Dose-Dependence of the Excitatory Effects of Acetylcholine on Common Snail Neurons after Orthodromic Tetanization

Neuroscience and Behavioral Physiology -     

The Effect of Extracellular Calcium on Thermal Excitability of the Sensory Units in the Tooth of the Cat

Intradental sensory nerve impulse activity was measured from dentinal cavities in canine teeth of anesthetized cats. No spontaneous activity was usually recorded in cavities filled with isotonic saline. Heat stimulation of 15–20^oC failed to give any impulse activity, while other stimuli, such as air blasts produced bursts of impulses. Lowering extracellular calcium ion concentration. by local application of sodium citrate, sodium oxalate or EDTA, induced impulse activity. Under these conditions, heat produced a rapid increase in discharge activity. which lasted as long as the stimulus was applied. Increased extracellular calcium concentration abolished this response to heat. The present findings show that a change in the extracellular calcium ion concentration modulates the excitability of intradental sensory units, and may thus also modulate the resulting experience of pain.     

Intradental nerve activity and jaw-opening reflex in response to mechanical deformation of cat teeth

Mechanical stress was applied to canine teeth in anaesthetized cats to excite intradental A-fibres and to produce digastric muscle EMG responses. Activity in the intradental sensory units was recorded by two electrodes, one inserted in a dentinal cavity, the other in contact with the gingival sulcus. A pneumatically driven piston was used to cause a mechanical stress (10-150 N) on the stabilized tooth crown for 30 s, with instantaneous onset and release. Application of a load of 30 N produced a momentary burst of impulses in 2 of 12 teeth; 8 out of 10 teeth responded when 150 N was used. Digastric EMG responses were obtained at and above 60 N. Removal of the coronal pulp or cooling of the tooth crown with ethyl chloride abolished this reflex, whereas percussion of the tooth still produced a digastric response. Our results suggest that load-induced deformation of teeth activates intradental sensory mechanisms and a reflex withdrawal reaction unrelated to periodontal stimulation.     

The Sensory Basis of Reading Problems

Learning to read is much more difficult than learning to speak. Most children teach themselves to speak with little or no difficulty. Yet a few years later when they come to learn to read they have to be taught how to do it; they do not pick up reading by themselves. This is because we speak in words and syllables, but we write in phonemes. Syllables do not naturally break down into the sounds of letters and letter units (i.e., phonemes) because these do not correspond to physiologically distinct articulatory gestures (Liberman, Shankweiler, & Studdert-Kennedy, 1967). Alphabetic writing was only invented when people realized that syllables could be artificially divided into smaller acoustically distinguishable phonemes that could be represented by a small number of letters. But these distinctions are arbitrary cultural artifacts, and their mastery was originally confined to a select social class. And until about 100 years ago it did not matter much if the majority of people could not read; the acquisition of reading probably had no serious disadvantages. Reading requires the integration of at least two kinds of analysis (Castles & Coltheart, 1993; Ellis, 1984; Manis, Seidenberg, Doi, McBride-Chang, & Petersen, 1996; Morton, 1969; Seidenburg, 1993). First, the visual form of words, the shape of letters, their order in words, and common spelling patterns, which is termed their orthography, has to be processed visually. Their orthography yields the meaning of familiar words very rapidly without needing to sound them out. But for unfamiliar words, and all words are fairly unfamiliar to the beginning reader, the letters have to be translated into the speech sounds (i.e., phonemes) that they stand for, and then those sounds have to be melded together in inner speech to yield the word and its meaning. Reading exclusively by the phonological route is more time consuming than if words can be accessed directly without requiring phonological mediation.     

局部兴奋全局抑制神经元振荡网络在医学图像分割中的应用

视觉皮层神经元之间存在的局部兴奋全局抑制机制能够使神经元根据接受到的视觉信息产生相应的振荡活动。在深入分析和探讨基于此生理振荡活动的具有局部兴奋全局抑制机制的视觉皮层神经元振荡网络模型的基础之上，运用最小交叉熵原理提出了一种自动确定参数的图像分割新算法。该算法应用于医学图像分割试验中，试验结果表明，这种以生物视觉感知机理为基础的神经计算方法可有效的检测出不同目标。由于该振荡网络具有高速并行运算，便于硬件实现等特点，因此这种方法在图像实时处理中具有很大的潜力和应用前景。     

Excitatory effects of serotonin on rat striatal cholinergic interneurones

We investigated the effects of 5-hydroxytryptamine (5-HT, serotonin) in striatal cholinergic interneurones with gramicidin-perforated whole-cell patch recordings. Bath-application of serotonin (30 μ m ) significantly and reversibly increased the spontaneous firing rate of 37/45 cholinergic interneurones tested. On average, in the presence of serotonin, firing rate was 273 ± 193% of control. Selective agonists of 5-HT_1A, 5-HT₃, 5-HT₄ and 5-HT₇ receptors did not affect cholinergic interneurone firing, while the 5-HT₂ receptor agonist α-methyl-5-HT (30 μ m ) mimicked the excitatory effects of serotonin. Consistently, the 5-HT₂ receptor antagonist ketanserin (10 μ m ) fully blocked the excitatory effects of serotonin. Two prominent after-hyperpolarizations (AHPs), one of medium duration that was apamin-sensitive and followed individual spikes, and one that was slower and followed trains of spikes, were both strongly and reversibly reduced by serotonin; these effects were fully blocked by ketanserin. Conversely, the depolarizing sags observed during negative current injections and mediated by hyperpolarization-activated cationic currents were not affected. In the presence of apamin and tetrodotoxin, the slow AHP was strongly reduced by 5-HT, and fully abolished by the calcium channel blocker nickel. These results show that 5-HT exerts a powerful excitatory control on cholinergic interneurones via 5-HT₂ receptors, by suppressing the AHPs associated with two distinct calcium-activated potassium currents.     

The Selective Action of Opioid Peptides on Excitability and the Various Sensory Inputs of Defensive Behavior Command Neurons LPl1 and RPl1 of the Common Snail

The nature of the effects of opioid peptides on the properties of electrogenic membranes and the responses of defensive behavior command neurons LPl1 and RPl1, evoked by sensory stimuli of different modalities and application sites was studied in semi-intact preparations from common snails. Application of met-enkephalin (10 M) to the snail CNS produced increases in membrane excitability along with facilitation of responses to application of dilute quinine solution to the animal's head and depression of responses to tactile stimulation of the head. Met-enkephalin (0.1 M) produced only depression of responses to tactile stimulation of the head. Application of leu-enkephalin (10 M) was accompanied by depression of responses to tactile stimulation of the head. Membrane excitability and responses to chemical sensory stimulation during application showed no change during application of this peptide. These effects of both peptides appeared 10–20 min from the start of application and lasted 15–30 min after washing was started. In addition, facilitation of the responses of neurons to chemical sensory stimulation was seen 30–50 min after the start of leu-enkephalin application. The responses of neurons to tactile stimulation of the snail's foot were not altered by application of peptides. The neuronal effects of peptides were suppressed by simultaneous application of naloxone (50 M). Thus, we observed the selective action of opioid peptides on the synaptic plasticity of neurons LPl1 and RPl1, both in relation to the location of sensory stimulation and in relation to sensory modality.     

The Effects of Glutamate on Spontaneous Acetylcholine Secretion Processes in the Rat Neuromuscular Synapse

Experiments on rat diaphragm muscles showed that glutamate (10 M – 1 mM) had no effect on the mean frequency, interspike intervals, and amplitude-time characteristics of miniature endplate potentials, but had a suppressive action on non-quantum secretion (the intensity of which was assessed in terms of the H effect). The effect of glutamate was markedly concentration-dependent and was completely overcome by blockade of NMDA receptors, inhibition of NO synthase, and by binding of NO molecules in the extracellular space by hemoglobin. It is suggested that glutamate can modulate the non-quantum release of acetylcholine, initiating the synthesis of NO molecules in muscle fibers via activation of NMDA receptors followed by the retrograde action of NO on nerve terminals.     

The Effects of Sensory Perceptual Isolation on Single Motor Unit Conditioning

Forty male volunteers were injected with bipolar fine-wire electrodes into the tibialis anterior muscle and trained to isolate and cunt nil a single motor unit. A light panel indicated trial onsets and correct and incorrect responses. Subjects were randomly assigned to the isolation or non-isolation condition for both sessions. Isolation condition was produced In an air-fluidized. ceramic-bead bed in a light attenuating chamber. A relearning session followed the initial session after a two week interim rest. The hypodynamic effects of sensory isolation increased the speed of learning to isolate and control an SMU. The results. suggested that subjects were better able to attend to the relatively weak proprioceptive information provided by the SMU through the reduction of the amount and/or variety of competing stimuli.     

Excitatory effects of GABA on procerebrum neurons in a slug

Classical neurotransmitters, such as glutamate and γ-aminobutyric acid (GABA), often have different actions on invertebrate neurons from those reported for vertebrate neurons. In the terrestrial mollusk Limax, glutamate was found to function as an inhibitory transmitter in the procerebrum (PC), but it has not yet been clarified how GABA acts in the PC. We thus examined what effects GABA exerts on PC neurons in the present study. For this purpose, we first applied GABA to isolated PC preparations and recorded postsynaptic currents and potentials in PC neurons. The GABA application reduced the amplitude of inhibitory postsynaptic currents and depolarization-induced outward currents recorded in nonbursting neurons and increased the number of spontaneous spikes of nonbursting neurons. However, direct GABA-induced currents were not observed in either bursting or nonbursting neurons. These results suggest a potential direct effect of GABA on outward currents resulting in enhanced excitability of PC neurons. Next, we measured the change in [Ca(2+)](i) in cultured PC neurons by application of GABA. The GABA application increased spontaneous Ca(2+) events in cultured neurons. These Ca(2+) events were ascribable to the influx of extracellular Ca(2+). We then confirmed the presence of GABA and GABA receptors in the PC. The GABA-like immunoreactivity was observed in the neuropil layers of the PC, and the mRNAs for both GABA(A) and GABA(B) receptors were expressed in the PC. In particular, GABA(B) receptor mRNA, rather than GABA(A), was found to be more abundantly expressed in the PC. These results suggest that GABA functions as an excitatory modulator for PC neurons via mainly GABA(B) receptors.     

Immunology of the Acetylcholine Receptor

Myasthenia gravis is a spontaneously occurring autoimmune disease in which antibodies and lymphocytes are specifically reactive with nicotinic ACh receptors of skeletal muscle. Antibodies reactive with junctional receptors of human muscle are found in 90% of patients with myasthenia gravis and not at all in other diseases. Their capacity to cross the placenta suggests their involvement in the pathogenesis of neonatal myasthenia. The role of the thymus in myasthenia gravis remains a mystery, but it has recently been established that the thymus contains nicotinic ACh receptors and that anti-receptor antibodies are present in myasthenic thymuses.

Antibodies of myasthenic patients detect only partial cross reactivity between ACh receptors of different species. However, greater antibody binding is observed with receptors isolated from denervated rat muscle than with receptors from normal rat muscle. This suggests that extrajunctional and junctional ACh receptors might express different antigenic determinants. Although human antibodies bind minimally to ACh receptors of the electric organs of eels and marine rays, lymphocyte reactivity to electric eel receptors is found in high incidence in myasthenic patients. This suggests that electric organ and mammalian muscle ACh receptors may share more lymphocyte-defined than serologically-defined antigenic determinants.

Both cellular and Numeral immune responses to ACh receptors can be induced experimentally. Sufficient antigenic homology exists between receptors of different species that electric organ receptors are capable of inducing in mammals experimental autoimmune myasthenia gravis. Syn-geneic muscle receptor also is immunogenic in rats. Induction of both myasthenia and antibodies to ACh receptor requires participation of thymus-derived lymphocytes. The majority of ACh receptors in myasthenic rat muscle exist complexed with antibody, but antibody is not bound directly to the receptor's ACh-binding site. Anti-receptor antibodies in vitro are capable of impairing the electrophysiological function of ACh receptors with minimal blocking of the ACh-binding site and in the absence of complement. Thus, myasthenia gravis and its experimental model provide unique biological tools for studying the structure, function and pathology of cell membrane receptors.