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F F Ebner

Publications and source records attributed to F F Ebner.

At least 19 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.

Animals↗
PubMed1989

Peripheral nerve damage facilitates functional innervation of brain grafts in adult sensory cortex.

The neural pathways that relay information from cutaneous receptors to the cortex provide the somatic sensory information needed for cortical function. The last sensory relay neurons in this pathway have cell bodies in the thalamus and axons that synapse on neurons in the somatosensory cortex. After cortical lesions that damage mature thalamocortical fibers in the somatosensory cortex, we have attempted to reestablish somatosensory cortical function by grafting embryonic neocortical cells into the lesioned area. Such grafts survive in adult host animals but are not innervated by thalamic neurons, and consequently the grafted neurons show little if any spontaneous activity and no responses to cutaneous stimuli. We have reported that transection of peripheral sensory nerves prior to grafting "conditions" or "primes" the thalamic neurons in the ventrobasal complex so that they extend axons into grafts subsequently placed in the cortical domain of the cut nerve. In this report we present evidence that the ingrowth of ventrobasal fibers leads to graft neurons that become functionally integrated into the sensory circuitry of the host brain. Specifically, the conditioning lesions made prior to grafting produce graft neurons that are spontaneously active and can be driven by natural activation of cutaneous receptors or electrical stimulation of the transected nerve after it regenerates. Furthermore, oxidative metabolism in these grafts reaches levels that are comparable to normal cortex, whereas without prior nerve cut, oxidative metabolism is abnormally low in neocortical grafts. We conclude that damage to the sensory periphery transsynaptically stimulates reorganization of sensory pathways through mechanisms that include axonal elongation and functional synaptogenesis.

Animals↗
PubMed1988

Maintenance of discrete somatosensory maps in subcortical relay nuclei is dependent on an intact sensory cortex.

Lesions of the rat barrelfield cortex drastically alter the discrete representations of the somatosensory periphery in the central nervous system. We have found that lesions placed in the parietal cortex, after the formation of barrels (postnatal day 5), can irreversibly abolish vibrissae- and extremity-related patterns of cytochrome oxidase activity in the principal sensory nucleus of the trigeminal nerve and in the dorsal column nuclei. Furthermore, abnormal patterns of enzymatic activity occur in the remaining primary somatosensory cortex and the ventrobasal nucleus of the thalamus. We conclude that cortical barrels are essential in maintenance of periphery-related discrete morphological organization in the rodent somatosensory system.

Afferent Pathways↗
PubMed1988

Time course of neocortical graft innervation by AChE-positive fibers.

Acetylcholinesterase (AChE)-containing axons are the only extrinsic fibers projecting to the adult cortex that readily innervate embryonic cortical grafts up to normal densities without prior manipulation of the host brain. In the present paper we compare the time course of AChE-positive fiber innervation in the normal mouse cortex with that seen in neocortical grafts by using AChE histochemistry as a marker for presumed cholinergic fibers. Donor tissue was taken at two different stages of gestation; before (embryonic days 12-14, or E12-14) and after (E17-19) the cortical plate is formed. Three features are analyzed: 1) the distribution and density of AChE-containing fibers, 2) the presence of AChE-positive cells, and 3) the distribution of butyrylcholinesterase (BuChE)-positive elements. The modification of Koelle's method used for AChE localization showed AChE-positive fibers in developing parietal neocortex as early as E18-19. The distribution of AChE-labeled fibers in the normal cortex achieves the mature pattern by the end of the third postnatal week. The rate of innervation of transplants takes longer and depends on the age of the donor tissue. Tissue from both donor ages first showed AChE-positive fibers crossing the host-transplant interface by 7 days postsurgery. E17-19 tissue approaches the density of AChE-positive fibers in the normal adult cortex by 15 weeks after grafting, whereas the E12-14 donor tissue does not approach normal innervation densities until after 20 weeks. While the degree of innervation in the E12-14 donor tissue never equalled the surrounding adult cortex within our range of survival times, a few of the E17-19 transplants did develop densities equal to that of the host cortex. AChE-positive cells are first detectable in the normal parietal cortex on the day of birth, peak by the end of the first postnatal week, and then decline in number to the low levels of the mature cortex after the second postnatal week. Grafted cells in E12-14 tissue stain lightly for AChE by 7 days postsurgery, achieve maximal densities by 3 weeks, and become markedly reduced in number and density by 10 weeks. Cells in E17-19 tissue are lightly reactive by 7 days postsurgery, reach maximal numbers by 2 weeks postsurgery, and become similar in number and density to those seen in the mature cortex after 4 weeks. The appearance of BuChE-reactive blood vessels, neurons, and glia in both normal development and in the transplants is described and discussed.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed1988

Peripheral nerve transection induces innervation of embryonic neocortical transplants by specific thalamic fibers in adult mice.

Embryonic neocortical tissue survives and differentiates when grafted to injured adult neocortex. While these transplants are readily innervated by the host cholinergic fibers, specific thalamic fibers fail to innervate them. The present study was designed to test whether changing the activity levels of the thalamic ventrobasal projection neurons would promote sprouting of their axons into the embryonic cortical implants placed in the barrel field cortex. To achieve this the main input to these thalamic neurons was eliminated two synapses away, by blocking the peripheral sensory input to the barrel field cortex. Adult hosts underwent unilateral transection of the infraorbital nerve and two days later the contralateral barrel field cortex was lesioned enough to insert an embryonic neocortical graft. Following a one month post-transplantation period we examined the amount of specific thalamic axon ingrowth into the transplants by injecting the ventrobasal nucleus with horseradish peroxidase. The control cases without prior nerve damage confirmed previous observations that ventrobasal nucleus neurons fail to innervate the implanted neocortex. Transection of the infraorbital nerve prior to transplantation resulted in an unprecedented ingrowth of specific thalamic axons into the transplants. There was no significant difference in the amount of thalamic fiber ingrowth into the transplants when the peripheral nerve was (transection) or was not (cautery) allowed to regenerate. However, transection of the infraorbital nerve permits the nerve to regenerate and at least partially reconnect the sensory periphery, thus leading to the possibility of functional integration of the neocortical transplants into the host trigeminal system. The morphology and distribution of host acetylcholinesterase-positive fibers that grow into the transplants under both experimental and control conditions were distinctly different from those of thalamic axons. These results provide the first demonstration of peripheral sensory nerve induction of regenerative propensity in specific thalamocortical projection neurons. The thalamic fiber ingrowth should lead to enhanced functional innervation of the neocortical implants and better incorporation of the graft into the adult host brain circuitry.

Acetylcholinesterase↗
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↗
PubMed1987

A physiological basis for a theory of synapse modification.

The functional organization of the cerebral cortex is modified dramatically by sensory experience during early postnatal life. The basis for these modifications is a type of synaptic plasticity that may also contribute to some forms of adult learning. The question of how synapses modify according to experience has been approached by determining theoretically what is required of a modification mechanism to account for the available experimental data in the developing visual cortex. The resulting theory states precisely how certain variables might influence synaptic modifications. This insight has led to the development of a biologically plausible molecular model for synapse modification in the cerebral cortex.

Action Potentials↗
PubMed1986

Tyrosine hydroxylase is expressed by neocortical neurons after transplantation.

Tyrosine hydroxylase [TyrOHase; L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2], an essential enzyme in the synthesis of catecholamines, is expressed normally by neurons in the brainstem but not by those in mature neocortex. When embryonic neocortex is transplanted into adult neocortex, TyrOHase-immunoreactive cells develop and continue to be present in the transplants for the life of the host animal. The percentage of transplant neurons that express TyrOHase is highly correlated with the age of the embryonic donor tissue at the time of transplantation. Many TyrOHase-immunoreactive cells are present in transplants from embryonic day 12 (E12) embryos. The labeled cells are frequently arrayed in striking clusters of cell bodies and their processes, which ramify densely within the transplants. Moderate numbers of cells are found scattered throughout transplants from E14 donors, while E17 donors consistently develop small numbers of TyrOHase-containing cells. Tissue removed for transplantation on the day before birth (E19) never contains cells that express TyrOHase. The TyrOHase-positive cells are mostly bipolar and stellate in shape and show neither immunoreactivity for other catecholamine-synthesizing enzymes nor catecholamine fluorescence. These results provide a demonstration of continued TyrOHase synthesis in central nervous system cells that normally do not express this enzyme. Because of these and similar results with other neurotransmitter enzymes, the transplantation paradigm is particularly useful as a technique for studying the factors that regulate enzyme induction and activity during development of the nervous system.

Animals↗
PubMed1985

The projection of three extrathalamic cell groups to the cerebral cortex of the turtle Pseudemys.

Three extrathalamic subcortical inputs to the part of the cerebral cortex that is known to receive thalamic fibers in the turtle were examined in the present study. Direct projections from the locus coeruleus, the superior medial raphe nucleus, and a wide area of the basal telencephalon that lies ventromedial to the globus pallidus were demonstrated with the horseradish peroxidase method. Fluorescence histochemistry confirmed the presence of catecholamine-containing fibers in the rostral half of dorsal cortex and also demonstrated a dense network of serotoninergic fibers. Biochemical analysis showed the concentration of both monoamines to be relatively high; the norepinephrine concentration was 709 ng/g and the serotonin concentration was 1,750 ng/g. No evidence was found to suggest the existence of either a dopamine fiber projection to cortex comparable to that of mammalian neocortex or the presence of an epinephrine pathway to turtle cortex equivalent to the epinephrine-containing fibers in the pallium of amphibians. The coexistence of the projections from the thalamus with noradrenergic projections from the locus coeruleus, serotoninergic projections from the superior medial raphe nucleus, and presumably cholinergic projections from the basal telencephalon provide at least four distinct subcortical inputs to the reptilian dorsal cortex. Neither thalamic nor similar extrathalamic inputs have been demonstrated in the dorsal pallium of amphibia. Mammalian neocortex, in contrast, has even more elaborately differentiated inputs of both types. These results support the idea that thalamic and extrathalamic inputs to cortex appear at the same time in vertebrate evolution, and that both types of inputs are required for the normal development and function of neocortex.

Animals↗
PubMed1985

Glutamic acid decarboxylase activity decreases in mouse neocortex after lesions of the basal forebrain.

Glutamic acid decarboxylase (GAD) activity was measured in the cerebral cortex of animals after acute and chronic lesions to basal forebrain cholinergic nuclei. Such lesions were shown to result in an extensive depletion of cholinergic markers in parietal cerebral cortex. A statistically significant 30% decrease in GAD activity was first detected at 6 weeks postlesion and was still measurable 8 months after the lesion. These results suggest that cholinergic inputs to cortex indirectly or directly influence GABAergic transmission in cortex.

Animals↗