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PubMed1994

The involvement of nucleus accumbens dopamine in appetitive and aversive motivation.

In recent years, considerable emphasis has been placed upon the putative role of nucleus accumbens dopamine systems in appetitive motivation and positive reinforcement. However, considerable evidence indicates that brain dopamine in general, and nucleus accumbens dopamine in particular, is involved in aspects of aversive motivation. Administration of dopamine antagonists or localized interference with nucleus accumbens dopamine systems has been shown to disrupt active avoidance behavior. In addition, accumbens dopamine release and metabolism is activated by a wide variety of stressful conditions. A review of the literature indicates that there are substantial similarities between the characteristics of dopaminergic involvement in appetitive and aversive motivation. There is conflicting evidence about the role of dopamine in emotion, and little evidence to suggest that the profound and consistent changes in instrumental behavior produced by interference with DA systems are due to direct dopaminergic mediation of positive affective responses such as hedonia. It is suggested that nucleus accumbens dopamine is involved in aspects of sensorimotor functions that are involved in both appetitive and aversive motivation.

Animals↗

PubMedDate not supplied

D-cycloserine, a novel cognitive enhancer, improves spatial memory in aged rats.

D-cycloserine, a partial agonist of the NMDA receptor-associated glycine site, can enhance cognition. The present experiment examines the behavioral effects of D-cycloserine on cognitive deficits in male Fischer-344 rats, 24 months old. Rats 24 months old (n = 42) received either vehicle or one of 3 doses of D-cycloserine prior to testing. Young rats, 4 months old (n = 13), received vehicle prior to testing. Place discrimination and repeated acquisition were tested in the water maze and a variety of sensorimotor tasks were given. Aging impaired performance in all tasks. D-cycloserine improved performance in place discrimination and repeated acquisition. No doses affected sensorimotor function. These results support the hypothesis that D-cycloserine has cognition enhancing properties and that it may be useful in treating disorders involving cognitive impairment.

Aging↗

PubMed1993

Surgical management of recurrent carpal tunnel syndrome.

An approach to the surgical management of recurrent carpal tunnel syndrome was evaluated in 30 patients with 35 involved wrists. This includes internal neurolysis of the median nerve and early post-operative mobilization of the wrist and fingers. The preferred surgical approach is through a second, more ulnar incision. Clinical assessment of sensorimotor function was converted into a numerical score ranging from zero (normal) to 9 (anaesthesia) and 10 (atrophy, severe). The average pre-operative score was mean 6.5 and median 7. At a mean follow-up of 23.5 months, the average post-operative score was mean 1.8 and median 0, a statistically significant improvement (P < 0.001).

Adult↗

PubMed1990

Selective neocortical and thalamic cell death in the gerbil after transient ischemia.

In animal models of transients ischemia, selective vulnerability and delayed neuronal death in the hippocampus have been extensively described. However, little is known about selective damage in the neocortex and the thalamus, even though deficits in sensorimotor function are common in humans surviving hypoxic/ischemic episodes. This study investigated the neurodegenerative effects of transient ischemia in the gerbil neocortex and thalamus with use of Cresyl Violet and silver impregnation staining methods. In addition, immunohistochemistry of an astrocyte-associated protein, glial fibrillary acidic protein, was used to assess the astrocytic response to ischemia. Pyramidal cells in layers 3 and 6 of somatosensory and auditory cortex were exceptionally sensitive to ischemia, whereas the neurons in layers 2, 4 and 5 were more resistant to ischemia. More pyramidal cells were killed in layer 3 than in layer 6. This bilaminar pattern of neuronal death developed after periods of ischemia ranging from 3 to 10 min and was identifiable at post-ischemic survival times of 6 h to one month. Somatodendritic argyrophilia in the neocortex was identified as early as 6-12 h after 5 min of ischemia. The greatest number of degenerating cortical neurons were stained two to four days after ischemia. With 10 min of ischemia, argyrophilic neurites and neurons were also found as early as 8 h after the occlusion. The most extensive damage was noted in the ventroposterior nucleus, the medial geniculate nucleus, and the intralaminar nuclei two to four days after ischemia. Thus, selective vulnerability and delayed neuronal death are evident in both the neocortex and the thalamus after transient ischemia. These regions need to be examined when considering the efficacy of potential neuroprotective drugs.

Animals↗

PubMed1990

Distribution of substance P-like immunoreactive fibres and terminals in the medulla oblongata of the human infant.

This study provides a detailed report of the distribution and density of substance P-like immunoreactive fibres and terminals within the human infant medulla. Seven brains with no signs of macroscopic alteration fixed usually within 24-48 h after death were used. Free floating transverse sections (50-60 microns) were then immunostained with a monoclonal antibody against substance P using the avidin-biotin-peroxidase technique. Morphologically three types of substance P-like immunoreactive fibres were observed: those with small varicosities of less than 1 micron, those with medium varicosities of 1-2 microns and those with large varicosities of 2-4 microns. Very dense substance P-like immunoreactivity was present within the spinal trigeminal nucleus, parts of the gracile and cuneate fasciculi and the paracommissural subnucleus of the solitary nucleus; dense substance P-like immunoreactivity was present within the dorsal nucleus of the vagus nerve, commissural, medial, dorsal, dorsolateral ventral and ventrolateral subnuclei of the solitary nuclear complex, parasolitary nucleus, raphe obscurus, inferior olivary complex (medial, dorsal, dorsomedial nuclei) and ventrolateral part of the dorsal reticular nucleus; moderate substance P-like immunoreactivity was present within the gelatinosus nucleus of the solitary tract, lateral reticular nucleus proper, intermediate reticular zone and parvocellular reticular nucleus; sparse substance P-like immunoreactivity was present within the hypoglossal nucleus, retroambigual nucleus and much of the reticular formation (dorsal, parvocellular, ventral gigantocellular, dorsal paragigantocellular nuclei): and very sparse substance P-like immunoreactivity was present within the nucleus ambiguus, medial vestibular nucleus and parts of the reticular formation (ventral, medial, gigantocellular, ventral gigantocellular, dorsal paragigantocellular nuclei). Substance P-like immunoreactivity was absent in the area postrema, intercalated nucleus, gracile and cuneate nuclei, in the epiolivary, subtrigeminal and parvocellular divisions of the lateral reticular nucleus, spinal vestibular nucleus, and in the solitary and pyramidal tracts. In several regions the substance P-like immunoreactive fibres formed distinct pericellular arrays around the somata and dendrites of neurons (hypoglossal nucleus, dorsal nucleus of the vagus nerve, retroambigual nucleus, intermediate reticular zone). The results indicate the high specificity of the localization of substance P in various structures of the brainstem and underline the presumed significance of this peptide in autonomic and sensorimotor functions of the brain.

Female↗

PubMed1993

Protective effects of SR 57746A in central and peripheral models of neurodegenerative disorders in rodents and primates.

Compounds possessing neurotrophic properties may represent a possible treatment for neurodegenerative disorders such as Alzheimer's disease. SR 57746A, 1-[2-(naphth-2-yl)ethyl]-4-(3-trifluoromethylphenyl)-1,2,5,6- tetrahydropyridine hydrochloride, is a new compound with neurotrophic activity in a number of in vitro preparations. The neurotrophic effects of this compound have been evaluated in vivo using four distinct rat models of neurodegeneration: transient global ischaemia produced by a four-vessel occlusion; septohippocampal lesion produced by injection of vincristine sulphate into the medial septum; sciatic nerve crushing; and acrylamide-induced peripheral neuropathy. Rats were administered vehicle or 2.5-10 mg/kg p.o. SR 57746A, after initiation of the degenerative process, then once daily for 10 days in the first two models, 16 days in the third and 26 days in the fourth model. Median scores for ischaemia-induced neuronal damage were reduced by 30-40% by SR 57746A treatment in hippocampal CA1, CA2, and CA3 regions, and in the dorsal striatum. Twelve days after intraseptal vincristine administration, there was a marked loss of septohippocampal cholinergic neurons, as indicated by reduced choline acetyltransferase activity in both the septum and hippocampus. SR 57746A dose-dependently reversed this reduction in both areas. These results were confirmed by histoenzymological evaluation of hippocampal acetylcholinesterase content. SR 57746A also reversed the loss of hippocampal choline acetyltransferase induced by intraseptal vincristine in marmosets. Behavioral deficits in these models (exploratory behaviour in the former and short-term social memory in the latter) were also significantly reduced by SR 57746A treatment. In the sciatic crush model, sensorimotor function improved more rapidly in rats treated with 10 mg/kg SR 57746A. In this same model, SR 57746A (10 mg/kg/day) also significantly increased the length of regenerated nerve eight days after the crush, as measured using the pinch test. Finally, SR 57746A retarded the onset, reduced the amplitude and accelerated the recovery of acrylamide-induced peripheral neuropathy. Thus, SR 57746A possesses notable neurotrophic activity in a variety of neurodegenerative models in vivo, suggesting that the compound may possess therapeutic potential for the treatment of neurodegenerative diseases.

Acetylcholinesterase↗

PubMed1981

Mesencephalic reticular formation stimulation effects on hypothalamic neuronal activity.

The effects of mesencephalic reticular formation (RF) single pulse, 0.5 msec and 0-500 microA, stimulation on lateral preoptic-lateral hypothalamic (LPA-LH) neuronal activity were determined in anesthetized rats. In addition, the effects of LH stimulation on neural activity in the RF and periaqueductal gray (PAG) were evaluated. Recordings from 117 neurons indicate reciprocal connections between the LPA-LH and the mesencephalon. Stimulation of the RF affected 70% of the LPA-LH neurons tested. Short latency decreases in activity predominated indicating an inhibitory synaptic input from the RF to the LPA-LH. Short latency increases in discharge frequency were observed infrequently. Stimulation of the LH affected only 32% of the mesencephalic neurons tested. Short latency decreases in activity were usually observed indicating reciprocal inhibitory synaptic connections between the LPA-LH and the RF and periaqueductal gray. Antidromic responses verified these interconnections and revealed relatively slow conduction velocities of approximately 1.0 m/sec. Results are discussed in terms of the involvement of the LPA-LH and RF in sensorimotor functions, spinal motor excitability, and ingestive behavior.

Action Potentials↗

PubMedDate not supplied

Behavioral and neurochemical sequelae in young rats of antenal hypoxia.

To test the hypothesis that perinatal hypoxia may have postnatal consequences via à vis learning memory, and neurochemical sequelae, we exposed pregnant Sprague-Dawley rats to 10.5% O2 for 4 h per day (0800-1200 h) or continuously from gestional day E15 to E20. On E20 we quantified ornithine decarboxylase activity and polyamine concentrations in fetal brain. We also conducted behavioral tests from postnatal day P3 to P110. Relatively mild antenatal hypoxia resulted in altered learning, memory, and delayed maturation of early developmental sensorimotor function. These behavioral changes disappeared at various postnatal ages, depending on the function. Perinatal hypoxia also altered the pharmacological response to dopaminergic drugs. In addition, antenatal hypoxia feminized a male nonreproductive sexual behavior, that of saccharin preference. Acute hypoxia also resulted in an increase in the enzyme ornithine decarboxylase and polyamines, which may affect brain development.

Animals↗

PubMed1993

Neural Darwinism: selection and reentrant signaling in higher brain function.

Variation and selection within neural populations play key roles in the development and function of the brain. In this article, I review a population theory of the nervous system aimed at understanding the significance of these processes. Since its original formulation in 1978, considerable evidence has accumulated to support this theory of neuronal group selection. Extensive neural modeling based on the theory has provided useful insights into several outstanding neurobiological problems including those concerned with integration of cortical function, sensorimotor control, and perceptually based behavior.

Animals↗

PubMed1995

Hypnotic catalepsy-induced changes of regional cerebral glucose metabolism.

In an attempt to elucidate the physiological basis of hypnosis, we investigated the changes of whole-brain and regional cerebral glucose metabolism, from a state of resting wakefulness to a hypnotized state with whole-body catalepsy, using positron emission tomography and the 2[18F]fluorodeoxyglucose method in 15 highly hypnotizable adults. Neither the random order of study conditions nor any of the other experimental factors had a measurable effect, and there was no statistically significant global activation or metabolic depression. However, repeated measures analysis of variance revealed a statistically significant heterogeneity of symmetric regional responses: Mainly the occipital areas, including visual and paravisual cortex, became relatively deactivated, while some metabolic recruitment was found in structures involved in sensorimotor functions. The observed pattern of changes of regional cerebral activity corresponds with the shift of attention away from normal sensory input that hypnosis is known to produce.

Adult↗

PubMed2004

NF-kappaB p50-deficient mice show reduced anxiety-like behaviors in tests of exploratory drive and anxiety.

The ubiquitous transcription factor nuclear factor (NF)-kappaB plays a prominent role in regulation of inflammatory immune responses and in cell survival. Recently, it has been found to be active in neurons, and mice lacking NF-kappaB subunits p50 or p65 show deficits in specific cognitive tasks. Here we demonstrate a strikingly low level of anxiety-like behavior in the p50(-/-) mouse. In an open field, the mutant mice showed significantly less defecation, more rearing, and more time spent in the center compartment relative to wild type control mice. The p50(-/-) mice also spent more time investigating a novel object placed in the open field. On the elevated plus maze, p50(-/-) mice spent more time on the open arms and had increased numbers of open arm entries relative to wild type. In group housing conditions, they did not establish dominant-subordinate hierarchies, whereas wild type control animals did so, in part, by whisker barbering and conspecific allogrooming. In tests of general health, sensorimotor function, and daily activity on a circadian rhythm, p50(-/-) mice were normal. Thus, absence of the p50 subunit of the NF-kappaB transcription factor, which results in altered NF-kappaB transcriptional activity in cells throughout the body and brain, alters neuronal circuitry underlying manifestation of emotional behavior. The p50 subunit appears to play a role in normal expression of certain forms of anxiety.

Animals↗

PubMed2005

Neurobehavioral characterization of APP23 transgenic mice with the SHIRPA primary screen.

The SHIRPA primary screen comprises 40 measures covering various reflexes and basic sensorimotor functions. This multi-test battery was used to compare non-transgenic controls with APP23 transgenic mice, expressing the 751 isoform of human beta-amyloid precursor protein and characterized by amyloid deposits in parenchyma and vessel walls. The APP23 mice were distinguishable from controls by pathological limb reflexes, myoclonic jumping, seizure activity, and tail malformation. In addition, this mouse model of Alzheimer's disease was also marked by a crooked swimming trajectory. APP23 mice were also of lighter weight and were less inclined to stay immobile during a transfer arousal test. Despite the neurologic signs, APP23 transgenic mice were not deficient in stationary beam, coat-hanger, and rotorod tests, indicating intact motor coordination abilities.

Alzheimer Disease↗

PubMed2005

Interleukin-1alphabeta gene-deficient mice show reduced nociceptive sensitivity in models of inflammatory and neuropathic pain but not post-operative pain.

The pro-inflammatory cytokine interleukin-1 (IL-1) has been implicated in both inflammatory processes and nociceptive neurotransmission. To further investigate the role of IL-1 in different pain states, gene-disrupted mice lacking both IL-1alpha and IL-1beta genes (IL-1alphabeta (-/-)) were characterized in inflammatory, neuropathic, and post-operative pain models. IL-1alphabeta (-/-) mice showed normal sensorimotor function as measured by the rotorod assay compared to control mice (BALB/c). Acute and persistent formalin-induced nocifensive behaviors were reduced by 20% in IL-1alphabeta (-/-) mice as compared to control mice. IL-1alphabeta (-/-) mice also showed reduced inflammatory thermal and mechanical hyperalgesia compared to controls following the intraplantar administration of carrageenan or complete Freund's adjuvant (CFA). The duration of inflammatory hyperalgesia was shortened in IL-1alphabeta (-/-) mice versus controls in the CFA model. In contrast, deletion of IL-1alphabeta did not change the extent or the duration of post-operative pain developing after skin incision of the hind paw. Finally, time to onset, duration, and magnitude of mechanical allodynia were reduced in two models of neuropathic pain, spinal nerve L5-L6 ligation and chronic constriction injury of the sciatic nerve, in IL-1alphabeta (-/-) mice versus controls. These results demonstrate that IL-1alphabeta modulates both the generation and the maintenance of inflammatory and chronic neuropathic pain and that IL-1 may modulate nociceptive sensitivity to a greater extent in conditions of chronic as compared to acute pain.

Acute Disease↗

PubMed2005

Behavioral performance of tfm mice supports the beneficial role of androgen receptors in spatial learning and memory.

In adulthood, androgens and androgen receptors might contribute to the sexually dimorphic performance in spatial learning and memory, but their roles seem complex. To study the potential role of androgen receptors in spatial learning and memory, we tested adult 6-8-month-old mutant mice with a naturally occurring defect in the androgen receptor gene (testicular feminization mutant or tfm) and C57Bl/6J wild-type mice. Because the trait is X-linked, only tfm males are completely androgen insensitive while female tfm mice are heterozygous, carrying one wild-type and one tfm copy of the androgen receptor. Here we show that female tfm carrier mice outperform tfm male mice in the water maze, while there are no gender differences in water maze performance in wild-type mice. In tfm mice, there were no gender differences in measures of anxiety in the open field or plus maze or sensorimotor function, indicating that potential differences in these measures did not contribute to the differences observed in the water maze. There were no differences in tfm and wild-type female and male mice in emotional learning and memory in the passive avoidance test. These findings support a beneficial role for androgen receptors in spatial learning and memory.

Androgen-Insensitivity Syndrome↗

PubMed2005

The pre-ischaemic neuroprotective effects of N1-dansyl-spermine in a transient focal cerebral ischaemia model in mice.

The pre-ischaemic neuroprotective potential of a novel polyamine/NMDA antagonist N1-dansyl-spermine (1-5 mg kg(-1)) was studied in a transient focal cerebral ischaemia model in mice in comparison to a reference compound, MK-801 (1 or 3 mg kg(-1)). The intraluminal suture transient middle cerebral artery occlusion (MCAO) model was used. N1-dansyl-spermine and MK-801 were administered (i.p.) 30 min prior to ischaemia. A range of histological and behavioural assessments was employed. N1-dansyl-spermine had a comparable effect to MK-801 at reducing the percentage hemisphere lesion volume (%HLV) at the doses tested. Furthermore, N1-dansyl-spermine reduced the ischaemic brain oedema, which MK-801 did not. N1-dansyl-spermine significantly reversed the decrease of locomotor activity (LMA) caused by the MCAO and showed a significant effect at improving the rotarod performance impaired by MCAO. In contrast, MK-801 had no beneficial effect on sensorimotor function and even worsened the LMA. These results clearly demonstrate the pre-ischaemic neuroprotective effect of N1-dansyl-spermine in a transient focal cerebral ischaemia model.

Animals↗

PubMed2006

Evidence for early activation of primary motor cortex and SMA after electrical lower limb stimulation using EEG source reconstruction.

Compared to median nerve somatosensory evoked potentials (SEP), less is known about activity evoked by nerve stimulation of the lower limb. To understand the mechanisms and the physiology of sensor- and motor control it is useful to investigate the sensorimotor functions as revealed by a standardized functional status. Therefore, we investigated SEPs of the lower limb in 6 healthy male volunteers. For each side, tibial and peroneal nerves were stimulated transcutaneously at the fossa poplitea. The tibial nerves were also stimulated further distally at the ankle joint. Source localization was applied to 64-EEG-channel data of the SEPs. In contrast to somatosensory areas, which are activated after median nerve stimulation, we found dipoles adjacent to motor areas near Brodmann area 4 (BA 4) for SEP components P 32/40 and P 54/60 and near the supplementary motor area (SMA) for the N 75/83 component. These sources could reliably be distinguished for each individual subject as well as for the grand mean data set. Our data show that afferent projections from the lower limb mainly reach primary motor areas (BA 4) and only subsequently, with a delay of 40 ms, higher order motor areas such as SMA. We conclude that a focused view on SEP of the lower limb could be a useful tool to investigate pathological states in motor control or peripheral deafferentiation.

Adult↗

PubMed2006

Peripheral median nerve block impairs precision pinch movement.

OBJECTIVE: The objective of this study was to investigate the effects of a simulated peripheral median nerve lesion on precision pinch movement by the thumb and index finger. METHODS: A median neuropathy was created by blocking the median nerve at the wrist using an anesthetic. The subjects (n=5) were asked to perform pulp-to-pulp precision pinch movements before and after the nerve block. Digit motion data was obtained with a marker-based motion analysis system. RESULTS: The radial offset of the thumb tip, as defined by the minimum distance of the thumb tip to the flexion-extension plane of the index finger, showed an increase of 11.2mm after the nerve block. For the thumb, the nerve block caused a decrease in the range of motion at the metacarpophalangeal (MCP) joint, and a compensatory increase in the range of motion at the interphalangeal (IP) joint. The range of motion ratio (MCP:IP) changed from 1:4.8 (pre-block) to 1:1.0 (post-block). The maximum flexion angle at the MCP joint increased from 18.8 degrees (pre-block) to 33.7 degrees (post-block), and maximum flexion angle at the IP joint decreased from 42.6 degrees (pre-block) to 18.8 degrees (post-block). For the index finger, the nerve block caused a decrease in the range of motion at the MCP joint, and compensatory increases in the ranges of motion at the proximal and distal interphalangeal (PIP and DIP) joints. The range of motion ratio (MCP:PIP:DIP) changed from 1:1.1:0.7 (pre-block) to 1:2.4:1.8 (post-block). The maximum flexion angle at the MCP joint decreased from 56.8 degrees (pre-block) to 34.6 degrees (post-block), and the maximum flexion angle at the PIP joint increased from 51.2 degrees (pre-block) to 76.0 degrees (post-block), but the change at the DIP joint was insignificant. CONCLUSIONS: The median nerve block caused remarkable degradation of the pinch performance as quantified by an inaccurate pulp-to-pulp contact of the thumb to the index finger and an alteration of joint motion of the digits. SIGNIFICANCE: Many fine manual tasks require accurate pulp-to-pulp positioning of the thumb to the index finger. Within the hand, the median nerve is critical to the fine sensorimotor function due to the motor supply and the sensory endings to the thumb and index finger. People with median neuropathies (for example, carpal tunnel syndrome) experience clumsiness while performing simple manual tasks. The current approach to the examination of precision pinch movement may be utilized to quantify the apparent hand clumsiness observed in individuals with peripheral neuropathy such as carpal tunnel syndrome.

Adult↗

PubMed2006

A long-term video-EEG and behavioral follow-up after endothelin-1 induced middle cerebral artery occlusion in rats.

The aim was to test the hypothesis that occlusion of the middle cerebral artery (MCA) results in the development of epilepsy in rats. Further, we investigated whether lesion volume, hippocampal pathology, early seizures, or severity of behavioral impairment is associated with the development and severity of epilepsy or interictal spiking. MCA occlusion was induced by intracerebral injection of endothelin-1 (ET; 120 pmol). One group of ET-injected rats were followed-up for 6 months (n = 15) and another for 12 months (n = 20). Sham-operated animals were injected with saline (n = 12). Occurrence of early and late seizures was monitored by intermittent video-electroencephalography. Sensorimotor function was tested with the running wheel and tapered beam-walking tests. Emotional learning and memory were assessed with the fear conditioning test and spatial learning and memory with the Morris water maze. Finally, brains were processed for histology. Only one rat developed late spontaneous seizures (i.e., epilepsy). Epileptiform interictal spiking was detected in 9 of 26 animals. Early seizures did not predict the development of epilepsy, spiking activity, or severity of behavioral impairment. Production of MCA stroke by intracerebral injection of ET was not a strong trigger of epileptogenesis in adult rats. Further studies are needed to investigate the effect of age, genetic background, and location of ET-injection on the development of hyperexcitability and the risk of post-stroke epileptogenesis.

Animals↗