Choline excites cortical neurons

In cats under halothane or methoxyflurane, iontophoretic applications of choline are only eight times weaker than applications of acetylcholine in evoking firing of neurons in the sensorimotor region of the cerebral cortex. The action of choline is suppressed by atropine but not by two agents that block choline uptake (hemicholinium-3 and triethylcholine), and is not potentiated by an anticholinesterase (physostigmine). Choline therefore appears to excite cortical neurons by a direct action, which may be a significant component of its beneficial therapeutic effects.     

Visual experience without lines: effect on developing cortical neurons

Kittens were reared in a planetarium-like visual environment that lacked straight line contours. Cortical neurons were subsequently highly sensitive to spots of light but not to straight lines, in marked contrast to those from a normal cat. If linear contour processing is an innate function it appears to be subject to substantial modification by early visual experience.     

Convergent projection of three separate thalamic nuclei on to a single cortical area

Three distinct sensory-motor nuclei in the thalamus project to parietal cortex in the Virginia opossum; the ventral posterior nucleus receives inputs from somatic sensory structures and projects to layers IV and III, the ventral anterolateral nucleus receives inputs from motor structures and projects to layers IV and III and inner I, and the central intralaminar nucleus receives inputs from sensory, motor, and other structures and projects to layers VI through outer I. The physiologically defined amalgamation of somatic sensory and motor cortex is correlated, therefore, with the extent of cortex that receives convergent somatic sensory and motor input from the thalamus.     

Drinking and eating elicited by cortical spreading depression

Single waves of unilateral and bilateral cortical spreading depression were administered to rats by electrophoretic injection of potassium ions into the occipital cortices. Aggressive and stereotyped eating, drinking, and exploratory behavior were elicited by unilateral and bilateral spreading depression. Onset of the elicited behaviors varied among rats from 4 to 8 minutes after injection of the ions. Direct activation of, or rebound from, inhibition of subcortical motivational mechanisms may be responsible for the effects.     

Retrograde amnesia gradients: effects of direct cortical stimulation

Electrical stimulation was delivered bilaterally to either the anterior or posterior cortex in rats from 0.1 second to 4 hours after a single training trial on an inhibitory avoidance task. As indicated by a retention test given 24 hours later, the length of the retrograde amnesia gradients ranged from 5 seconds to 240 minutes, depending on the brain region stimulated and the intensity of the stimulating current. The stimulation intensity that was threshold for amnesia varied directly with the length of the interval between training and treatment.     

Thalamocortical relay neurons: antidromic invasion of spikes from a cortical epileptogenic focus

Thalamocortical relay neurons whose axons project into a penicillininduced cortical epileptogenic focus generate bursts of action potentials during spontaneous interictal epileptiform discharges. These bursts originate in intracortical axons and propagate antidromically into thalamic neurons. Repetitive spike generation in cortical axons and presynaptic terminals could produce a potent excitatory drive and contribute to the generation of the large depolarization shifts which are seen in cortical elements during focal epileptogenesis.     

Intracellular potentials of cortical neurons during focal epileptogenic discharges

Focal electroencephalographic discharges in lesions of cortex induced by freezing are associated with prolonged membrane depolarizations and hyperpolarizations in neurons located at various depths in the lesion sites. Transmembrane potential changes have properties similar to those of postsynaptic potentials. The temporal relationship between intracellular potentials and paroxysmal discharges indicates that the latter are extracellularly recorded summations of synchronously developing depolarizations and hyperpolarizations in complex synaptic organizations of neurons.     

Ventral posterior thalamic neurons differentially responsive to noxious stimulation of the awake monkey

Of 76 cutaneously activated neurons recorded from the ventral posterior thalamus of awake, behaving monkeys, nine were weakly excited by innocuous skin stimulation and responded maximally only when noxious mechanical cutaneous stimuli were delivered within small, contralateral receptive fields. These results show that neurons capable of encoding the spatial and temporal features of noxious stimuli are located in the ventral posterior thalamus of the awake primate.     

Serotonin-containing neurons in brain: depression of firing by monoamine oxidase inhibitors

Monoamine oxidase inhibitors were administered to rats while the activities of single, serotonin-containing neurons of the midbrain raphe nuclei were being monitored with microelectrodes. All the inhibitors tested (pargyline, tranylcypromine, phenelzine, iproniazid) caused depression of raphe unit firing rate. The ability of monoamine oxidase inhibitors to depress raphe units was impaired by prior treatment with p-chlorophenylalanine, an inhibitor of serotonin synthesis.     

大鼠大脑皮质神经元体外分离培养和纯化研究

为建立动物中枢神经疾病的细胞作用模型,根据大鼠大脑皮质神经元的生存特性。按照抑制筛选的原理,对大鼠大脑皮质神经元进行了体外培养、纯化和鉴定。结果表明:培养的大脑皮质神经元在体外发育良好,经神经元特异性的烯醇化酶(NSE)免疫组织化学染色证明其纯度较高,可以用于进一步细胞作用模型的建立。     

Representation of action sequence boundaries by macaque prefrontal cortical neurons

Complex biological systems such as human language and the genetic code are characterized by explicit markers at the beginning and end of functional sequences. We report here that macaque prefrontal cortical neurons exhibit phasic peaks of spike activity that occur at the beginning and endpoint of sequential oculomotor saccade performance and have the properties of dynamic start- and end-state encoders accompanying responses to sequential actions. Sequence bounding may thus reflect a general mechanism for encoding biological information.     

Zinc selectively blocks the action of N-methyl-D-aspartate on cortical neurons

Large amounts of zinc are present in synaptic vesicles of mammalian central excitatory boutons and may be released during synaptic activity, but the functional significance of the metal for excitatory neurotransmission is currently unknown. Zinc (10 to 1000 micromolar) was found to have little intrinsic membrane effect on cortical neurons, but invariably produced a zinc concentration-dependent, rapid-onset, reversible, and selective attenuation of the membrane responses to N-methyl-D-aspartate, homocysteate, or quinolinate. In contrast, zinc generally potentiated the membrane responses to quisqualate or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and often did not affect the response to kainate. Zinc also attenuated N-methyl-D-aspartate receptor-mediated neurotoxicity but not quisqualate or kainate neurotoxicity. The ability of zinc to specifically modulate postsynaptic neuronal responses to excitatory amino acid transmitters, reducing N-methyl-to-aspartate receptor-mediated excitation while often increasing quisqualate receptor-mediated excitation, is proposed to underlie its normal function at central excitatory synapses and furthermore could be relevant to neuronal cell loss in certain disease states.     

Acetylcholine facilitation, atropine block of synaptic excitation of cortical neurons

Sinigle neurons in cat visual cortex were driven by afferent stimuli to determine the effects of drugs liberated from multibarreled micropipettes on synaptic transmission. Acetylcholine increased, and atropine decreased, the number of neuron discharges fired in response to stimulation of the mesencephalic reticular formation without necessarily affecting responses to other stimuli or affecting spontaneous firing.     

Role of subplate neurons in functional maturation of visual cortical columns

The subplate forms a transient circuit required for development of connections between the thalamus and the cerebral cortex. When subplate neurons are ablated, ocular dominance columns do not form in the visual cortex despite the robust presence of thalamic axons in layer 4. We show that subplate ablation also prevents formation of orientation columns. Visual responses are weak and poorly tuned to orientation. Furthermore, thalamocortical synaptic transmission fails to strengthen, whereas intracortical synapses are unaffected. Thus, subplate circuits are essential not only for the anatomical segregation of thalamic inputs but also for key steps in synaptic remodeling and maturation needed to establish the functional architecture of visual cortex.     

Muscarinic depression of long-term potentiation in CA3 hippocampal neurons

Behavioral studies have suggested that muscarinic cholinergic systems have an important role in learning and memory. A muscarinic cholinergic agonist is now shown to affect synaptic plasticity in the CA3 region of the hippocampal slice. Long-term potentiation (LTP) of the mossy fiber-CA3 synapse was blocked by muscarine. Low concentrations of muscarine (1 micromolar) had little effect on low-frequency (0.2 hertz) synaptic stimulation but did significantly reduce the magnitude and probability of induction of LTP. Experiments under voltage clamp showed that muscarine blocked the increase in excitatory synaptic conductance normally associated with LTP at this synapse. These results suggest a possible role for cholinergic systems in synaptic plasticity.     

Lack of coincidence between neural and behavioral manifestations of cortical spreading depression

The presence of cortical spreading depression is typically inferred from the presence of hypesthesia. The electrocorticogram and slow-potential change were recorded during cortical spreading depression and it was found that hypesthesia remained long after the cortex recovered from neural depression. Hypesthesia, therefore, is an unreliable indicant of cortical spreading depression; if cortical spreading depression is used as a research tool, neural activity must be monitored. These data offer a special problem for memory transfer studies.     

Effects of alcohol on the generation and migration of cerebral cortical neurons

Prenatal exposure to alcohol produces many developmental defects of the central nervous system, such as microcephaly, mental retardation, motor dysfunction, and cognitive deficiencies. Therefore, the generation of neurons in the cerebral cortex was examined in the offspring of female rats fed a diet containing ethanol. Prenatal exposure to ethanol delayed and extended the period during which cortical neurons were generated, reduced the number of neurons in the nature cortex with the same time of origin, and altered the distribution of neurons generated on a particular day. Thus, the proliferation and migration of cortical neurons are profoundly affected by in utero exposure to ethanol.