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F F Ebner

Publications and source records attributed to F F Ebner.

18 recordsLinked to original sources
PubMed1992

Somatic sensory responses in the rostral sector of the posterior group (POm) and in the ventral posterior medial nucleus (VPM) of the rat thalamus: dependence on the barrel field cortex.

The projection from the whiskers of the rat to the S-I (barrel) cortex is segregated into two separate pathways--a lemniscal pathway relayed by the ventral posterior medial nucleus (VPM) to cortical barrels, and a paralemniscal pathway relayed by the rostral sector of the posterior complex (POm) to the matrix between, above, and below barrels. Before investigating how the barrel cortex integrates these sensory pathways, it is important to learn more about the influence of the various inputs to the two thalamic nuclei. Based on the greater density of descending versus ascending projections to POm, it seemed likely that corticofugal inputs play an important role in the sensory activity of POm. To test this, the responses of POm and VPM cells to sensory stimuli were measured before, during, and after suppression of the S-I cortex. S-I was suppressed by application of magnesium or by cooling; the status of the barrel cortex was assessed continuously by an electrocorticogram. All VPM cells (n = 8) responded vigorously to whisker movement even when the barrel cortex was profoundly depressed. In contrast, all POm cells (n = 9) failed to respond to whisker movement once the barrel cortex became depressed, typically about 25 minutes after the start of cortical cooling or magnesium application. POm cells regained responsiveness about 30 minutes after the cessation of cortical cooling or the washoff of magnesium. These findings indicate that the transmission of sensory information through the lemniscal pathway occurs independently of the state of cortex, whereas transmission through the paralemniscal pathway depends upon the state of the cortex itself.

Animals↗
PubMed1992

Somatic sensory responses in the rostral sector of the posterior group (POm) and in the ventral posterior medial nucleus (VPM) of the rat thalamus.

The rodent barrel field cortex integrates somatosensory information from two separate thalamic nuclei, the ventral posterior medial nucleus (VPM) and the rostral sector of the posterior complex (POm). This paper compares the sensory responses of POm and VPM cells in urethane-anesthetized rats as a first step in determining how cortex integrates multiple sensory pathways. A complete representation of the contralateral body surface was identified in POm. Trigeminal receptive fields (RFs) of POm and VPM cells were mapped by computer-controlled displacement of individual whiskers; responses were quantified by using peristimulus time histograms. Average RF size was similar in POm (5.1 whiskers) and VPM (4.4 whiskers), but evoked responses in the two nuclei differed significantly according to all other measures. VPM cells were maximally responsive to one single whisker--the "center RF." Stimulating this whisker evoked, on average, a response of 1.4 spikes/stimulus at a latency of 7 ms; surrounding whiskers evoked responses of less than 1 spike/stimulus at latencies of greater than 8 ms. In contrast, POm cells were nearly equally responsive to several whiskers. Quantitative criteria allowed us to designate a single whisker as the "center RF" and stimulating this whisker evoked, on average, a response of 0.5 spikes/stimulus at a latency of 19 ms. VPM cells, but not POm cells, were able to "follow" repeated whisker deflection at greater than 5 Hz. We conclude that, when a single whisker is deflected, VPM activates the related cortical barrel-column at short latency--before the onset of activity in POm. The timing of activation could allow POm cells to modulate the spread of activity between cortical columns.

Animals↗
PubMed1992

Induction of high frequency activity in the somatosensory thalamus of rats in vivo results in long-term potentiation of responses in SI cortex.

Extracellular single-unit techniques were employed to record unitary activity simultaneously from the thalamic ventral posterior medial (VPM) nucleus and the ipsilateral primary somatosensory cortex of adult rats. Cross-correlation analysis triggered by the spontaneous firing of thalamocortical relay neurons in VPM and the discharge of layer IV neurons in the corresponding ipsilateral cortical barrel indicated that the paired-units included in this study were strongly correlated in their activity. The baseline responses of highly correlated cortical/thalamic pairs to a 10 ms deflection of a vibrissa on the contralateral side were measured using poststimulus time histograms. After establishing the baseline response, high frequency activity in VPM was induced in one of two ways: i) direct electrical stimulation of thalamic neurons or ii) whisker stimulation in the presence of bicuculline methiodide (BIC) released near the thalamic neurons. Both methods resulted in a conditioning stimulus (CS) paradigm consisting of "burst" of high-frequency activity (50-100 Hz) with an inter-burst interval of 150 ms (approximately 7 Hz). Almost immediately following the presentation of the CS, the response of layer IV cortical neurons to vibrissa stimulation increased by 37-62% over baseline values, which was maintained after the effects of BIC had worn off in VPM. This enhancement in the response of the cortical neurons was not accompanied by a concomitant increase in the thalamic responses. Thus, these results strongly suggest that the potentiation first occurred at the thalamocortical synapse.

Animals↗
PubMed1991

Horizontal long-term potentiation of responses in rat somatosensory cortex.

The search for mechanisms in neocortex that change synaptic efficacy and produce associative learning through activity-dependent processes has focused on the role of glutamate receptors of the N-methyl-D-aspartate (NMDA) type. NMDA receptor activation is necessary for the induction of long-term potentiation (LTP) in hippocampus and in neocortex. The effect of NMDA receptor activation is modulated in several ways, including Mg2+ block of the NMDA-dependent channel which prevents Ca2+ entry until neurons become partially depolarized. We report that when NMDA receptor activation is facilitated by lowering the extracellular [Mg2+] in the bathing medium, a low-frequency train presented in layer VI induces potentiated responses throughout a wide horizontal extent of layer II/III in neocortical slices. The response amplitudes potentiated by 34-200% over baseline values depending on the intensity of the repetitive conditioning stimulus and the distance of the recording site from the stimulus. At the same time that pre-existing evoked responses were potentiated, horizontal spread of activity in layer II/III was facilitated resulting in responses appearing at sites more than 1 mm from the stimulus. This enhanced transmission of responses persisted for greater than 2 h, and its induction was prevented by selective NMDA receptor antagonists. The results show that the horizontal spread of activity can be increased by altering the conditions of the stimulus presentation. We conclude that the mechanisms supporting LTP could determine the area of neocortex that is activated by a sensory input.

Animals↗
PubMed1990

Thalamic retrograde degeneration following cortical injury: an excitotoxic process?

Traumatic or stroke-like injuries of the cerebral cortex result in the rapid retrograde degeneration of thalamic relay neurons that project to the damaged area. Although this phenomenon has been well documented, neither the basis for the relay neuron's extreme sensitivity to axotomy nor the mechanisms involved in the degenerative process have been clearly identified. Physiological and biochemical studies of the thalamic response to cortical ablation indicate that pathological overexcitation might contribute to the degenerative process. The responses of thalamic projection neurons, protoplasmic astrocytes, and inhibitory thalamic reticular neurons in adult mice were examined from one to 120 days following ablation of the somatosensory cortex as part of an investigation of the role of excitotoxicity in thalamic retrograde degeneration. The responses of thalamic neurons to cortical ablation were compared with those produced by intracortical injection of the convulsant excitotoxin kainic acid, since the degeneration of neurons in connected brain structures distant to the site of kainic acid injection is also thought to occur via an excitotoxic mechanism. Within two days after either type of cortical injury, protoplasmic astrocytes in affected regions of the thalamic ventrobasal complex and the medial division of the posterior thalamic nuclei became reactive and expressed increased levels of immunohistochemically detectable glial fibrillary acidic protein. Within the affected regions of the ventrobasal complex an increased intensity of puncta positive for glutamate decarboxylase immunoreactivity, presumably due to an increase in its content within the terminals of the reciprocally interconnected thalamic reticular neurons, was also evident. These immunohistochemically detectable alterations in the milieu of the damaged thalamic neurons preceded the disappearance of the affected relay neurons by at least two days following cortical ablation and by seven to 10 days following intracortical kainic acid injection. Regions of the thalamus containing reactive astrocytes corresponded very closely to the regions undergoing retrograde degeneration. Protoplasmic astrocytes in these areas remained intensely reactive up to 60 days after cortical injury. Levels of glutamate decarboxylase were only transiently elevated in the degenerating regions of the ventrobasal complex following cortical ablation and returned to normal by 14 days. Increased glutamate decarboxylase immunoreactivity was transiently seen through the entire ventrobasal complex following intracortical kainic acid injection but was markedly more intense in degenerating regions. These patterns of labeling did not return to normal until 50 days after intracortical kainic acid injection, well after the death of the relay neurons. Cortical ablation and intracortical kainic acid injection produce similar alterations in thalamic neuronal and glial populations.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Intracortical processes regulating the integration of sensory information.

The mechanisms that link sensory inputs in spatially separated regions of cortex can be elucidated by analyzing the mechanisms that generate receptive field properties in cortical neurons under conditions that mimic the waking state; a state when learning, memory and the modification of synaptic strength can be most readily demonstrated. Important advances in understanding receptive field mechanisms in sensory cortex have arisen from studying the precise relationship between the mystacial vibrissae or "whiskers" and their neural representation in separate cortical domains or "barrels". The anatomical precision of whisker projections to barrels permits a unique delineation of thalamocortical and intracortical components of cortical cell responses based on latency and security of response to peripheral receptor stimulation. When recorded in awake animals or even under very light anesthesia, cortical neurons show two components to their response to whisker movement. Neurons in layer IV of a whisker's primary projection zone respond with short latency (7-10 msec) and a high response magnitude (two or more action potentials (spikes) per stimulus). This "Center Receptive Field" (CRF) for layer IV cells is generated in large part by sensory fiber inputs from the thalamus. The CRF is restricted to 1.4 whiskers on average and is the only response detectable when cortical responses are depressed by deep anesthesia. In the "waking state" the same neuron often will respond to deflection of 4-6 surrounding whiskers, but only at longer latency (15-40 msec) and with fewer spikes per stimulus. These more labile responses form an excitatory surround receptive field (SRF). Sensory information that is transduced by individual whiskers and that generates the SRF of a cortical neuron achieves this added response complexity through intracortical mechanisms. The control of the mechanisms that determine the dissemination of sensory information within cortex include: (1) regulating the level of GABAergic inhibition; and (2) potentiation or depression of the response level generated by repeated sensory experience. State-dependent "modulatory" inputs to cortex, such as the noradrenergic and cholinergic fiber system, could regulate the degree of horizontal spread of a sensory input, in part through global changes in the level of inhibition and/or regulating the amplitude of cortical responses, thereby determining the level of associative interactions between sensory inputs.

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PubMed1988

Basal forebrain lesions facilitate adult host fiber ingrowth into neocortical transplants.

The ability of mature host thalamic neurons to innervate embryonic (E19) cortex when implanted into the cortex of adult hosts was compared in normal and basal forebrain lesioned mice. The ingrowth of mature horseradish peroxidase-labeled thalamic axons into the transplants is facilitated by prior basal forebrain lesions. We discuss the possible reasons for the lesion-induced enhancement of axonal ingrowth, including the possibility that the enhanced ingrowth of thalamic fiber systems may be related to the loss of cortical innervation by extrathalamic brainstem inputs, especially cholinergic afferent fibers. The results support the interpretation that extrathalamic inputs to cortex play a modulatory role in regulating the growth and connections of specific sensory fiber systems during brain responses to injury.

Acetylcholinesterase↗
PubMed1988

The effect of thiamine deficiency on the structure and physiology of the rat forebrain.

Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological properties of neurons in the thalamus and somatosensory cortex. The regimen for experimentally inducing thiamine deficiency produced large lesions in the thalamus of every case; the lesions included most, if not all, of the neurons in the intralaminar thalamic nuclei. The extent of the lesion in the intralaminar thalamus was highly correlated with the loss of bilaterally synchronous spontaneous activity in the cerebral cortex. This correlation was seen in animals analyzed as early as 1-18 hr after the appearance of opisthotonus, the crisis state of thiamine deficiency, and as late as 2-9 weeks of recovery following thiamine replacement therapy. The loss of bilateral synchronous bursting neuronal activity following intralaminar thalamic lesions is consistent with the proposed role of the intralaminar thalamus as a pacemaker for rhythmic cortical activity (Armstrong-James et al., Exp. Brain Res., 1985; Fox and Armstrong-James, Exp. Brain Res. 63: 505-518, 1986). The location and size of the central lesions within the thalamus suggest that the observed neuronal loss could result from a nonhemorrhagic infarction in the ventromedial branches of the superior cerebellar arteries. Experimental thiamine deficiency also produced alterations in the receptive field properties of the somatosensory cortex neurons in all animals examined. Changes in cortical receptive field properties were correlated with the destruction of sensory relay neurons in the thalamic ventrobasal complex. The loss of the central lateral thalamic input to the cortex and the loss of somatosensory relay neurons in the ventrobasal thalamus in experimental thiamine deficiency produce alterations in cortical function which may contribute to deficits in memory and cognition analogous to those which characterize Korsakoff's psychosis in humans.

Animals↗
PubMed1978

Connections of the visual cortex in the hedgehog (Paraechinus hypomelas). II. Corticocortical projections.

Cortical subdivisions based on cytoarchitectural and myeloarchitectural observations of normal tissue were correlated with the topography of corticocortical connections in the visual system of the Pakistani hedgehog. Large subpial aspiration lesions were made in both visual and non-visual cortical regions to determine the areal limits of the corticocortical connections of the visual cortex. Subsequently, discrete electrolytic lesions were placed within the visual cortex. After appropriate survival periods, the brains were processed and stained with the Fink-Heimer technique. The results of these studies show that the visual cortex may be subdivided into four distinct regions from lateral to medial; the lateral parastriate cortex, the lateral and medial part of striate cortex, and the medial parastriate cortex. Within these regions, interhemispheric connections between visual cortices arise mainly in the lateral striate and lateral parastriate regions and terminate in a single band within the lateral portion of the cytoarchitecturally defined striate cortex. These corticocortical projections, therefore, substantially overlap with the geniculostriate projections. Lateral striate cortex and lateral parastriate cortex project in a reciprocal fashion that correlates well with the physiologically defined mirror image representation of two retinotopic maps of the binocular visual field on cortex. These connections are reflected about a line that is closely correlated with the medial edge of the band of commissural axon terminals that is located within the lateral striate cortex, instead of corresponding exactly with the striate-parastriate border as they do in other mammals. Medial striate cortex projects to medial parastriate cortex, indicating that the monocular portion of V I is related to a separate secondary area of cortex on the medial wall of the hemisphere.

Animals↗
PubMed1978

Interlaminar connections of the visual cortex in the hedgehog (Paraechinus hypomelas).

The contribution of each cortical lamina to intracortical circuitry was studied in the visual neocortex of the Pakistani hedgehog. Punctate laminar lesions were made electrolytically within the visual cortex, and after five to seven days the brains were processed and stained with the Fink-Heimer technique. The results of this study suggest that both horizontal and vertical connections are important to the organization of visual cortex in the hedgehog. The horizontal projections originate at three distinct cortical depths. Lesions in layer II reveal projections that traverse the inner one-half of layer I; lesions in layers III and IV reveal projections that traverse layer IV and that enter the cortical white matter; lesions in layers V and VI reveal projections that traverse the outer one-half of layer VI and that enter the cortical white matter. The vertical projections are oriented perpendicular to the pial surface. Layers II and III project to underlying layer V. Layers V and VI in turn contribute to a reciprocal projection back to all superficial cortical laminae. This anatomical data about intracortical circuitry is discussed with reference to the functional organization of visual cortex.

Animals↗
PubMed1976

Localization of function in corpus callosum: tactual information transmission in Macaca mulatta.

Different portions of the corpus callosum were transected in 28 juvenile rhesus monkeys. These animals were then taught a tactual roughness discrimination task while using their right hands and tested for transfer of training while using their left. Animals with some part of the posterior body region of the corpus callosum preserved exhibited intermediate or high levels of transfer of training. Animals with other portions of the commissures preserved, including the splenium, the anterior body, the genu, and/or the anterior commissure but with the posterior body region transected generally failed to show such transfer. It is concluded that tactual information is transmitted between the hemispheres through the posterior body region of the corpus callosum.

Animals↗
PubMed1975

Synaptic patterns in the visual cortex of turtle: an electron microscopic study.

The part of turtle general cortex that receives afferent fibers from the dorsal lateral geniculate nucleus and that shows evoked potentials to light stimuli has been studied with the electron microscope. This cortex consists of an outer molecular layer, a perikaryal layer, and a subcellular layer lying on a row of ependymal cell bodies. Neurons in the perikaral lamina are characterized by long spine-bearing apical dendrites ascending through the outer molecular layer and short finer basal dendrites in the subcellular zone. Scattered neurons without apical dendrites occur in both the molecular and subcellular zones. Two types of dendritic spines can be distinguished. Some are large, have a complex irregular shape, contain a variety of membranous sacs and mitochondria, and occasionally, a single bundle of microtubules embedded in an electron-dense background [corrected] opacity. These large spines are the most common postsynaptic element in the outer third of the molecular layer, where they are located on the distal enlargement that contains only electron-dense fuzz. They are the most common post-synaptic element in the lower two-thirds of the molecular layer where they arise from the proximal portion of apical dendrites. Most synaptic contacts are found on the dendritic spines and are of the "round-asymmetrical" type. Not infrequently "flat-symmetrical" synapses are coupled to "round-asymmetrical" contacts on individual large spines. The few contacts present on spine-bearing dendritic shafts are of both types. Axo-somatic contacts are mainly of the "flat-symmetrical" variety. Thus the synaptic patterns on the principal cells of turtle visual cortex are remarkably similar to those found on pyramidal cells of mammalian neocortex. In addition, however, axon terminals, dendrites and glial (ependymal) processes were often seen to give rise to membranous pouches containing large vacuoles and invaginating into dendritic shafts or spines. Rarely, axon terminals were seen to form contacts, identical in appearance to synaptic contacts, on cell bodies in the ependymal lining. More frequently, unusual types of membrane differentiations were present at the site of apposition of the membranes of axon terminals and ependymal processes. They are interpreted as functional neuroependymal contacts.

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