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PubMed1984

The pharmacology of hippocampal theta cells: evidence that the sensory processing correlate is cholinergic.

The firing repertoires of theta cells in the CA1 and dentate layers of the hippocampal formation of the freely moving rabbit were analyzed during 3 behavioral conditions: (1) voluntary motor patterns, termed type 1 theta behaviors; (2) automatic motor patterns, termed type 2LIA behaviors; (3) alert immobility with presentation of sensory stimuli, termed type 2 theta behavior. Cholinergic manipulations were shown to effect the firing repertoires of theta cells during the type 2 theta behavior condition (sensory processing) and not the other two behavioral conditions. A hypothesis of a sensorimotor processing function of the hippocampal formation is presented and discussed.

Animals↗
PubMed1984

Evidence that the neurotrophic actions of alpha-MSH may derive from its ability to mimick the actions of a peptide formed in degenerating nerve stumps.

The ability of alpha-MSH to facilitate the recovery of sensorimotor nerve function following crush lesion is restricted to a critical period following such a lesion. This period coincided with the initiation of sprouting and the disappearance of the 150 kD neurofilament protein from the degenerating distal stump of the nerve. Degenerating nerve contains a factor that is active in a bioassay system for MSH. This factor could not be detected in control nerves. The hypothesis is forwarded that a neurotrophic factor known to be present in degenerating nerve stumps is an alpha-MSH-like peptide formed by the breakdown of the 150 kD neurofilament protein.

Animals↗
PubMed1994

Unilateral AMPA lesions of nucleus basalis magnocellularis induce a sensorimotor deficit which is differentially altered by arecoline and nicotine.

One week after unilateral alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) lesions of nucleus basalis magnocellularis, rats showed significant lateralised bias in spontaneous turning and in turning induced by tail pinch or by placing the rat on a 45 degrees grid. Turning was biased to the lesioned side and this side also showed increased responsiveness to pin-prick stimulation of the skin (somaesthesia), snout and whisker stimulation and ammonia olfaction. Arecoline (0.5 mg/kg), at a dose which did not affect responses to sensorimotor stimulation in sham-operated rats, corrected the lesion-induced biased turning to tail pinch and the 45 degrees grid test and reduced the bias in the open field. In contrast, nicotine (0.05 mg/kg), at a dose which also did not substantially affect responses to sensorimotor stimulation in sham-operated rats, switched the lesion-induced turning bias towards the contralateral side. Neither cholinoceptor agonist reduced the lesion-induced increased sensory responsiveness. The effects of nicotine were blocked by the centrally acting nicotinic antagonist, mecamylamine (1.0 mg/kg), but not by hexamethonium (1.0 mg/kg), or ondansetron (0.01 mg/kg). Amphetamine (up to 1.0 mg/kg) did not affect the lesion-induced motor asymmetry. The results confirm that the basal forebrain cholinergic system plays a role in sensorimotor cortical functions, but suggest different functional roles for muscarinic and nicotinic receptors.

Afferent Pathways↗
PubMedDate not supplied

Discoordination of laryngeal and respiratory movements in aged rats.

Voice and swallowing actions require the coordination of multiple motor systems, and this coordination may be impaired with aging. Although recent work has reported impairments in age-related laryngeal kinematics in rats, the temporal relationship of laryngeal excursions to the respiratory cycle is unknown. The goal of this study was to assess laryngeal-respiratory coordination by examining temporal interrelationships between change in laryngeal aperture and chest wall movement during quiet breathing in a rat model. Glottal images were recorded, digitized, and synchronized with respiratory signals, and temporal features were measured. In the young animals, glottal opening began before the onset of inspiration, and glottal and respiratory cycles were phasic and stereotypic. In old animals, however, inspiration often began during the glottal closing phase, and both respiratory signals were asymmetric. Discoordination of laryngeal and respiratory motor actions associated with aging may be caused by a generalized decline in sensorimotor cranial functions and may contribute to age-related swallowing and communication impairment.

Aging↗
PubMed1992

[Cerebellar dysarthria--a review of the literature].

This review summarizes and discusses the literature on speech deficits in cerebellar diseases and on the topography of cerebellar dysarthria. Clinical descriptions of dysarthric features in cerebellar diseases, parametric investigations of ataxic dysarthria, and experimental studies in animals concerning the effects of lesions on vocalization and the representation of sensorimotor orofacial functions in the cerebellum are considered. Signs of cerebellar dysarthria include a slowing down of articulatory movements, increased variability of pitch and loudness, monotonous and "scanning" speech, and articulatory impreciseness. The available data indicate that the paramedian regions of the superior cerebellar hemispheres are relevant for the development of cerebellar dysarthria.

Articulation Disorders↗
PubMed2002

NADPH-diaphorase and calcium binding proteins in the trigeminal nucleus oralis of rats.

We have examined the distribution of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and the calcium binding proteins (CBPs), calbindin D-28k (CB), calretinin (CR) and parvalbumin (PV), in the trigeminal nucleus oralis (Sp5O). NADPH-d was detected by histochemistry while CBP was detected by immunohistochemistry. NADPH-d-positive neurons were distributed in the medial rostro-dorsomedial part (RDMsp5O) and dorsomedial part (DMsp5O) of Sp5O, and the rostrolateral part of the nucleus of the solitary tract (NTS). CB- and CR-positive neurons were mainly distributed in the dorsal part of Sp5O. In contrast, PV-positive neurons were mainly distributed in the ventral part of Sp5O. NADPH-d colocalized with CB (40%) and CR (20%) but not with PV in neurons of DMsp5O/ NTS. The mean cell sizes of neurons in RDMsp5O were larger than those in DMsp5O/NTS. PV-positive neurons were larger than NADPH-d-positive neurons. NADPH-d-, CB- and CR-positive neurons were generally small in RDMsp5O and DMsp5O/NTS. Few neurons were retrogradely labeled in RDMsp5O and DMsp5O from the thalamus, when numerous labeled neurons were in the principal and interpolar nuclei. These data indicate that NADPH-d histochemistry and CB, CR and PV immunohistochemistry identify a discrete cell population in Sp5O. Those labeled neurons in RDMsp5O and DMsp5O/NTS were considered to be involved in sensorimotor reflexive function of the intra-oral structures.

Animals↗
PubMed1988

Multiple potassium conductances and their functions in neurons from cat sensorimotor cortex in vitro.

1. Potassium conductances were studied in large layer V neurons using an in vitro slice preparation of cat sensorimotor cortex. The kinetics and pharmacological sensitivity of K+ currents were studied directly using single microelectrode voltage clamp and indirectly by evoking single or multiple spikes and recording the spike repolarization and subsequent afterhyperpolarizations (AHPs). 2. A fast-decaying afterhyperpolarization (fAHP) and a subsequent medium-duration afterhyperpolarization (mAHP) followed a single spike. The amplitude and duration of the mAHP increased when multiple spikes were evoked at a fast rate (e.g., 100 Hz), and a slower afterhyperpolarization (sAHP) appeared only after sustained repetitive firing. 3. All AHPs were reduced by membrane potential hyperpolarization and raised extracellular K+ concentration, suggesting they were caused by an increased K+ conductance. Only the mAHP and sAHP reversed at the estimated value of potassium equilibrium potential (-100 mV), whereas the mean reversal potential of the fAHP was nearly identical to the mean value of resting potential (-71 mV). 4. Mechanisms underlying spike repolarization, the fAHP, and the mAHP were investigated. Two rapidly activating outward currents, a fast-inactivating current and a slowly inactivating delayed rectifier, were detected by voltage clamp. Both currents were reduced rapidly by tetraethylammonium (TEA). The fast transient current was reduced slowly after divalent cations were substituted for Ca2+ (through a mechanism unrelated to blockade of Ca2+ channels), whereas the delayed rectifier was unaffected. 5. Spike duration was increased and the fAHP was abolished only by blocking agents that reduced the fast outward currents. Effects of extracellular and intracellular TEA were similar. Effects of TEA and Ca2+-free perfusate were additive and resembled the effects of intracellular Cs+. The addition of apamin, d-tubocurare, or Cd2+ was ineffective. We conclude that the two fast outward currents reflect pharmacologically and kinetically separate K+ conductances that are primarily responsible for spike repolarization and the fAHP. 6. Voltage-clamp studies revealed two additional outward currents, which were persistent and Ca2+-mediated. Each current activated and deactivated slowly, but the kinetics of one component were approximately 10 times slower than the other. The decay of these currents gave rise to AHPs resembling the mAHP and the early sAHP. 7. Neither the mAHP nor the sAHP was reduced by TEA. The mAHP was reduced when divalent cations were substituted for Ca2+ or when Cd2+, apamin, or d-tubocurare were added.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1994

Synaptic plasticity in the thalamo-cortical pathway as one of the neurobiological correlates of forelimb flexion conditioning: electrophysiological investigation in the cat.

1. In a previous study, using a chronic cat preparation subjected to an associative conditioning procedure, we described the plasticity of the thalamo-cortical pathway by qualitatively and quantitatively analyzing the motor responses induced by stimulating each of the relays on the cerebello-thalamo-cortical pathway. In the present study, it was proposed to analyze the effects on the synapses located between thalamic endings and cortical neurones, using a twofold behavioral and electrophysiological approach, with a view to correlating the patterns of synaptic plasticity with the changes in the motor responses recorded. 2. For this purpose, a reduced, functionally organized sensorimotor circuit, which can be taken to be a neuronal analog of associative conditioning, was studied in an awake chronic animal preparation. This circuit was defined on the basis of the sites at which conditioned (CS) and unconditioned stimuli (UCS) were applied: the CS was applied at a site on the cerebellar interpositus nucleus which activated the forepaw musculature so as to induce flexion movements and the UCS was applied to the skin of the distal part of that paw so as to induce reflex flexion movements. By repetitively activating the central nervous pathways by the associated CS and UCS according to a predefined temporal pattern, the efficiency of the thalamo-cortical pathway's contribution to the movement production was enhanced, and its capacity to convey the cerebellar inputs to neurons in the motor cortex increased. 3. The associative nature of the conditioning was tested using previously established criteria. The setting up of motor and central changes in response to the repetitive presentation of paired CS and UCS, the fact that these changes were reversible because they could be abolished by applying extinction procedures, and the consistency of their occurrence whenever the CS was applied repeatedly alone for several days to naive animals, all showed that the stimuli of both kinds (CS and UCS) had to be applied together for the plasticity of the thalamo-cortical pathway to be expressed. 4. By determining whether the waves constituting the cerebello-cortical responses were excitatory or inhibitory, the nature of the changes in the transmission of the cerebellar impulses to neurons in the motor cortex was established.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Ankle sensorimotor control and eversion strength after acute ankle inversion injuries.

We performed this study to monitor changes in ankle eversion strength and sensorimotor control functions after acute ankle inversion injury. Forty-four patients with clinical grade II to III first-time ankle inversion sprains were tested for 1) pathologic talar tilt and anterior talar translation at 1 and 12 weeks after injury; 2) isometric eccentric ankle eversion strength and 3) peroneal reaction time to sudden ankle inversion at 3, 6, and 12 weeks after injury; and 4) accuracy of inversion position assessment 1, 3, 6, and 12 weeks after injury. Not all patients could perform all tests at the early follow-up visits. There was mechanical instability in 19 of 40 tested patients at 1 week and in 4 patients at 12 weeks after injury. Eversion strength was 88% of the contralateral side 3 weeks after injury, rising to 96% after 12 weeks. The magnitude of error of inversion position sense was 190% of the contralateral side 1 week after injury; this was still affected after 12 weeks, but fell to 133%. Patients with pathologic talar tilt or anterior talar translation, or both, at 1 week after injury did not show significantly greater error in position assessment or reduction in eversion strength when compared with patients with ankles that remained stable after injury.

Acute Disease↗
PubMed2005

Nitric-oxide-directed synaptic remodeling in the adult mammal CNS.

In adult mammals, learning, memory, and restoration of sensorimotor lost functions imply synaptic reorganization that requires diffusible messengers-mediated communication between presynaptic and postsynaptic structures. A candidate molecule to accomplish this function is the gaseous intercellular messenger nitric oxide (NO), which is involved in synaptogenesis and projection refinement during development; however, the role of NO in synaptic reorganization processes in adulthood remains to be established. In this work, we tested the hypothesis that this free radical is a mediator in the adult mammal CNS synaptic remodeling processes using a model of hypoglossal axonal injury recently developed by us. Axonal injury-induced disconnection of motoneurons from myocytes produces withdrawal of synaptic inputs to motoneurons and concomitant upregulation of the neuronal isoform of NO synthase (NOS-I). After recovery of the neuromuscular function, synaptic coverage is reestablished and NOS-I is downregulated. We also report, by using functional and morphological approaches, that chronic inhibition of the NO/cGMP pathway prevents synaptic withdrawal evoked by axon injury, despite the persistent muscle disconnection. After successful withdrawal of synaptic boutons, inhibition of NO synthesis, but not of cGMP, accelerated the recovery of synaptic coverage, although neuromuscular disconnection was maintained. Furthermore, protein S-nitrosylation was upregulated after nerve injury, and this effect was reversed by NOS-I inhibition. Our results suggest that during synaptic remodeling in the adult CNS, NO acts as a signal for synaptic detachment and inhibits synapse formation by cGMP-dependent and probably S-nitrosylation-mediated mechanisms, respectively. We also suggest a feasible role of NO in neurological disorders coursing with NOS-I upregulation.

Animals↗
PubMed2004

Parallel FoxP1 and FoxP2 expression in songbird and human brain predicts functional interaction.

Humans and songbirds are two of the rare animal groups that modify their innate vocalizations. The identification of FOXP2 as the monogenetic locus of a human speech disorder exhibited by members of the family referred to as KE enables the first examination of whether molecular mechanisms for vocal learning are shared between humans and songbirds. Here, in situ hybridization analyses for FoxP1 and FoxP2 in a songbird reveal a corticostriatal expression pattern congruent with the abnormalities in brain structures of affected KE family members. The overlap in FoxP1 and FoxP2 expression observed in the songbird suggests that combinatorial regulation by these molecules during neural development and within vocal control structures may occur. In support of this idea, we find that FOXP1 and FOXP2 expression patterns in human fetal brain are strikingly similar to those in the songbird, including localization to subcortical structures that function in sensorimotor integration and the control of skilled, coordinated movement. The specific colocalization of FoxP1 and FoxP2 found in several structures in the bird and human brain predicts that mutations in FOXP1 could also be related to speech disorders.

Animals↗
PubMed1994

Physiological identification of jaw-movement-related neurons in the trigeminal nucleus of cats.

Although neurons responsive to jaw movements have been identified in most parts of the trigeminal brainstem nuclei, little is known about how this information is relayed to the thalamus and ultimately to the cortex for kinesthetic functions and sensorimotor integration. The present extracellular recording experiments showed that a substantial amount of movement-related information is relayed to the thalamus through the caudal part of subnucleus interpolaris (Vi) in adult cats. Vertical jaw displacements, natural mechanical stimuli, and electrical stimulation of the masseter nerve were used to determine the receptive fields and response properties of movement-related neurons. Movement-related responses were observed in 161 units. The receptive fields of these units were located in the masseter muscle, other deep structures, hairy skin, oral mucosa, or some combination of these structures (i.e., convergent). The latency of units responding to masseter nerve stimulation ranged from 1.0 msec to 20 msec, which suggested that some movement-related information was provided by smaller-diameter muscle afferents. Movement responses were either tonic or phasic. Tonic units showed continuous firing at some jaw position; some of these showed a "dynamic" response to jaw displacement. Phasic units were only active, or showed increased activity, when the jaw moved through a specific position. Seventy-one movement-related units were activated by stimulation from the contralateral ventroposteromedial nucleus (VPM) of the thalamus. Most of the brainstem recording sites were located in the dorsal part of Vi between the caudal pole of the facial motor nucleus and the obex. Neurons in caudal Vi may be important for facial kinesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMedDate not supplied

Some conceptual remarks about supraspinal mechanisms in the control of voluntary and reflex motor activities.

The present paper analyses the supraspinal control of motor functions and sensorimotor integrations. Attention was paid mainly to three phenomena involved in these mechanisms: the Bereitschaftspotential, the long latency reflex responses and the short latency somatosensory evoked potentials (SEPs). The study includes the problems of long loop motor control and dyscontrol, the gating process of SEPs by movement, the role of N18 component of SEP and the analysis of supraspinal modulation of the H-reflex excitability curve in healthy subjects and in patients with some cerebral dysfunction. It was found that the amplitude of the Bereitschaftspotential increased with peripheral nerve stimulation. The experiments have shown a positive relationship between the long latency reflex latencies and the distance of the corresponding muscle from the brain. The amplitude of the long latency reflex response was found to be higher and its synchronization better in phasic movements than in a slightly sustained contraction. The short latency somatosensory evoked potentials were distinctly attenuated by movement gating. By its wide spread negativity, the N18 component probably facilitates the cortical transfer of the long latency muscle response. The H-reflex excitability curves in patients with various cerebral dysfunction exhibited a characteristic course corresponding approximately to the degree of dysfunction in focal cerebral lesions, arterial hypertension and neurasthenias.

Adult↗
PubMed1980

[Ultrastructure of the functional element links of the sensorimotor cortex in endotoxic shock].

Endotoxin shock in rabbits and dogs was induced by intravenous administration of endotoxin B. typhosus. Dystrophic changes and hemodynamic disturbances with dilatation and hyperemia of capillaries, increasing permeability of blood-brain barrier were observed in light microscopy of the brain sensomotor cortex. Ultrastructural alterations in neurons were characterized by swelling and destruction of mitochondria, hypertrophy of Golgi complex, increasing lysosome number. In cytoplasm of astrocytes the glycogen disappeared, the secondary lysosomes increased in number. There was a vacuolar dystrophy in olygodendrocytes. These changes were resulted from the shifts occurring in fine structure of capillaries. Hypoxia played an important role in disturbances of the brain integrative activity.

Animals↗
PubMed1993

Paw-reaching, sensorimotor, and rotational behavior after brain infarction in rats.

BACKGROUND AND PURPOSE: Functional tests that are stable and consistent over time are an advantage for long-term evaluation of treatment in experimental stroke research. Because little information on this subject is available in rodents with focal cerebral ischemia, we investigated the outcome of three behavioral tests for a period of 3 months after the insult. METHODS: Spontaneously hypertensive rats were sham-operated (n = 27) or underwent an occlusion (n = 36) of the right middle cerebral artery. Before surgery all rats were tested for amphetamine-induced rotational behavior, and half of the rats were trained in a paw-reaching task. One, 2, and 3 months after surgery the tests were repeated, together with a test for sensorimotor function. Infarct size was measured morphometrically. RESULTS: In the lesion group, total hemisphere area was reduced by 22%, caudate putamen by 47%, and the thalamus by 24%. Contralateral to the lesion, paw-reaching was highly impaired, regardless of whether or not the rats had been pretrained, and lesion size correlated significantly to paw-reach performance. Ipsilateral rotation increased and sensorimotor function recovered with time in infarcted rats. CONCLUSIONS: In contrast to amphetamine-induced rotation and sensorimotor behavior, the paw-reaching test provides a stable behavioral parameter after a middle cerebral artery occlusion. Moreover, the lesion-induced deficit in paw-reaching is highly correlated to the extent of the infarct, suggesting that this test is useful in evaluating treatment effects for a longer period of time.

Amphetamine↗
PubMed2003

Baseline glutamate levels affect group I and II mGluRs in layer V pyramidal neurons of rat sensorimotor cortex.

Possible functional roles for glutamate that is detectable at low concentrations in the extracellular space of intact brain and brain slices have not been explored. To determine whether this endogenous glutamate acts on metabotropic glutamate receptors (mGluRs), we obtained whole cell recordings from layer V pyramidal neurons of rat sensorimotor cortical slices. Blockade of mGluRs with (+)-alpha-amino-4-carboxy-alpha-methyl-benzeacetic acid (MCPG, a general mGluR antagonist) increased the mean amplitude of spontaneous excitatory postsynaptic currents (sEPSCs), an effect attributable to a selective increase in the occurrence of large amplitude sEPSCs. 2S-2-amino-2-(1S,2S-2-carboxycyclopropyl-1-yl)-3-(xanth-9-yl)propanoic acid (LY341495, a group II antagonist) increased, but R(-)-1-amino-2,3-dihydro-1H-indene-1,5-dicarboxylic acid (AIDA) and (RS)-hexyl-HIBO (group I antagonists) decreased sEPSC amplitude, and (R,S)-alpha-cyclopropyl-4-phosphonophenylglycine (CPPG, a group III antagonist) did not change it. The change in sEPSCs elicited by MCPG, AIDA, and LY341495 was absent in tetrodotoxin, suggesting that it was action potential-dependent. The increase in sEPSCs persisted in GABA receptor antagonists, indicating that it was not due to effects on inhibitory interneurons. AIDA and (S)-3,5-dihydroxyphenylglycine (DHPG, a group I agonist) elicited positive and negative shifts in holding current, respectively. LY341495 and (2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine (DCG-IV, a group II agonist) elicited negative and positive shifts in holding current, respectively. The AIDA and LY341495 elicited currents persisted in TTX. Finally, in current clamp, LY341495 depolarized cells by approximately 2 mV and increased the number of action potentials to a given depolarizing current pulse. Thus ambient levels of glutamate tonically activate mGluRs and regulate cortical excitability.

Amino Acids↗
PubMed2001

Structural and functional characteristics of neurons in the sensorimotor cortex of rats with different resistance to emotional stress.

Wistar rats behaviorally active in the open field test (resistant to emotional stress) are characterized by polymorphism of neurons in layer V of the sensorimotor cortex and the presence of hyperchromatic cells, which probably determines resistance to emotional stress in these rats. Atrophy of hyperchromatic neurons reflecting transient inhibition of cell activity was noted in Wistar rats subjected to stress. In the sensorimotor cortex of behaviorally passive animals (predisposed to emotional stress) groups of densely packed hyperchromatic cells and pronounced pericellular edema were revealed. In these rats stress caused irreversible changes in cortical neurons and death of some cells. The presence of ischemic cortical neurons in rats subjected to emotional stress suggests that cerebral hypoxia plays a role in structural and functional disorganization of the sensorimotor cortex during emotional stress.

Animals↗