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Introduction Scientific misconduct is a global issue. There is low awareness among health professionals regarding plagiarism, particularly in developing countries, including Pakistan. There is no formal training in the ethical conduct of research or writing for under- and post-graduate students in the majority of medical schools in Pakistan. Internet access to published literature has made plagiarism easy. The aim of this study was to document the effectiveness of focused workshops on reducing scientific misconduct as measured using a modified version of the attitude towards plagiarism questionnaire (ATPQ) assessment tool. Materials and methods A cross-sectional study was conducted with participants of workshops on scientific misconduct. Demographic data were recorded. A modified ATPQ was used as a pre- and post-test for workshop participants. Data were entered in SPSS v20 (IBM< Armonk, NY, US). Frequencies and descriptive statistics were analyzed. An independent sample t-test was run to analyze differences in mean scores on pre-workshop ATPQ and differences in mean scores on post-test scores. Results There were 38 males and 42 females (mean age: 26.2 years) who participated in the workshops and completed the pre- and post-assessments. Most (59; 73.75%) were final-year medical students. One-third (33.8%) of the respondents had neither attended workshops related to ethics in medical research nor published manuscripts in medical journals (32.5%). More than half (55%) admitted witnessing unethical practices in research. There was a significant improvement in attitudes toward plagiarism after attending the workshop (mean difference = 7.18 (6.2), t = 10.32, P < .001). Conclusions Focused workshops on how to detect and avoid scientific misconduct can help increase knowledge and improve attitudes towards plagiarism, as assessed by the modified ATPQ. Students, residents, and faculty members must be trained to conduct ethical medical research and avoid all forms of scientific misconduct.
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INTRODUCTION : The Pakistan military has been actively engaged in the war against terror for more than a decade. Many officers and soldiers have lost their limbs in this war. But the data on traumatic lower limb amputations in Pakistan is sparse. The aim of this study is to prospectively document the epidemiological profile of lower limb military amputees presenting at the largest rehabilitation centre of Pakistan over a three-year period. MATERIALS & METHODS : A prospective three-year survey was conducted at the Armed Forces Institute of Rehabilitation Medicine (AFIRM), Pakistan. One hundred twenty-three consecutive patients with lower limb amputations were enrolled in the survey. The demographic data, etiology, associated injuries, complications profile, and type of prosthesis provided were documented. The data analysis was done using the statistical analysis tool SPSS V 20 (IBM®,NY, USA). RESULTS : All patients were male. Most had traumatic amputation (119), were between 20-40 years (106), with unilateral amputation (115). Mine blast injury was the leading cause in 73 (59.3%) and most (58.5%) were fitted with modular prosthesis. Transtibial amputation was the commonest level (65), followed by transfemoral (30). The time of surgical amputation was not documented in 87% of the patients. Half of the patients (54%) had associated injuries. Seventy-nine patients had at least one complication with phantom pain being the commonest in 25% cases. CONCLUSIONS : This is the largest prospective demographic survey of lower limb amputees in Pakistan military to date. Scores of soldiers and civilians in Pakistan have suffered lower limb amputation. The availability of demographic data can improve the trauma and rehabilitation services for better understanding and management of such cases. There is a need to conduct large scale community-based epidemiological surveys to direct future policies and develop amputee rehabilitation services in the public sector.
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Alkaptonuria is a rare inborn error of metabolism, which is classified as an orphan disease. It is due to the lack of an enzyme homogentisate 1,2-dioxygenase, which results in an accumulation of homogentisic acid in different areas of the body, including sclera, skin, cardiac valves, articular cartilage of the large joints and intervertebral disks. We present two cases of alkaptonuria resulting in ochronotic arthropathy with advanced secondary generalized osteoarthritis, intervertebral disk calcifications, skin and scleral pigmentation. In these case reports, both patients had symptoms for >10 years before being diagnosed. Conservative management in the form of high-dose ascorbic acid, exercises, and gait aids was offered to both of them, which resulted in some symptomatic improvement in the first case, while the second case was lost to follow-up. Alkaptonuria is a rare disease, and although it does not clearly impact mortality, early diagnosis may improve the quality of life.
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1. To examine the effects of glucose on the central components of the vago-vagal reflex control of gastric function, we performed both in vivo and in vitro experiments on neurones in the medial nucleus of the tractus solitarius (mNTS) and in the dorsal motor nucleus of the vagus (DMV). 2. In the in vivo anaesthetized rat preparation, unilateral microinjection of D-glucose (10 or 50 mM (60 nl)(-1)) in mNTS produced inhibition of gastric motility and an increase in intragastric pressure. D-glucose had no effect in the DMV. 3. In the in vitro rat brainstem slice preparation, whole-cell recordings of DMV neurones showed that increasing the glucose concentration of the perfusion solution from 5 mM to 15 or 30 mM produced outward currents of 35 +/- 5 pA (n = 7) and 51 +/- 10 pA (n = 11), respectively. These were blocked by tetrodotoxin and picrotoxin, indicating that glucose was acting indirectly to cause the release of GABA. Decreasing the glucose concentration of the perfusing solution by one-half produced an inward current of 36 +/- 5 pA (n = 7). 4. Stimulation of the NTS evoked inhibitory postsynaptic currents (IPSCs) in DMV neurones. The amplitude of the evoked IPSCs was positively correlated with glucose concentration. Perfusion with the ATP-sensitive K(+) (K(ATP)) channel opener diazoxide mimicked the effect of reduced glucose, while perfusion with the K(ATP) channel blocker glibenclamide mimicked the effects of increased glucose. 5. Our data indicate that glucose had no direct excitatory effect on DMV neurones, but DMV neurones appear to be affected by an action of glucose on cell bodies of mNTS neurones via effects on an ATP-sensitive potassium channel.
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Vaciamiento Gástrico/efectos de los fármacos , Glucosa/farmacología , Núcleo Solitario/fisiología , Nervio Vago/fisiología , Animales , Potenciales Postsinápticos Excitadores/efectos de los fármacos , Potenciales Postsinápticos Excitadores/fisiología , Espacio Extracelular/metabolismo , Vaciamiento Gástrico/fisiología , Masculino , Microinyecciones , Neuronas/efectos de los fármacos , Neuronas/fisiología , Técnicas de Cultivo de Órganos , Técnicas de Placa-Clamp , Presión , Terminales Presinápticos/efectos de los fármacos , Terminales Presinápticos/fisiología , Ratas , Ratas Sprague-Dawley , Núcleo Solitario/citología , Núcleo Solitario/efectos de los fármacos , Estómago/inervación , Estómago/fisiología , Vagotomía , Nervio Vago/citología , Nervio Vago/cirugíaRESUMEN
In the aftermath of prolonged continuous seizure activity (status epilepticus, SE), neuronal cell death occurs in the brain regions through which the seizure propagates. The vulnerability to adrenalectomy-induced apoptotic neuronal death was recently reported to be reduced by prior exposure to repeated daily noninjurious electroconvulsive shock (ECS). The present studies identified apoptosis and apoptosis-associated gene products in the neurodegenerative response to experimentally controlled periods (1 or 2 h) of SE in the rat, and determined whether exposure to ECS can interrupt these apoptotic responses mechanisms. Internucleosomal DNA fragmentation and the presence of apoptotic-like neurons (as assessed by in situ double labeling technique) was detected in hippocampus and rhinal cortex at 24 h after SE. Under these conditions, levels of both mRNA and protein encoded by the 'death promoting' bcl-XS gene were increased in the same brain areas. Pretreatment of animals for 7 days with low intensity (minimal) ECS conferred resistance to SE-evoked neurodegeneration, as assessed histopathologically by silver staining. Associated with this neuroprotective action was a reduction in the incidence of apoptosis-like neuronal morphology and DNA fragmentation, and a prevention of the increase in Bcl-XS protein and mRNA in hippocampus and rhinal cortex. These data suggest that pre-exposure to controlled, brief noninjurious seizures decreases vulnerability to programmed neuronal cell death, that this neuroprotective action occurs upstream from Bcl-XS, and that increases in bcl-XS gene expression may serve as a sensitive indicator of neurodegeneration following SE.
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Apoptosis , Terapia Electroconvulsiva , Neuronas/patología , Estado Epiléptico/patología , Estado Epiléptico/terapia , Animales , Biomarcadores , Fragmentación del ADN , Corteza Entorrinal/patología , Corteza Entorrinal/fisiología , Agonistas de Aminoácidos Excitadores , Expresión Génica , Hipocampo/patología , Hipocampo/fisiología , Ácido Kaínico , Masculino , Degeneración Nerviosa/inducido químicamente , Degeneración Nerviosa/patología , Degeneración Nerviosa/terapia , Neuronas/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/genética , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , ARN Mensajero/análisis , Ratas , Ratas Sprague-Dawley , Estado Epiléptico/inducido químicamente , Proteína bcl-XRESUMEN
Our previous data obtained in the cat suggest that the neurons of the ventrolateral subnucleus of the tractus solitarius (vlNTS) act as an inspiratory off-switch and terminate the inspiratory phase of the respiratory cycle (Berger et al., Eur. J. Pharmacol. 277 (1995) 195-208; Gillis et al., Neurosci. Abstr. 23 (1997) 725). The purpose of the present study was to determine whether inhibition of the region of the vlNTS of the rat using drugs that hyperpolarize, disfacilitate or block both axonal conduction and action potential generation would alter the inspiratory phase of the respiratory cycle. Experiments were conducted in anesthetized, vagotomized and spontaneously breathing rats while monitoring diaphragmatic electromyogram activity. Vagus nerves were sectioned in order to rule out prolongation of inspiration evoked by microinjection of agents into the vlNTS which block excitatory drive from lung afferent inputs. Bilateral microinjection of the inhibitory amino acid gamma-aminobutyric acid (GABA) 25 nmol/45 nl produced an immediate prolongation of inspiratory duration (484+/-18 to 1291+/-84 ms) and an apneustic pattern of breathing. Other effects observed were a significant shortening of expiratory duration (778+/-36 to 432+/-38 ms), rise in blood pressure (83+/-4 to 108+/-6 mmHg) and a small but significant increase in heart rate (439+/-17 to 452+/-18 beats/min). Bilateral microinjection of the ionotropic glutamate receptor antagonist kynurenic acid (1 nmol) and the Na(+) channel blocker tetrodotoxin (10 pmol) into the region of the vlNTS consistently produced a similar prolongation of inspiratory duration and an apneustic pattern of breathing. These results support the hypothesis that neurons in the region of the vlNTS promote the transition from inspiration to expiration and function as part of the 'Inspiratory Off Switch'.
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Inhalación/fisiología , Ácido Quinurénico/farmacología , Neuronas/fisiología , Mecánica Respiratoria , Núcleo Solitario/fisiología , Ácido gamma-Aminobutírico/farmacología , Potenciales de Acción/efectos de los fármacos , Potenciales de Acción/fisiología , Animales , Axones/efectos de los fármacos , Axones/fisiología , Gatos , Lateralidad Funcional , Inhalación/efectos de los fármacos , Ácido Quinurénico/administración & dosificación , Masculino , Microinyecciones , Neuronas/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Mecánica Respiratoria/efectos de los fármacos , Núcleo Solitario/efectos de los fármacos , Transmisión Sináptica/efectos de los fármacos , Transmisión Sináptica/fisiología , Tetrodotoxina/administración & dosificación , Tetrodotoxina/farmacología , Nervio Vago/fisiología , Ácido gamma-Aminobutírico/administración & dosificaciónRESUMEN
The purpose of our study was to test the hypothesis that 5-hydroxytryptamine (5-HT)(1A) receptor agonists counteract morphine-induced respiratory depression. Studies were conducted in anesthetized rats, and respiratory activity was monitored with diaphragm electromyography. Morphine was administered i.v. in doses that produce apnea. Once apnea was established, i.v. administration of the 5-HT(1A) receptor agonist drug 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) at 10 or 100 microgram/kg restored normal breathing in each animal (n = 24). This antagonistic effect of 8-OH-DPAT on morphine-induced respiratory depression was observed in both spontaneously breathing and artificially ventilated animals. Results obtained with 8-OH-DPAT were mimicked by buspirone (50 microgram/kg i.v.), another 5-HT(1A) receptor agonist drug. Pretreatment with 4-(2'-methoxyphenyl)-1-[2'[N-(2'-pyridinyl]-p-iodo-benzamido]ethyl]pi perazine, an antagonist of 5-HT(1A) receptors, prevented 8-OH-DPAT from counteracting morphine-induced apnea. These results indicate that activation of central nervous system 5-HT(1A) receptors is an effective way of reversing morphine-induced respiratory depression. Most important, this is the third model of disturbed respiratory function in which drugs that stimulate 5-HT(1A) receptors have been shown to restore breathing to near-normal levels.
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Apnea/inducido químicamente , Morfina/farmacología , Receptores de Serotonina/efectos de los fármacos , Antagonistas de la Serotonina/farmacología , Agonistas de Receptores de Serotonina/farmacología , 8-Hidroxi-2-(di-n-propilamino)tetralin/farmacología , Aminopiridinas/farmacología , Animales , Buspirona/farmacología , Diafragma/efectos de los fármacos , Interacciones Farmacológicas , Electromiografía , Masculino , Contracción Muscular/efectos de los fármacos , Piperazinas/farmacología , Ratas , Ratas Sprague-Dawley , Receptores de Serotonina/clasificaciónRESUMEN
Seizures evoked by electroshock induce rapid changes in the expression of several genes in the adult brain, including those encoding for neurotrophic factors. Some of the neurotrophic factors induced by brief seizures such as basic fibroblast growth factor and nerve growth factor have been shown to have neuroprotective action. We reasoned therefore that these seizures may protect against neural injury. To test this hypothesis, we examined the effect of electroshock-induced seizures on the vulnerability to cell death in the hippocampus. Cell death was induced by adrenalectomy, which results in a highly selective apoptotic neuronal death in the dentate granule cell layer of the hippocampus. Daily electroshock seizures were administered for seven days to sham-operated and adrenalectomized rats. Neuronal degeneration was evaluated by the highly sensitive and reliable cupric-silver impregnation method. Animals experiencing electroshock seizures were completely protected against adrenalectomy-induced cell death, whereas adrenalectomized animals not exposed to electroshock seizures exhibited substantial neuronal cell degeneration in the dentate granule cell layer. Daily restraint stress did not prevent the adrenalectomy-induced neuronal death, indicating that the neuroprotective effect of the seizure treatment is not accounted for by stress. We conclude that brief controlled seizure-evoked neural activation may allow the sparing of otherwise vulnerable neuronal populations in the injured adult brain. This prompts a need to explore the possibility that controlled administration of electroshock seizures may have therapeutic potential in treating neurodegenerative disorders.
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Adrenalectomía , Apoptosis/fisiología , Hipocampo/fisiopatología , Convulsiones/etiología , Convulsiones/fisiopatología , Animales , Atrofia , Giro Dentado/patología , Electrochoque , Hipocampo/patología , Masculino , Ratas , Ratas Sprague-Dawley , Convulsiones/patología , Timo/patologíaRESUMEN
The role of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors in the initiation and propagation of limbic motor seizures in rats was examined by the intracerebral and systemic administration of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (f) quinoxaline (NBQX), a selective antagonist of the AMPA subtype of glutamate receptor. Limbic motor seizures were evoked focally by the application of the gamma-aminobutyric acid receptor antagonist, bicuculline, into area tempestas, an epileptogenic site in the deep anterior piriform cortex. Before eliciting seizures, NBQX was applied focally into either 1) area tempestas or 2) perirhinal or posterior piriform cortex ipsilateral to the area tempestas from which seizures were evoked. In addition, pretreatment with i.p. NBQX was evaluated for anticonvulsant actions against area tempestas-evoked clonic or systemically evoked tonic seizures. In all conditions, a dose-dependent decrease in the severity of seizures was obtained with NBQX. With focal intracerebral administration, a dose of 500 pmol of NBQX consistently protected against limbic motor seizures, with partial protection achieved with 100 pmol. After i.p. administration, 2.5 and 5.0 mg/kg significantly protected the rats from both limbic motor seizures and tonic extensor seizures. No overt disturbance of spontaneous behavior was associated with the anticonvulsant doses of NBQX. Moreover, both forebrain substrates of limbic motor seizures and hindbrain substrates of tonic extensor seizures were highly susceptible to disruption by NBQX. The results indicate that AMPA subtype of glutamate receptors are crucial mediators of seizure propagation via perirhinal and piriform cortics.
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Corteza Motora/fisiopatología , Receptores AMPA/fisiología , Convulsiones/fisiopatología , Animales , Masculino , Quinoxalinas/farmacología , Ratas , Ratas Sprague-Dawley , Receptores AMPA/antagonistas & inhibidores , Convulsiones/inducido químicamenteRESUMEN
This is a prospective open study of randomly selected 35 patients with a single sore of cutaneous leishmaniasis who were treated with paromomycin sulphate topical ointment for 4 weeks. According to the observations made on days 0, 15, 45 and 105 after the careful application twice a day in 2 lengths from one side of the lesion to the other at right angles to each other and then smeared to cover the whole surface of the sore, the overall efficacy of the ointment as therapeutic agent was 91%. There was a mild and temporary adverse reaction in the form of painless, non-itching nodulation around the ulcers in 10 (28%) patients after 15 days application which disappeared within 5-7 days of further application. It thus proved a promising, simple and inexpensive remedial agent without any undesirable side effects as compared to other complicated and unpredictable therapeutic regimens.
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Amebicidas/uso terapéutico , Leishmaniasis Cutánea/tratamiento farmacológico , Paromomicina/uso terapéutico , Adolescente , Adulto , Amebicidas/administración & dosificación , Estudios de Evaluación como Asunto , Humanos , Masculino , Pomadas , Paromomicina/administración & dosificación , Estudios Prospectivos , Resultado del TratamientoRESUMEN
Previous studies showed that brainstem seizures can still be evoked after transections that separate forebrain from brainstem. We sought to determine whether forebrain-evoked electrographic seizures require brainstem connections for initiation and generalization. Male Sprague-Dawley rats weighing 295-320 g implanted with epidural electrodes had brain transections placed at the pre-, mid-, or postcollicular level. In experiment 1, the transections were limited to severing the brainstem, sparing the telencephalon laterally; these are referred to as "core" transections. In experiment 2, the transections severed the brainstem and also cut through the lateral telencephalon. These "extended" transections were either (a) bilateral, (b) unilateral (i.e., a hemitransection confined to one hemisphere), or (c) partial (sparing pathways ventral to the pretectal nuclei). All transections were performed under ether anesthesia, and seizures were initiated 3 h later by focal infusion of bicuculline (BIC) into the area tempestas (AT) through a previously implanted guide cannula. In experiment 1, bilateral forebrain electrographic seizures occurred in the complete absence of connections between forebrain and brainstem, showing that the brainstem is not required for forebrain-evoked seizures. In experiment 2, forebrain seizures evoked by BIC in AT were suppressed by bilateral extended transections which interrupted connections between AT and the caudal lateral telencephalon. Under these circumstances, application of carbachol with BIC reinstated the forebrain seizure response. These results indicate that carbachol application served to compensate for loss of an excitatory influence on AT resulting from the severing of connections with the caudal telencephalon. The demonstration of direct projections from entorhinal cortex to AT using Fluoro-Gold tracing together with the finding that extended brain transections caudal to the telencephalon do not suppress focally evoked forebrain seizures provided further support for the notion that AT afferents from the caudal telencephalon regulate the sensitivity of AT to BIC. The present findings provide further evidence that seizure substrates in the forebrain and brainstem are separable and independent.
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Bicuculina , Tronco Encefálico/fisiología , Prosencéfalo/fisiología , Convulsiones/inducido químicamente , Estilbamidinas , Vías Aferentes/anatomía & histología , Vías Aferentes/efectos de los fármacos , Vías Aferentes/fisiología , Animales , Bicuculina/farmacología , Tronco Encefálico/anatomía & histología , Tronco Encefálico/efectos de los fármacos , Carbacol/farmacología , Electrodos Implantados , Electroencefalografía , Colorantes Fluorescentes , Sistema Límbico/anatomía & histología , Sistema Límbico/efectos de los fármacos , Sistema Límbico/fisiología , Masculino , Vías Nerviosas/anatomía & histología , Vías Nerviosas/fisiología , Pentilenotetrazol/farmacología , Prosencéfalo/anatomía & histología , Prosencéfalo/efectos de los fármacos , Ratas , Ratas Sprague-DawleyRESUMEN
Immunocytochemistry using antisera directed against dopamine-beta-hydroxylase (DBH) was used to determine the organization of the noradrenergic (NE) input to the hamster's superior colliculus (SC). Immunocytochemistry for DBH was combined with retrograde transport of fluorogold (FG) to determine the sources of NE input to SC. Microiontophoretic techniques were used together with extracellular single unit recording and receptive field mapping techniques to determine the manner in which NE influenced the responses of individual SC neurons. The hamster's SC contained numerous DBH-positive fibers but no immunopositive cells. These fibers formed a plexus that was most dense in the lower stratum griseum superficiale (SGS). The density of DBH-positive fibers was very low in the stratum opticum (SO) and increased in density in the stratum griseum intermediale (SGI) and the other deep layers. When FG injections into the SC were combined with immunocytochemical detection of DBH, double-labeled cells were observed in the contralateral locus ceruleus. DBH-positive neurons were observed in several other portions of the mesencephalon and pons, but none of these were labelled with FG. The effects of NE iontophoresis were assessed for a total of 135 SC neurons. In 74% (N = 100), NE reduced spontaneous and/or stimulus evoked activity. In 3% (N = 4 cells), NE increased activity, and in 23% (N = 31 cells) it had no effect. These percentages were essentially the same for superficial layer visual cells and somatosensory neurons in the deep laminae. The effect of NE iontophoresis upon signal to noise ratios was assessed for 46 visual and 56 somatosensory neurons. For 54% (N = 25) of the visual cells and 16% (N = 9) of the somatosensory cells, NE iontophoresis decreased signal to noise ratios. For 13% (N = 6) of the visual cells and 21% (N = 12) of the somatosensory cells, NE iontophoresis increased signal to noise ratios. The effects of NE on the responsivity of SC neurons were antagonized by propranolol (86% of the 21 cells tested), sotalol (67% of the six cells tested), and atenolol (effective in the single cell tested). All these agents are beta-adrenergic antagonists. The single alpha-adrenergic antagonist that we evaluated, corynanthine, potentiated the effects of NE on the responsivity of the two SC neurons that we tested.
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Cricetinae/anatomía & histología , Dopamina beta-Hidroxilasa/metabolismo , Neuronas Aferentes/fisiología , Norepinefrina/metabolismo , Colículos Superiores/fisiología , Vías Visuales/fisiología , Potenciales de Acción/efectos de los fármacos , Animales , Cricetinae/fisiología , Femenino , Inmunohistoquímica , Masculino , Neuronas Aferentes/efectos de los fármacos , Norepinefrina/farmacología , Norepinefrina/fisiología , Estimulación Luminosa , Propranolol/farmacología , Colículos Superiores/citología , Colículos Superiores/metabolismo , Vías Visuales/efectos de los fármacosRESUMEN
Multiple retrograde labelling techniques were used to determine whether the superior collicular (SC) cells that project to the spinal cord in hamster and rat also innervate the contralateral colliculus. In 25 rats and 13 hamsters, various combinations of the tracers horseradish peroxidase, True blue, Diamidino yellow, fluorogold and rhodamine-labelled latex microspheres were used to label tectospinal and SC commissural neurons. No double-labelled cells were observed in any of these experiments. Analysis of neurons that were retrogradely labelled with horseradish peroxidase showed further that SC commissural neurons were much smaller than tectospinal cells. The average soma area for tectospinal cells in hamster was 225.9 micron 2 and that for such neurons in rat was 214.4 micron 2. The mean soma areas for SC commissural neurons in hamster and rat were 85.4 micron 2, respectively. In additional experiments (6 rats and 6 hamsters), True blue was injected into the left predorsal bundle and Diamidino yellow was deposited into the left SC. In both hamsters and rats, these injections invariably produced a small number of double-labelled cells in the deep layers of the right SC. In a final group of animals (7 rats and 2 hamsters), large thalamic deposits of Diamidino yellow were combined with bilateral injections of True blue into the spinal cord. This combination also produced small numbers of double-labelled neurons in both colliculi. These results indicate that the tectospinal and SC commissural pathways arise from distinct neuronal populations, but that a small number of cells that send axons into the predorsal bundle also have commissural collaterals. They demonstrate further that some tectospinal cells also send axon collaterals to the thalamus.
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Médula Espinal/anatomía & histología , Colículos Superiores/anatomía & histología , Animales , Cricetinae , Vías Nerviosas/anatomía & histología , Ratas , Ratas Endogámicas , Colículos Superiores/citología , Núcleos Talámicos/anatomía & histologíaRESUMEN
Stimulation of the superior colliculus in rats produces movements of the head and body that resemble either orientation and approach towards a contralateral stimulus, or avoidance of, or escape from, such a stimulus. A variety of evidence indicates that the crossed descending pathway, which runs in the contralateral predorsal bundle to the pontomedullary reticular formation and the spinal cord, is involved in orienting movements. The nature of this involvement was investigated, by assessing the effects on tectally-elicited movements of midbrain knife-cuts intended to section the pathway as it crosses midline in the dorsal tegmental decussation. As expected, ipsilateral movements resembling avoidance or escape were little affected by dorsal tegmental decussation section, whereas contralateral circling movements of the body were almost abolished. However, contralateral movements of the head in response to electrical stimulation were not eliminated, nor were orienting head movements to visual or tactile stimuli. There was some suggestion that section of the dorsal tegmental decussation increased the latency of head movements from electrical stimulation at lateral sites, and decreased the accuracy of orienting movements to sensory stimuli. These results support the view that the crossed tectoreticulospinal system is concerned with approach rather than avoidance movements. However, it appears that other, as yet unidentified, tectal efferent systems are also involved in orienting head movements. It is possible that this division of labour may reflect functional differences between various kinds of apparently similar orienting responses. One suggestion is that the tectoreticulospinal system is concerned less in open-loop orienting responses (that are initiated but not subsequently guided by sensory stimuli), than in following or pursuit movements.
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Orientación/fisiología , Formación Reticular/fisiología , Médula Espinal/fisiología , Colículos Superiores/fisiología , Animales , Mapeo Encefálico , Vías Eferentes/fisiología , Estimulación Eléctrica , Reacción de Fuga/fisiología , Femenino , Masculino , Movimiento , Ratas , Especificidad de la EspecieRESUMEN
Some studies have reported that stimulation of the superior colliculus in rats produces orienting responses, as it does in a number of species. However, other studies have reported movements resembling avoidance and escape, which are not characteristic of collicular stimulation in other mammals. This apparent discrepancy was investigated by systematically recording the effects on head and body movements of electrical stimulation at a large number of sites throughout the superior colliculus (SC) and surrounding structures. It was found that the nature of the movements observed depended on the location of the stimulating electrode. Contralateral head and body movements resembling orienting and approach were obtained from sites in the intermediate and deep layers in rostral colliculus, the intermediate white layer and immediately surrounding tissue in central colliculus, and in all layers except deep white in caudal colliculus. At the remaining responsive sites, movements resembling avoidance and escape were obtained. The most common response was an ipsilateral cringelike movement of the body that developed into ipsilateral locomotion, followed by running and jumping as the current was increased. These movements were obtained from sites in the superficial and intermediate layers rostrally; from the intermediate gray and the medial superficial and deep layers in central colliculus; and from the deep layers and underlying tegmentum caudally. The distributions of sites, together with evidence from other studies, suggested the following conclusions: Within the superficial layers, avoidance responses were obtained from a region of the superior colliculus that appeared to represent the upper visual field, whereas orienting responses were obtained from a region apparently representing the lower visual field. Stimulation of the area containing the cells of origin of the predorsal bundle produced orientation and approach movements, whereas the avoidance and escape movements were probably mediated by parts of the ipsilateral descending pathway. The stimulation-induced avoidance and escape may reflect the importance of such responses to visual "events," particularly in the upper part of the visual field, in animals, like rats, with many predators.