Neuromuscular control of prey capture in frogs.
(9/597)
While retaining a feeding apparatus that is surprisingly conservative morphologically, frogs as a group exhibit great variability in the biomechanics of tongue protraction during prey capture, which in turn is related to differences in neuromuscular control. In this paper, I address the following three questions. (1) How do frog tongues differ biomechanically? (2) What anatomical and physiological differences are responsible? (3) How is biomechanics related to mechanisms of neuromuscular control? Frog species use three non-exclusive mechanisms to protract their tongues during feeding: (i) mechanical pulling, in which the tongue shortens as its muscles contract during protraction; (ii) inertial elongation, in which the tongue lengthens under inertial and muscular loading; and (iii) hydrostatic elongation, in which the tongue lengthens under constraints imposed by the constant volume of a muscular hydrostat. Major differences among these functional types include (i) the amount and orientation of collagen fibres associated with the tongue muscles and the mechanical properties that this connective tissue confers to the tongue as a whole; and (ii) the transfer of intertia from the opening jaws to the tongue, which probably involves a catch mechanism that increases the acceleration achieved during mouth opening. The mechanisms of tongue protraction differ in the types of neural mechanisms that are used to control tongue movements, particularly in the relative importance of feed-forward versus feedback control, in requirements for precise interjoint coordination, in the size and number of motor units, and in the afferent pathways that are involved in coordinating tongue and jaw movements. Evolution of biomechanics and neuromuscular control of frog tongues provides an example in which neuromuscular control is finely tuned to the biomechanical constraints and opportunities provided by differences in morphological design among species. (+info)
Serotonergic modulation of the hyperpolarizing spike afterpotential in rat jaw-closing motoneurons by PKA and PKC.
(10/597)
Intracellular recordings were obtained from rat jaw-closing motoneurons (JCMNs) in slice preparations to investigate the effects of serotonin (5-HT) on the postspike medium-duration afterhyperpolarization (mAHP) and an involvement of protein kinases in the effects. Application of 50 microM 5-HT caused membrane depolarization and increased input resistance in the most cells without affecting the mAHP, whereas not only membrane depolarization and an increase in input resistance, but also the suppression of the mAHP amplitude was induced by higher dose of 5-HT (100 or 200 microM). On the other hand, when the mAHP amplitude was increased by raising [Ca(2+)](o) from 2 to 6 mM, 5-HT-induced attenuation of the mAHP amplitude was enhanced, and even 50 microM 5-HT reduced the mAHP amplitude. This 5-HT-induced suppression of the mAHP could be mimicked by application of membrane-permeable cAMP analogue 8-Bromo-cAMP, potentiated by the cAMP-specific phosphodiesterase inhibitor Ro 20-1724 and antagonized by protein kinase A (PKA) inhibitor H89. The enhancement of the mAHP attenuation induced by 50 microM 5-HT under raised [Ca(2+)](o) was blocked by a protein kinase C (PKC) inhibitor chelerythrine, suggesting an involvement of PKC in this enhancement. On the other hand, the attenuation of the mAHP induced by PKC activator phorbol 12-myristate 13-acetate was blocked almost completely by H89, suggesting that the PKC action on the mAHP requires PKA activation. Neither 5-HT(1A) antagonist NAN-190 or 5-HT(4) antagonist SB 203186 blocked 5-HT-induced attenuation of the mAHP. We conclude that 5-HT induces dose-dependent attenuation of the mAHP amplitude through cAMP-dependent activation of PKA and that PKC-dependent PKA activation is also likely to be involved in the enhancement of 5-HT-induced attenuation of the mAHP under raised [Ca(2+)](o). Because the slope of the linear relationship between firing frequency and injected current was increased only when the mAHP amplitude was decreased by 5-HT, it is suggested that the relation between incoming synaptic inputs and firing output in JCMNs varies according to serotonergic effects on JCMNs and calcium-dependent modulation of its effects. (+info)
Comparison of external load compensation during rhythmic arm movements and rhythmic jaw movements in humans.
(11/597)
Experiments were performed on human elbow flexor and extensor muscles and jaw-opening and -closing muscles to observe the effect on rhythmic movements of sudden loading. The load was provided by an electromagnetic device, which simulated the appearance of a smoothly increasing spring-like load. The responses to this loading were compared in jaw and elbow movements and between expected and unexpected disturbances. All muscles showed electromyographic responses to unexpected perturbations, with latencies of approximately 65 ms in the arm muscles and 25 ms in the jaw. When loading was predictable, anticipatory responses started in arm muscles approximately 200 ms before and in jaw muscles 100 ms before the onset of loading. The reflex responses relative to the anticipatory responses were smaller for the arm muscles than for the jaw muscles. The reflex responses in the arm muscles were the same with unexpected and expected perturbations, whereas anticipation increased the reflex responses in the jaw muscles. Biceps brachii and triceps brachii showed similar sensory-induced responses and similar anticipatory responses. Jaw muscles differed, however, in that the reflex response was stronger in masseter than in digastric. It was concluded that reflex responses in the arm muscles cannot overcome the loading of the arm adequately, which is compensated by a large centrally programmed response when loading is predictable. The jaw muscles, particularly the jaw-closing muscles, tend to respond mainly through reflex loops, even when loading of the jaw is anticipated. The differences between the responses of the arm and the jaw muscles may be related to physical differences. For example, the jaw was decelerated more strongly by the load than the heavier arm. The jaw was decelerated strongly but briefly, <30 ms during jaw closing, indicating that muscle force increased before the onset of reflex activity. Apparently, the force-velocity properties of the jaw muscles have a stabilizing effect on the jaw and have this effect before sensory induced responses occur. The symmetrical responses in biceps and triceps indicate similar motor control of both arm muscles. The differences in reflex activity between masseter and digastric muscle indicate fundamental differences in sensory feedback to the jaw-closing muscle and jaw-opening muscle. (+info)
Effects of gravitational load on jaw movements in speech.
(12/597)
External loads arising as a result of the orientation of body segments relative to gravity can affect the achievement of movement goals. The degree to which subjects adjust control signals to compensate for these loads is a reflection of the extent to which forces affecting motion are represented neurally. In the present study we assessed whether subjects, when speaking, compensate for loads caused by the orientation of the head relative to gravity. We used a mathematical model of the jaw to predict the effects of control signals that are not adjusted for changes to head orientation. The simulations predicted a systematic change in sagittal plane jaw orientation and horizontal position resulting from changes to the orientation of the head. We conducted an empirical study in which subjects were tested under the same conditions. With one exception, empirical results were consistent with the simulations. In both simulation and empirical studies, the jaw was rotated closer to occlusion and translated in an anterior direction when the head was in the prone orientation. When the head was in the supine orientation, the jaw was rotated away from occlusion. The findings suggest that the nervous system does not completely compensate for changes in head orientation relative to gravity. A second study was conducted to assess possible changes in acoustical patterns attributable to changes in head orientation. The frequencies of the first (F1) and second (F2) formants associated with the steady-state portion of vowels were measured. As in the kinematic study, systematic differences in the values of F1 and F2 were observed with changes in head orientation. Thus the acoustical analysis further supports the conclusion that control signals are not completely adjusted to offset forces arising because of changes in orientation. (+info)
A new primate from the Middle Eocene of Myanmar and the Asian early origin of anthropoids.
(13/597)
A new genus and species of anthropoid primate, Bahinia pondaungensis gen. et sp. nov., is described from the Yashe Kyitchaung locality in the Late Middle Eocene Pondaung Formation (Myanmar). It is related to Eosimias, but it is represented by more complete remains, including upper dentition with associated lower jaw fragment. It is interpreted as a new representative of the family Eosimiidae, which corresponds to the sister group of the Amphipithecidae and of all other anthropoids. Eosimiidae are now recorded from three distinct Middle Eocene localities in Asia, giving support to the hypothesis of an Asian origin of anthropoids. (+info)
oto is a homeotic locus with a role in anteroposterior development that is partially redundant with Lim1.
(14/597)
Genetic control of mammalian head development involves mechanisms that are shared with trunk development as well as mechanisms that are independent. For example, mutations in the nodal gene disrupt axis formation and head development while mutations in the Otx2 or Lim1 genes block head development without disrupting development of the trunk. We show here that the oto mutation on mouse chromosome 1 defines a locus with a critical role in anterior development. The oto mutation disrupts development of the telencephalic and optic vesicles, the pharyngeal endoderm and the first branchial arch. Also, oto embryos have dose-dependent, posterior homeotic transformations throughout the axial skeleton. To further dissect the role of the oto locus in head development, we crossed mice carrying oto and Lim1 mutations. Interactions between the two mutations indicate that the role of oto in the regulation of head development is partially redundant with that of Lim1. The phenotype of oto embryos points to an early and critical role for oto in the development of forebrain subregions. Transformations of the vertebrae in oto embryos reveal a Lim1-independent role in the establishment of positional information in the trunk. (+info)
Comparative susceptibility of rainbow trout Oncorhynchus mykiss and brown trout Salmo trutta to Myxobolus cerebralis, the cause of salmonid whirling disease.
(15/597)
The susceptibility of rainbow trout Oncorhynchus mykiss and brown trout Salmo trutta to Myxobolus cerebralis, the cause of salmonid whirling disease, was assessed following dosed exposures to the infectious stages (triactinomyxons). Parallel groups of age-matched brown trout and rainbow trout were exposed to 10, 100, 1000 or 10,000 triactinomyxons per fish for 2 h and then placed in aquaria receiving single pass 15 degrees C well water. Severity of infection was evaluated by presence of clinical signs (whirling and/or black tail), prevalence of infection, severity of microscopic lesions, and spore counts 5 mo after exposure. Clinical signs of whirling disease, including a darkened caudal region (black tail) and radical tail chasing swimming (whirling), occurred first among rainbow trout at the highest dose at 6 to 7 wk post exposure. Black tail and whirling occurred among rainbow trout receiving 1000 and 100 triactinomyxons per fish at 8 to 9 wk post exposure. Only 1 of 20 fish had a black tail among rainbow trout receiving 10 triactinomyxons per fish, although 30% of the fish were infected at 5 mo post exposure. Black tails were observed in brown trout at 1000 and 10,000 triactinomyxons per fish beginning at 11 and 7 wk post exposure, respectively. There was no evidence of the tail chasing swimming (whirling) in any group of brown trout. The prevalence of infection, spore numbers, and severity of microscopic lesions due to M. cerebralis among brown trout were less at each exposure dose when compared to rainbow trout. Infections were found among rainbow trout at all doses of exposure but only among brown trout exposed to doses of 100 triactinomyxons per fish or greater. Risk of infection analyses showed that rainbow trout were more apt to be infected at each exposure dose than brown trout. Spore counts reached 1.7 x 10(6) per head among rainbow trout at the highest dose of exposure compared to 1.7 x 10(4) at the same exposure dose among brown trout. Spore numbers increased with dose of exposure in rainbow trout but not in brown trout. As microscopic lesion scores increased from mild to moderate, spore numbers increased in rainbow trout but not brown trout. The mechanisms by which brown trout resist infections with M. cerebralis were not determined. Cellular immune functions, including those of eosinophilic granular leukocytes that were more prominent in brown trout than rainbow trout, may be involved. (+info)
Synaptic modulation contributes to firing pattern generation in jaw motor neurons during rejection of seaweed in Aplysia kurodai.
(16/597)
Japanese species, Aplysia kurodai, feeds well on Ulva but rejects Gelidium (Geli.) or Pachydictyon (Pach.) with different rhythmic patterned movements of the jaws and radula. During ingestion the jaws open at the radula-protraction phase and remain half open at the initial phase of the radula-retraction, whereas during rejection the jaws open similarly but start to close immediately after the onset of the radula-retraction. These can be induced not only by the natural seaweed but by the extract solutions. We previously showed that the change of the patterned jaw movements from the ingestion to the rejection may result from the decrease in the delay of the firing onset of the jaw-closing (JC) motor neurons during their depolarization. This diminished delay produces a phase advance relative to the radula-retraction phase. In that study, we showed that during ingestion the buccal multiaction (MA) neurons may generate the delay of firing onset of the JC motor neurons by producing monosynaptic inhibitory postsynaptic potentials (IPSPs) during the initial portion of their depolarization. In the present experiments, the firing patterns in the MA neurons induced by application of the Geli. or Pach. extract to the lips were explored in the semi-intact preparations. During the Pach. response the duration and the firing frequency of the MA firing at each depolarizing phase were decreased in comparison with the Ulva response. No decreases in the MA firing were observed during the Geli. response, suggesting that the similar patterned jaw movements during rejection of Geli. and Pach. may be generated by different neural mechanisms. Moreover, the size of the MA-induced IPSP in the JC motor neurons was largely decreased by application of the Geli. or Pach. extract to the lips in the reduced preparations consisting of the tentacle-lips and the cerebral-buccal ganglia. Voltage-clamp experiments on the JC motor neurons showed that the size of synaptic current induced by the MA spikes was decreased by application of these solutions to the lips. The decrease was induced when the buccal ganglia were bathed in a solution to block polysynaptic pathways. These results suggest that the advance of the onset of the JC firing at each depolarizing phase during the Geli. or Pach. response may be mainly or partly caused by the decrease in the size of the MA-induced IPSP in the motor neurons. Modulatory action of cerebral neurons or peripheral afferent neurons in the lip region may contribute to this synaptic plasticity. (+info)