not supplied

Mechanisms of recovery following unilateral labyrinthectomy: a review.

This paper reviews the literature on the mechanisms responsible for the behavioural recovery which occurs following unilateral labyrinthectomy (UL), UL causes a syndrome of ocular motor and postural disorders, which diminish over time in a process of behavioural recovery known as vestibular compensation. Electrophysiological studies show that the VIIIth nerve does not undergo a functional recovery, therefore vestibular compensation has been attributed to CNS plasticity. However, the nature of the plasticity responsible for vestibular compensation is not understood. Single-neuron studies have demonstrated that a significant recovery of resting activity has occurred in the vestibular nuclei (VN) ipsilateral to the UL by the time symptoms such as spontaneous nystagmus and roll head tilt (static symptoms) have largely disappeared. However, many of the deficits in the response of VN neurons to head acceleration persist and may be permanent. This lack of recovery in the response of neurons to head acceleration correlates with the incomplete and sometimes poor recovery of the vestibulo-ocular and vestibulo-spinal reflex responses to head movement (dynamic symptoms). The major neuronal change in the VN during vestibular compensation appears to be the recovery of resting activity in the VN ipsilateral to the UL, although this recovery is more pronounced in the medial VN than in the lateral VN. The mechanism responsible for the regeneration of resting activity in VN neurons is unknown. In frogs, there is evidence to suggest that transcommissural synaptic input to the VN, from the contralateral (intact) labyrinth, increases in efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Variations in the Hoffmann reflex recovery curve related to clinical manifestations of schizoaffective disorder.

Recovery curves of the Hoffmann reflex (H reflex) were measured in both legs of 10 unmedicated inpatients with schizoaffective disorder, depressed type. Neither recovery curve height of the right leg nor that of the left leg was significantly correlated with clinical psychopathology, although a consistent negative relation was noted between recovery curve height of the left leg and psychopathology. Right-left differences in recovery curve height significantly correlated with both Brief Psychiatric Rating Scale and Hamilton Rating Scale for Depression ratings of psychopathology, such that relative elevation of the recovery curve of the right leg or relative lowering of the recovery curve of the left leg correlated with symptom severity. Three patients who later developed psychotic symptoms when treated with bupropion, a dopaminergic agent, had lower recovery curves, indicative of increased central dopaminergic activity. Relatively lower left-sided recovery curves may reflect increased dopaminergic activity on the right side of the brain in schizoaffective disorder, compared to the left in schizophrenia.

Adult↗

PubMed1987

Environmental enrichment and recovery from contralateral sensory neglect in rats with large unilateral neocortical lesions.

Previous investigations of the potential value of postoperative environmental enrichment in enhancing functional recovery in brain-lesioned rats have yielded contradictory results. The present study sought to resolve some of the contradictions by drawing a clear distinction between the contribution of environmental enrichment to the processes of compensation for sensory loss and recovery per se. By using unilateral lesions, thus avoiding total loss in any sensory modality, and examining a behavioural deficit not anyway thought to be, primarily, a consequence of sensory loss, it was hoped to arrive at an experimental test in which reinstatement of preoperative performance would necessarily reflect recovery rather than compensation. Recovery from the effects of large unilateral neocortical removals on performance on the 'bracelets' test, recently proposed by Schallert and Whishaw, Behavioural Neuroscience, 1984, 98: 518-540, as a model of simultaneous extinction in humans, was investigated. Lesions significantly impaired bracelet removal from the contralateral paw and a degree of recovery from this impairment was observed. However, recovery was not enhanced by postoperative environmental enrichment. The reasons for this were discussed and possible explanations of the recovery that did occur were considered. Implications for Schallert and Whishaw's model were also discussed. It was concluded that the present results were consistent with the view that any restorative value that postoperative environmental enrichment may have lies in facilitating compensation rather than recovery.

Animals↗

PubMed1996

The ACTH(4-9) analog ORG 2766 and recovery after brain damage in animal models--a review.

Treatment with adrenocorticotrophic hormone (ACTH), as well as with ACTH fragments and analogues, can influence behaviour of animals and humans. Furthermore it facilitates recovery of damaged peripheral nervous tissue. The question whether ACTH/MSH peptides affect recovery processes after injury to the central nervous system as well is addressed in the present review. The effects of administration of the ACTH(4-9) analog ORG 2766 after brain lesions has been studied frequently. However, the interpretation of the available data is confused by the variability of the results. Several factors can be identified which influence the efficacy of the peptide: (i) not all behavioural tests are equally suitable to reveal a peptide effect on behavioural recovery; (ii) the affected brain area; (iii) whether cell bodies or terminals are affected; (iv) the post-operative housing conditions; and (v) the onset and duration of peptide administration. Two possible explanations of peptide efficacy on functional recovery are considered: first, the peptide may accelerate spontaneously occurring recovery processes and second, the peptide may induce compensatory mechanisms underlying functional recovery without recuperation of the damaged neurons. These compensatory mechanisms seem to rely mainly on enhanced non-selective attention by activation of limbic structures. It is as yet unknown to which receptor system ORG 2766 binds; the analog lacks affinity for the known melanocortin (MC) receptors in brain, yet ORG 2766 is able to modulate the activity of endogenous opioids and the NMDA-receptor. A modulating influence of the peptide on NMDA-receptor activity might indirectly account for both enhanced attention--with ensuing behavioural recovery--and the acceleration of spontaneous recovery.

Adrenocorticotropic Hormone↗

PubMed1992

Suppression of atrial natriuretic peptide (ANP) receptor recovery from homologous down-regulation by 8-bromo-cGMP in endothelial cells.

In a previous study we reported that cyclic GMP (cGMP) selectively down-regulates the atrial natriuretic peptide clearance receptor (C-ANP receptor) in the cultured bovine pulmonary artery endothelial (CPAE) cell line. Our efforts in the current study are directed towards determining the effects of cGMP on C-ANP receptor recycling and de novo synthesis following homologous down-regulation by atriopeptin III (APIII, rat ANP 103-126). [125I]APIII binding to CPAE cells was decreased to 45.3 +/- 1.0% of control following the pretreatment with 100 nM APIII for 24 h. After the removal of APIII, the decreased [125I]APIII binding gradually recovered up to 68.8 +/- 1.8% of control for 24 h: a 'long-term recovery'. When CPAE cells were pretreated with 1 nM APIII for 30 min, [125I]APIII binding was also decreased to 62.6 +/- 2.6% of control. Following the removal of APIII, the decrease in [125I]APIII binding quickly recovered to 87.7 +/- 2.7% of control for 1 h: a 'short-term recovery'. 8-bromo-cGMP suppressed the long-term recovery of ANP receptor in a dose-dependent manner, while it had no effect on the short-term recovery. Both actinomycin D (1 ng/ml) and cycloheximide (10 ng/ml) significantly (P less than 0.01) suppressed the long-term recovery, but failed to affect the short-term recovery, whereas, the short-term recovery was significantly (P less than 0.01) inhibited by either 10 mM NH4Cl or 0.2 mM chloroquine which inhibits the recycling of internalized ANP receptor. These findings suggest that new ANP receptor synthesis is necessary for long-term but not for short-term recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2006

Recovery of Escherichia coli ATCC 25922 in phosphate buffered saline after treatment with high hydrostatic pressure.

Escherichia coli ATCC 25922 in phosphate buffered saline solution (PBS, pH 7.1, 10(8) CFU/ml) was inactivated by high hydrostatic pressure (HHP, 400 to 600 MPa) treatment at 25 degrees C for 10 min. Colonies of E. coli were not detected on non-selective plate count agar immediately after a HHP-treatment of at least 550 MPa. E. coli subjected to at least 500 MPa in PBS were incubated at 4, 25, and 37 degrees C for 120 h. No colonies were detected on plate count agar throughout the 120-h incubation period at 4 or 37 degrees C. In contrast, the number of E. coli during storage at 25 degrees C increased from an undetectable level (< 1 CFU/ml) to the level of initial cell counts regardless of the treatment pressure level. The recovery in PBS required a maximum time of 48 h, while the period during which cell numbers remained at an undetectable level increased from 24 to 72 h as the treatment pressure increased. E. coli treated at 550 and 600 MPa in PBS were inoculated into trypticase soy broth (TSB) and stored at 4, 25, and 37 degrees C for 120 h. No recovery was recorded in TSB during the 120-h storage at 37 degrees C. In contrast, the number of E.coli during storage at 25 degrees C in TSB increased beyond the level of initial cell counts regardless of the treatment pressure level. The recovery of cell numbers observed in TSB was faster than that in PBS samples, as bacterial growth in TSB assisted faster recovery. When the incubation temperature in PBS was shifted to 25 degrees C after 120-h at 4 or 37 degrees C, recovery of E. coli was observed in samples shifted from 4 to 25 degrees C regardless of the treatment pressure. However, the time during which cell numbers remained at an undetectable level was extended by increasing the level of treatment pressure, and recovery required a maximum time of 48 h. On the other hand, no recovery was observed with HHP-treated E. coli subjected to an incubation temperature shift from 37 to 25 degrees C. This study indicates that an appropriate incubation temperature after HHP-treatment is needed to optimize the recovery of HHP-injured bacteria and thus prevent overestimation of the lethal effect of HHP-treatment.

Colony Count, Microbial↗

PubMed2006

Intervertebral disc recovery after dynamic or static loading in vitro: is there a role for the endplate?

In vivo studies on disc mechanics show loss of fluid from the intervertebral disc (IVD) during loading and full recovery during rest. Previous work indicated that in vitro recovery is hampered after static loading. The aim of the present study was to investigate the role of the endplate after dynamic and static loading on mechanical recovery in vitro. Lumbar spines (caprine) were obtained from the local slaughterhouse and stored frozen. Twenty-four intervertebral discs were thawed and subjected to a compression test in a saline bath (37 degrees C). The discs were pre-loaded at 20 N for 15 min. Three 15-min loading cycles (static: 2.0 MPa or dynamic: average load 2.0 MPa at 0.5 Hz) were applied, each followed by a 30-min period of unloading (20 N). After this protocol, the endplates of half of the discs were blocked with silicone paste and the long-term recovery protocol was applied; the discs were subjected to a single loading cycle (15 min of static or dynamic loading) followed by 10h of unloading at 20 N. All specimens showed a net loss of height and a gain in stiffness during the first part of the test. Eventually, height and stiffness were restored during a long-term recovery test. The difference in recovery between blocked and free endplates was marginal. If fluid flow plays a role during recovery in vitro, the role of the endplate appears to be limited. Our findings show no influence of loading type on recovery in vitro.

Animals↗

PubMed2005

Urea as an endogenous surrogate in human microdialysis to determine relative recovery of drugs: analytics and applications.

During in vivo microdialysis studies time-consuming and laborious bedside calibration methods, e.g. retrodialysis, have to be performed. To reduce the burden on the patient it would be desirable to establish a reliable, time-saving calibration technique to obtain the in vivo recovery describing the relative drug transfer across the membrane of the microdialysis probe. The performed study aimed to evaluate and validate the use of urea as an endogenous reference compound to determine relative in vivo recovery of anti-infectives, e.g. linezolid used herein as model drug. In order to meet the special requirements imposed by microdialysis to measure urea concentrations in very small sample volumes ( approximately 10 microL) a photometric assay in 96-well microtiter plates was established based on the method of Berthelot. Subsequently, concentration- and flow rate-dependence were evaluated in vitro to determine the relative recovery (RR) of urea. Finally, urea and linezolid concentrations in human microdialysis samples were measured. The developed assay was validated according to international guidelines and met all requirements. Relative in vitro recovery was found to be independent from concentration and dependent on flow rate. Subsequently, relative in vivo recovery of urea was correlated with relative in vivo recovery of linezolid obtained by the traditional retrodialysis method. In healthy volunteers, the mean ratio of the relative recovery of linezolid to the relative recovery of urea was 0.6 for the subcutaneous (s.c.: CV 33.4%, n = 48) and 0.7 for the intramuscular probe (i.m.: CV 18.8%, n = 40), respectively. In critically ill patients this ratio was 0.7 for both tissues (s.c.: CV 32.8%, n = 18; i.m.: CV 22.1%, n = 17). Successful calibration of the urea reference technique without the need to use in vitro data will further promote the application of microdialysis in clinical studies especially in critically ill patients, as it reduces the imposed burden to a minimum.

Acetamides↗

PubMed2006

Aging may adversely affect testicular sperm recovery in patients with Klinefelter syndrome.

OBJECTIVES: To investigate the clinical parameters or laboratory analyses that may have a predictive value for successful sperm retrieval in Klinefelter syndrome (KS). METHODS: A total of 74 patients with nonmosaic KS were included in this study. All patients were azoospermic and underwent microdissection testicular sperm extraction for sperm recovery. The predictive values of patient age, testicular volume, serum follicle-stimulating hormone, luteinizing hormone, and testosterone levels were assessed for successful sperm recovery. RESULTS: Testicular sperm recovery was successful in 42 (56.7%) of 74 men. The serum follicle-stimulating hormone, luteinizing hormone, and total testosterone levels did not show any difference between the patients with successful and those with unsuccessful sperm recovery. However, the patients with successful sperm recovery were significantly younger (31.6 +/- 4.3 years) than those with failed attempts (35 +/- 5.1 years, P = 0.002). In the receiver operating characteristics curve analysis, a cutoff of 30.5 years of age had a sensitivity of 78% and a specificity of 48% for successful sperm retrieval. Logistic regression analysis showed that sperm recovery was inversely related to patient age (odds ratio 0.854, 95% confidence interval 0.76 to 0.95). CONCLUSIONS: Microdissection testicular sperm extraction is an effective sperm recovery technique in patients with KS. Our data have demonstrated that aging might adversely affect the sperm recovery rate in men with KS. These results suggest that earlier infertility assessment and testicular sperm extraction in men with KS might play a critical role in their treatment.

Adult↗

PubMed2001

Important pressure recovery in patients with aortic stenosis and high Doppler gradients.

Pressure recovery has been described in aortic stenosis and may explain the difference occasionally observed between Doppler- and catheter-measured gradients. A narrow ascending aorta (AA) and moderately severe stenosis favors pressure recovery. The aims of this study were to investigate the degree to which these conditions are present in patients with aortic stenosis and high Doppler gradients and to evaluate the magnitude of pressure recovery. One hundred sixteen patients were examined with Doppler echocardiography before aortic valve replacement. Patients with a maximum gradient >70 mm Hg (n = 81) were included. The diameter of the AA was measured and compared with the diameter in an age- and body size-matched group of normal controls (n = 23). Pressure recovery was estimated from a previously validated equation by measuring the maximum Doppler gradient, the effective orifice area (EOA), and the diameter of the AA. The diameter of the AA was similar for patients (mean 3.0 cm, range 2.1 to 4.1) and normal controls (mean 3.0 cm, range 2.3 to 3.5). The maximum Doppler gradient was 107 mm Hg (range 71 to 170) and the EOA was 0.6 cm(2) (range 0.2 to 1.3). The calculated pressure recovery was 18 mm Hg (range 6 to 37), which gives a net gradient of 89 mm Hg (range 51 to 151). Twenty-three percent had a net gradient <70 mm Hg. A cutoff of EOA/AA diameter at >0.2 cm identified 84% of patients (16 of 19) with a net gradient <70 mm Hg. In conclusion, we found that important pressure recovery can be expected in most patients with aortic stenosis and high Doppler gradients. Pressure recovery may explain why some patients with high Doppler gradients are asymptomatic. Also, pressure recovery is a factor to consider in patients with atypical symptomatology and high Doppler gradients when one must decide on valvular replacement.

Aortic Valve↗

PubMed2001

Prolonged cardiac recovery from exercise in asymptomatic adults late after atrial correction of transposition of the great arteries: evaluation with magnetic resonance flow mapping.

After atrial correction of transposition of the great arteries (TGA), dysfunction of the systemic right ventricle at rest and during exercise has been reported. Information on changes in systemic right ventricular function during recovery from exercise is lacking. This study evaluates cardiac recovery from supine exercise using magnetic resonance (MR) imaging in patients with asymptomatic TGA after atrial correction. Flow in the ascending aorta, representing stroke volume of the systemic ventricle, was assessed with MR flow mapping in 10 asymptomatic patients with atrially corrected TGA and in 12 controls at rest during exercise and an 8-minute recovery period. In response to exercise, the patients had a smaller increase in heart rate, stroke volume, and cardiac output than did controls. After exercise, no significant difference in halftime of heart rate recovery was observed (patients, 48 +/- 7 seconds; controls, 39 +/- 4 seconds [p >0.05]). In the patients, the time course of stroke volume recovery was significantly different (p <0.001). Stroke volume in the patients, as a percent difference from rest, remained significantly elevated, from 2.5 minutes (+16 +/- 5% vs +7 +/- 6%; p <0.05) to 8 minutes (+4 +/- 7% vs -3 +/- 5%; p <0.05) after exercise. Subsequently, cardiac output remained significantly elevated, from 4.5 minutes (+27 +/- 13% vs +15 +/- 11%; p <0.05) to 7 minutes (+22 +/- 11% vs +12 +/- 12%; p <0.05) after exercise. We conclude that heart rate recovery is within normal limits in patients with atrially corrected TGA. Furthermore, cardiac recovery from exercise, assessed with MR flow mapping, is prolonged in patients with asymptomatic TGA after atrial correction. Abnormal recovery may reflect dysfunction of the systemic right ventricle and an altered metabolic response to exercise.

Adolescent↗

PubMed2000

Immune-recovery uveitis in patients with cytomegalovirus retinitis taking highly active antiretroviral therapy.

PURPOSE: To investigate the clinical features associated with immune recovery in human immunodeficiency virus (HIV)-infected patients with cytomegalovirus retinitis who are taking highly active antiretroviral therapy. METHODS: Sixteen patients were evaluated prospectively at the National Eye Institute, Bethesda, Maryland. Evaluation included a medical history and a complete ophthalmologic examination. The examination included best-corrected visual acuity score measured by means of logarithmic charts, slit-lamp biomicroscopy, dilated retinal examination, retinal photography, and fluorescein angiography. Immune-recovery uveitis was defined as the ocular inflammation associated with clinical immune recovery in patients taking potent antiretroviral regimens. The ophthalmic characteristics of immune-recovery uveitis were identified, and their effect on visual acuity was statistically analyzed. RESULTS: The mean CD4+ T-lymphocyte count for the 16 patients taking highly active antiretroviral therapy at the time of evaluation was 393 cells/microl (range, 97-1,338 cells/microl). Immune-recovery uveitis was characterized by vitreitis and optic disk and macular edema. Clinically important complications of immune-recovery uveitis included cataract and epiretinal membrane formation. The visual acuity scores were significantly worse in the 23 eyes with cytomegalovirus retinitis (mean, 67.2 letters, 20/50) than in the nine eyes without cytomegalovirus retinitis (mean, 89.8 letters, 20/16) (P <.001). Regression analysis showed that a lower visual acuity score was associated with the presence of moderate to severe macular edema on fluorescein angiography and vitreous haze (P < or =. 001). CONCLUSIONS: Immune-recovery uveitis is an important cause of visual morbidity in HIV-infected patients with cytomegalovirus retinitis in the era of highly active antiretroviral therapy. Although immune recovery associated with highly active antiretroviral therapy has allowed some patients to discontinue specific anticytomegalovirus therapy, the rejuvenated immune response can be associated with sight-threatening inflammation.

AIDS-Related Opportunistic Infections↗

PubMed1996

Recovery from C-type inactivation is modulated by extracellular potassium.

Extracellular potassium modulates recovery from C-type inactivation of Kv1.3 in human T lymphocytes. The results of whole-cell patch clamp recordings show that there is a linear increase in recovery rate with increasing [K+]o. An increase from 5 to 150 mM K+o causes a sixfold acceleration of recovery rate at a holding potential of -90 mV. Our results suggest that 1) a low-affinity K+ binding site is involved in recovery, 2) the rate of recovery increases with hyperpolarization, 3) potassium must bind to the channel before inactivation to speed its recovery, and 4) recovery rate depends on external [K+] but not on the magnitude of the driving force through open channels. We present a model in which a bound K+ ion destabilizes the inactivated state to increase the rate of recovery of C-type inactivation, thereby providing a mechanism for autoregulation of K+ channel activity. The ability of K+ to regulate its own conductance may play a role in modulating voltage-dependent immune function.

Binding Sites↗

PubMed2002

Theophylline-induced respiratory recovery following cervical spinal cord hemisection is augmented by serotonin 2 receptor stimulation.

Cervical spinal cord hemisection leads to a disruption of bulbospinal innervation of phrenic motoneurons resulting in paralysis of the ipsilateral hemidiaphragm. We have previously demonstrated separate therapeutic roles for theophylline, and more recently serotonin (5-HT) as modulators to phrenic nerve motor recovery; mechanisms that likely occur via adenosine A1 and 5-HT2 receptors, respectively. The present study was designed to specifically determine if concurrent stimulation of 5-HT2 receptors may enhance motor recovery induced by theophylline alone. Adult female rats (250-350 g; n=7 per group) received a left cervical (C2) hemisection that resulted in paralysis of the ipsilateral hemidiaphragm. Twenty-four hours later rats were given systemic theophylline (15 mg/kg, i.v.), resulting in burst recovery in the ipsilateral phrenic nerve. Theophylline-induced recovery was enhanced with the 5-HT2A/2C receptor agonist, (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI; 1.0 mg/kg). DOI-evoked augmentation of theophylline-induced recovery was attenuated following subsequent injection of the 5-HT2 receptor antagonist, ketanserin (2.0 mg/kg). In a separate group, rats were pretreated with ketanserin, which did not prevent subsequent theophylline-induced respiratory recovery. However, pretreatment with ketanserin did prevent DOI-induced augmentation of the theophylline-evoked phrenic nerve burst recovery. Lastly, using immunocytochemistry and in situ hybridization, we showed for the first time a positive co-localization of adenosine A1 receptor mRNA and immunoreactivity with phrenic motoneurons of the cervical ventral horns. Taken together, the results of the present study suggest that theophylline may induce motor recovery likely at adenosine A1 receptors located at the level of the spinal cord, and the concurrent stimulation of converging 5-HT2 receptors may augment the response.

Action Potentials↗

PubMed2003

The effect of bicuculline application on azimuth-dependent recovery cycle of inferior collicular neurons of the big brown bat, Eptesicus fuscus.

The recovery cycle of auditory neurons is an important neuronal property, which determines a neuron's ability to respond to pairs of sounds presented at short inter-sound intervals. This property is particularly important for bats, which rely upon analysis of returning echoes to extract the information about targets after emission of intense orientation sounds. Because target direction often changes throughout the course of hunting, the changing echo direction may affect the recovery cycle and thus temporal processing of auditory neurons. In this study, we examined the effect of sound azimuth on the recovery cycle of inferior collicular (IC) neurons in the big brown bat, Eptesicus fuscus, under free-field stimulation conditions. Our study showed that the recovery cycle of most IC neurons (42/49, 86%) was longer when determined with sounds delivered at 40 degrees ipsilateral (i40 degrees ) than at 40 degrees contralateral (c40 degrees ) to the recording site. To study the contribution of GABAergic inhibition to sound azimuth-dependent recovery cycle, we compared the recovery cycle of IC neurons determined at two sound azimuths before and during iontophoretic application of bicuculline, an antagonist for GABA(A) receptors. Bicuculline application produced a greater decrease of the recovery cycle of these neurons at i40 degrees than at c40 degrees. As a result, the azimuth-dependent recovery cycle of these neurons was abolished or greatly reduced. Possible mechanisms underlying these observations and biological relevance to bat echolocation are discussed.

Acoustic Stimulation↗

PubMed1998

Effects of the alkylating agent EEDQ on regulatory G proteins and recovery of agonist and antagonist alpha2-adrenoceptor binding sites in rat brain.

The aim of this study was to assess the effect of N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ)-induced alpha2-adrenoceptor inactivation on regulatory G proteins and the recovery of agonist and antagonist binding sites. EEDQ induced a rapid increase in the abundance of rat brain cortical Galphai1/2 proteins (30% at 6 h) which reached a maximum at 4 days (45%) and which then slowly returned (7-30 days) to control values. EEDQ did not alter significantly the levels of Galphai3 and Galphao proteins. By using the standard monoexponential model, the analysis of the recovery of alpha2-adrenoceptor density (6 h-30 days) with [3H]UK 14304 (bromoxidine) and [3H]RX 821002 (2-metoxy idazoxan) in the cerebral cortex did not reveal differences in receptor turnover parameters. However, the recovery of [3H]UK 14304 binding fitted best to a new biphasic recovery model, suggesting the existence of two distinct phases of recovery of agonist sites (r1 and r2 = 15.7 and 7.4 fmol mg protein(-1) day(-1); k1 and k2 = 0.51 and 0.25 day(-1); (t1/2)1 and (t1/2)2 = 1.4 and 2.7 days). In contrast, the recovery of [3H]RX 821002 antagonist sites did not fit to the biphasic model (r = 8.1, k = 0.14, t1/2 = 4.9). Because agonist binding requires coupling to G proteins, the present results suggest that the rapid over-expression of Galphai1/2 proteins induced by EEDQ is related to the biphasic recovery of [3H]UK 14304 binding. The possible implication of the faster recovery of alpha2-adrenoceptor function after EEDQ inactivation is discussed.

Adrenergic alpha-2 Receptor Agonists↗

PubMed1995

Regulated expression of a contractile protein gene correlates with recovery of contractile function after reversible metabolic inhibition in cultured myocytes.

Little is known of the relation between recovery of contraction and the regulation of contractile protein gene expression in ventricular myocytes after severe ATP depletion. We have examined alterations in activation of an MLC-2 luciferase fusion gene in cultured neonatal rat ventricular myocytes produced by exposure to 2 mM Na CN and 20 mM 2-deoxyglucose, and after recovery is serum or serum free medium. The effects of metabolic inhibition followed by recovery on expression on an RSV-luciferase activity were also investigated. Myocytes were co-transfected with a CMV beta-galactosidase fusion gene, and luciferase activities were normalized relative to beta-galactosidase activity to control for transfection efficiency. Two hours of metabolic inhibition produced significant cell injury, as documented by disorganization of myofilaments, and reduction in luciferase and beta-galactosidase activity within transfected cells. Cells allowed to recover for 48 h in serum free hormone supplemented medium showed a further decline in corrected luciferase activity, consistent with a marked reduction in MLC-2 gene transcription. Cells recovered from severe metabolic inhibition in serum free medium also showed failure to redevelop contractile activity, and failure of redevelopment of organized myofibrils. In contrast, myocytes exposed to serum during the 48 h recovery period had a marked increase in luciferase activity, resumed contractile activity and re-established organized myofilaments. There were no significant differences between RSV luciferase activities in cells recovered in serum versus serum free media. In ventricular myocytes in which contraction was inhibited by exposure to 10 microM verapamil, MLC-2 luciferase activity declined by 87%. However, even when contractile activity was inhibited by exposure to verapamil during recovery from metabolic inhibition, exposure to serum containing medium caused a significantly greater increase in MLC-2 luciferase activity than did serum free medium. Thus, the effects of serum on MLC-2 gene expression were not solely due to an effect of serum on recovery of contractile activity. Verapamil had no consistent effect on expression of RSV luciferase. These results suggest that expression of the MLC-2 gene is markedly reduced following recovery from severe metabolic inhibition, an effect largely due to cessation of myocyte contractile activity. Resupply of growth factors present in fetal calf serum reactivate expression of this gene, and this is associated with resumption of contractile activity and redevelopment of organized myofibrils. These results suggest that reactivation of contractile protein gene expression during recovery from metabolic inhibition may be beneficial in allowing cells to recover from this insult.

Analysis of Variance↗