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H J Luhmann

Publications and source records attributed to H J Luhmann.

54 records · Page 3Linked to original sources
PubMed1996

Characterization of neuronal migration disorders in neocortical structures: I. Expression of epileptiform activity in an animal model.

Hypoxia, ischemia and other forms of brain injury during the pre- and perinatal period may cause neuronal migration disorders which results in irreversible structural modifications. In human neocortex, these malformations have been associated with severe mental retardation, motor dysfunction and the manifestation of therapy-resistant epilepsy. We were interested in analyzing the expression of epileptiform activity in an animal model of neocortical migration disorders. Newborn rats received a focal freeze lesion and were investigated anatomically and in vitro electrophysiologically after survival times of up to five months. Anatomic abnormalities included loss of normal cortical lamination (focal microgyrus) and presence of ectopic cell clusters in layer I and in the white matter (heterotopia). The functional in vitro analyses with eight extracellular recording electrodes revealed a prominent hyperexcitability of the disorganized neocortical network. Electrical stimulation of the afferents elicited epileptiform responses that propagated over > 4 mm in the horizontal direction. In untreated and sham-operated animals, this spread of evoked activity was restricted to 0.5-1 mm. Epileptiform responses were not significantly affected by APV but blocked by NBQX, indicating that AMPA receptors play a prominent role in the generation and propagation of this pathophysiological activity. Our data suggest that the experimentally induced migration disturbances cause long-term structural and/or functional modifications in the neocortical network which may form the basis for the expression of epileptiform activity.

Animals↗
PubMed1995

Ischaemia-induced long-term hyperexcitability in rat neocortex.

The long-term structural and functional consequences of transient forebrain ischaemia were studied with morphological, immunohistochemical and in vitro electrophysiological techniques in the primary somatosensory cortex of Wistar rats. After survival times of 10-17 months postischaemia, neocortical slices obtained from ischaemic animals were characterized by a pronounced neuronal hyperexcitability in comparison with untreated age-matched controls. Extra- and intracellular recordings in supragranular layers revealed all-or-none long-latency recurrent responses to orthodromic synaptic stimulation of the afferent pathway. These responses were characterized by durations up to 1.7 s, by multiple components and by repetitive synaptic burst discharges. The reversible blockade of this late activity by DL-amino-phosphonovaleric acid (APV) suggested that this activity was mediated by N-methyl-D-aspartate (NMDA) receptors. The peak conductance of inhibitory postsynaptic potentials was significantly smaller in neurons recorded in neocortical slices obtained from ischaemic animals than those from the controls. However, the average number of parvalbumin (PV)-labelled neurons per mm3, indicative of a subpopulation of GABAergic interneurons, and the average number and length of dendritic processes arising from PV-containing cells was not significantly different between ischaemic and control cortex. The prominent dysfunction of the inhibitory system in ischaemic animals occurred without obvious structural alterations in PV-labelled cells, indicating that this subpopulation of GABAergic interneurons is not principally affected by ischaemia. Our data suggest a long-term down-regulation of inhibitory function and a concurrent NMDA receptor-mediated hyperexcitability in ischaemic neocortex. These alterations may result from structural and/or functional properties of inhibitory non-PV-positive neurons or permanent functional modifications on the subcellular molecular level, i.e. alterations in the phosphorylation status of GABA and/or NMDA receptors. The net result of these long-term changes is an imbalance between the excitatory and inhibitory systems in the ischaemic cortex with the subsequent expression and manifestation of intracortical hyperexcitability.

Animals↗
PubMed1995

Impairment of intracortical GABAergic inhibition in a rat model of absence epilepsy.

The WAG/Rij rat strain is characterized in its EEG by the manifestation of spike-wave discharges which resemble in their spontaneous appearance and pharmacological sensitivity the absence epilepsy observed in humans. In order to test the hypothesis whether cellular intrinsic membrane and/or synaptic network properties in the neocortex are modified in this form of epilepsy, we analyzed with extra- and intracellular recording techniques the functional status of neocortical slices obtained from adult epileptic WAG/Rij rats and compared them with the data acquired from non-epileptic control Wistar rats. Intrinsic membrane properties, like resting membrane potential, neuronal input resistance and basic cellular firing characteristics, did not differ between these two strains. However, the analysis of extra- and intracellularly recorded synaptic responses revealed an intracortical hyperexcitability which was accompanied by a significant reduction in the efficiency of GABAergic inhibition. Our data indicate that the imbalance between intracortical excitatory and inhibitory mechanisms may at least contribute to the expression and augmentation of spike-wave discharges in epileptic WAG/Rij rats.

Animals↗
PubMed1995

Development of excitatory and inhibitory postsynaptic potentials in the rat neocortex.

The postnatal development of synaptic potentials in the rat neocortex is characterized by the sequential appearance of functional excitatory and inhibitory synapses. Morphological and electrophysiological studies provided evidence that at early stages of development, pyramidal cells are extensively coupled to each other, presumably via gap junctions. Thus, immature neurons are able to communicate through pathways that are not available or only weakly expressed in the mature neocortex. During the very early postnatal period, excitatory synaptic inputs prevail. Excitatory postsynaptic potentials (EPSPs) are characteristically long in duration and show high sensitivity to frequent stimulation. Although spontaneous inhibitory postsynaptic potentials (IPSPs) and mature responses to exogenously applied gamma-aminobutyric acid (GABA) have been described during the first postnatal week, evoked IPSPs do not develop before postnatal day 10 (P10). During the period of maximum synaptogenesis (P11 to P20), GABA-mediated synaptic inhibition develops and pyramidal cells respond to afferent activation with efficient EPSPs and IPSPs. These postsynaptic potentials gradually mature during the late postnatal period. The delayed development of synaptic inhibition in the neocortex simultaneously promotes synaptic plasticity while increasing seizure susceptibility. On the one hand, the functional lack of synaptic inhibition during early stages of development enables a period of enhanced neuronal activity and augmented synaptic plasticity necessary to form proper synaptic connections. On the other hand, the absence of inhibitory control over excitatory processes increases the vulnerability of the developing neocortex to seizure activity during postnatal ontogenesis.

Aging↗
PubMed1994

Dextromethorphan attenuates hypoxia-induced neuronal dysfunction in rat neocortical slices.

We investigated the effects of the antitussive dextromethorphan (DM; 100 microM) on the extracellular DC potential, extracellular calcium concentration ([Ca2+]o) and on stimulus-evoked field potential (FP) responses in rat neocortical slices during hypoxia. DM significantly reduced the amplitude of the anoxic depolarization (AD) and the associated [Ca2+]o decrease by 47.6% and 48.5%, respectively, but did not change the onset latency and the duration of the AD. DM did not affect the preservation or recovery of excitatory synaptic transmission and significantly suppressed paired-pulse inhibition in the postanoxic recovery phase. These results indicate that DM exerts its potential neuroprotective action by reducing the hypoxia-induced depolarization and Ca2+ influx.

Animals↗
PubMed1994

Lesion-induced transient suppression of inhibitory function in rat neocortex in vitro.

The structural and functional consequences of a local thermolesion were examined in rat neocortex with electrophysiological in vitro techniques and immunocytochemistry. Age-matched untreated and sham-operated animals served as controls and were analysed in the same way. The lesions consisted of a core of coagulated tissue 2-3 mm in diameter and reached ventrally into the deep cortical layers. After two days reactive astrocytes and after nine days a dense gliosis were observed in the immediate vicinity. Modifications in the intrinsic membrane characteristics and the synaptic network properties were investigated with intra- and extracellular recording techniques after survival times of one to eight days. Neurons recorded in the surrounding of lesions in neocortical slices revealed a significantly more depolarized resting membrane potential and a higher neuronal input resistance. In comparison to cells in control slices, maximal discharge rates to injection of depolarizing current pulses of neurons close to a focal lesion were not significantly altered and intrinsic burst firing was never observed. However, between postlesion days 1 and 5, neurons in the surroundings of lesions showed a transient increase in synaptic excitability. This hyperactivity was most clearly pronounced at a distance of 2-3 mm from the centre of the lesion (i.e. about 1-1.5 mm away from the lesion border) and characterized by long-duration field potential responses and multiphasic long-lasting excitatory postsynaptic potentials to orthodromic stimulation of the afferent input. This lesion-induced hyperexcitability was associated with a significant reduction in the peak conductance of the Cl(-)-dependent fast inhibitory postsynaptic potential and the K(+)-dependent long-latency inhibitory postsynaptic potential, suggesting that the intracortical GABAergic system was functionally impaired. The decrease in synaptic inhibition was associated with prolonged N-methyl-D-aspartate receptor-mediated activity, which could be reversibly blocked by D-amino-phosphonovaleric acid. In addition, neurons recorded in the vicinity of the lesion responded to an orthodromic synaptic stimulus with a long-lasting burst. The lesion-induced disturbance in the balance between the excitatory and inhibitory system may not only have profound influences on the mechanisms of intracortical information processing, but may also lead to the expression of epileptiform activity and long-term functional deficits.

Action Potentials↗
PubMed1993

Role of NMDA receptors and voltage-activated calcium channels in an in vitro model of cerebral ischemia.

In an in vitro model of cerebral ischemia we investigated the functional consequences of repeated hypoxias and the potential protective effect of the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovaleric acid (D-APV) and the calcium channel blocker verapamil in preventing the expression of pathophysiological activity. Rat neocortical slices were exposed to nitrogen for 2-13 min and the hypoxia-induced functional modifications were monitored in layer II/III by recording the extracellular DC potential, the extracellular calcium concentration ([Ca2+]o) and the stimulus-evoked synaptic responses. Hypoxia caused a reversible 2.4-24.6 mV negative shift in the extracellular DC potential associated with a [Ca2+]o decrease from 1.2 to 0.2 mM and a complete loss of synaptic responsiveness. Repeating hypoxias induced an increase in the amplitude of this anoxic depolarization (AD) and a significant decrease in the AD onset latency. Synaptic responses partially recovered at 20 and 60 min intervals between subsequent hypoxic periods, indicating that the initial AD did not induce any short-term irreparable functional deficits. Verapamil (50 microM) caused an increase in the AD onset latency. However, in comparison to untreated controls, verapamil induced a reduction of excitatory and inhibitory responses during hypoxia probably by blocking voltage-activated calcium conductances. In addition, verapamil did not have any significant effect on the hypoxia-induced reduction of [Ca2+]o. Bath application of D-APV (30 microM) prevented the significant reduction in the AD onset latency to the second hypoxia, but had no significant effect on the AD amplitude and duration. The hypoxia-induced decrease in [Ca2+]o was not altered after addition of D-APV to the bathing medium. These data indicate that the influx of calcium through voltage-activated calcium channels and the NMDA receptor-gated ionophore does not significantly contribute to the massive depolarization observed under hypoxic conditions.

2-Amino-5-phosphonovalerate↗
PubMed1993

Influence of hypoxia on excitation and GABAergic inhibition in mature and developing rat neocortex.

To analyze the functional consequences of hypoxia on the efficacy of intracortical inhibitory mechanisms mediated by gamma-aminobutyric acid (GABA), extra- and intracellular recordings were obtained from rat primary somatosensory cortex in vitro. Hypoxia, induced by transient N2 aeration, caused a decrease in stimulus-evoked inhibitory postsynaptic potentials (IPSPs), followed by a pronounced anoxic depolarization. Upon reoxygenation, the fast (f-) and long-latency (l-) IPSP showed a positive shift in the reversal potential by 24.4 and 14.9 mV, respectively. The peak conductance of the f- and l-IPSP was reversibly reduced in the postanoxic period by 72% and 94%, respectively. Extracellular field potential recordings and application of a paired-pulse inhibition protocol confirmed the enhanced sensitivity of inhibitory synaptic transmission for transient oxygen deprivation. Intracellular recordings from morphologically or electrophysiologically identified interneurons did not reveal any enhanced susceptibility for hypoxia as compared to pyramidal cells, suggesting that inhibitory neurons are not selectively impaired in their functional properties. Intracellularly recorded spontaneous IPSPs were transiently augmented in the postanoxic period, indicating that presynaptic GABA release was not suppressed. Developmental studies in adult (older than postnatal day 28), juvenile (P14-18), and young (P5-8) neocortical slices revealed a prominent functional resistance of immature tissue for hypoxia. In comparison with adult cortex, the hypoxia-induced reduction in excitatory and inhibitory synaptic transmission was significantly smaller in immature cortex. Our data indicate a hypoxia-induced distinct reduction of postsynaptic GABAergic mechanisms, leading to the manifestation of intracortical hyperexcitability as a possible functional consequence.

2-Amino-5-phosphonovalerate↗
PubMed1992

Hypoxia-induced functional alterations in adult rat neocortex.

1. Brief periods of hypoxia (2-7 min) were induced in rat neocortical slices maintained in an interface-type recording chamber at 34-35 degrees C by changing the aerating gas from 95% O2-5% CO2 to 95% N2-5% CO2. Field potential (FP) and intracellular recordings were obtained in layers II/III of primary somatosensory cortex. Intracellular injection of biocytin revealed the characteristic morphology of supragranular spiny pyramidal neurons. 2. Excitatory synaptic transmission reversibly decreased by 45% as estimated from FP responses to orthodromic stimulation of the underlying white matter/layer VI. Excitatory postsynaptic potentials (EPSPs) were suppressed by 36% in amplitude and recovered within 2-3 min after reoxygenation. During the recovery period, EPSPs showed a reversible increase in duration by 72%. 3. Inhibitory synaptic transmission was completely blocked as determined in FP responses with a paired-pulse inhibition protocol. The fast inhibitory postsynaptic potential (IPSP) declined by 58% during hypoxia. The long-lasting IPSP was suppressed by 75% and showed incomplete recovery. During hypoxia, the amplitude of both IPSPs was significantly more strongly suppressed than the EPSP. 4. In 40% of the cells, hypoxia induced an early anoxic hyperpolarization with a reversal potential of E = -80.8 mV, followed by a postanoxic hyperpolarization (E = -89.4 mV). In a second group of cells (37%), a gradual anoxic depolarization with E = -57.5 mV was observed instead of an early hyperpolarization. In both groups of cells, the anoxic response was associated with a marked decrease in input resistance, by 42 and 31%, respectively. 5. The spike discharge frequency was reversibly suppressed by 71% during hypoxia. A transient hyperexcitability accompanied with a rise in input resistance and discharge rate was observed in 38% of the cells on reoxygenation. 6. The reversal potential of the anoxic hyperpolarization was unaffected by tetrodotoxin (TTX) but was significantly altered by application of the ATP-sensitive K+ channel (KATP) blocker gliquidone. Application of gliquidone additionally resulted in a significantly smaller hypoxia-induced decline in paired-pulse inhibition. 7. Increases in tissue high-energy phosphates induced by preincubating the slices in 25 mM creatine for greater than 2 h had a pronounced protective effect on excitatory and inhibitory synaptic transmission. 8. These data suggest a selective vulnerability of the neocortical inhibitory system during hypoxia. Our results further indicate that hypoxia activates a pre- and postsynaptic KATP conductance because of the decline in intracellular ATP.

Adenosine Triphosphate↗
PubMed1991

Postnatal maturation of the GABAergic system in rat neocortex.

1. The postnatal maturation of intracortical inhibitory circuitry and the development of responses to applied gamma-aminobutyric acid (GABA) and baclofen were studied in pyramidal and nonpyramidal neurons from layers II and III of the rat primary somatosensory and primary visual cortex, in vitro. 2. Depolarizing spontaneous inhibitory postsynaptic potentials (IPSPs) could be recorded in approximately 70% of the young (postnatal day 4-10; P4-10), juvenile (P11-16), and adult cells (P28-41), respectively, when they were loaded with nitrate. At all ages these spontaneous events could be blocked by application of the GABAA receptor antagonist bicuculline methiodide (BMI), indicating that they were mediated by activation of GABAA receptors. 3. In 122 of the 130 adult cells tested, standardized electrical stimulation of the white matter or layer VI evoked a brief excitatory postsynaptic potential (EPSP), followed by both a fast (f-) and a long-latency (l-)IPSP. Similar stimuli evoked a biphasic IPSP in only 51 of the 98 juvenile and in only 1 of the 56 young neurons studied. The mean peak conductance of the f-IPSP and the l-IPSP increased significantly from 50.2 and 7.5 nS, respectively, in juvenile cells to 84.2 and 18.0 nS, respectively, in adult neurons. 4. Application of the N-methyl-D-aspartate (NMDA) receptor antagonist D-amino-phosphonovaleric acid (D-APV) to juvenile cells induced a significant negative shift in the reversal potential of both the f-IPSP and l-IPSP. This effect was accompanied by a reduction in the peak conductance during these events by 31 and 48%, respectively, indicating that a prominent long-lasting NMDA receptor-mediated EPSP occurs concurrent with the early and late IPSP in immature neurons. In adult neurons, D-APV had no significant effect on the reversal potential of the f- and l-IPSP, although the peak conductance decreased by 20 and 5%, respectively, suggesting that there was a smaller concurrent activation of NMDA receptors in this age group. 5. The functional maturation of GABAA and GABAB receptors was studied using focal applications of GABA to the soma and the apical dendrite. Somatic GABA applications to adult neurons held at depolarized membrane potentials evoked a triphasic response, consisting of 1) a GABAA-mediated hyperpolarizing fast component (GABAhf; reversal potential, -76 mV), 2) a GABAA-mediated depolarizing phase (GABAd; -54 mV), and 3) a hyperpolarizing late response (GABAhl; -80 mV). The GABAd response could be demonstrated at all ages in almost every neuron.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1990

Control of NMDA receptor-mediated activity by GABAergic mechanisms in mature and developing rat neocortex.

The effects of diazepam and low concentrations of bicuculline methiodide (BMI) on the expression of long-latency N-methyl-D-aspartate (NMDA) receptor-mediated activity was studied in supragranular layers of juvenile (14-18 days old) and adult rat (greater than or equal to 28 days) primary somatosensory cortex. In juvenile slices, orthodromic stimulation of layer VI/white matter evoked a long-lasting oscillatory field potential response which could be blocked by the NMDA receptor antagonist D(-)-2-amino-5-phosphonovaleric acid (D-APV) and by diazepam. Similar D-APV-sensitive responses could be observed in adult slices when the GABAergic system was slightly suppressed by adding low doses of BMI to the bathing solution. Our findings indicate that a small decrease in the efficacy of the inhibitory system, whether caused by developmental events or by processes that modulate inhibitory electrogenesis, can lead to NMDA receptor-mediated synchronized afterdischarges, which might play an important role in the functional maturation of the neocortex and in susceptibility to epileptogenesis.

2-Amino-5-phosphonovalerate↗
PubMed1990

Burst generating and regular spiking layer 5 pyramidal neurons of rat neocortex have different morphological features.

Intracellular recordings were obtained from pyramidal neurons in layer 5 of rat somatosensory and visual cortical slices maintained in vitro. When directly depolarized, one subclass of pyramidal neurons had the capacity to generate intrinsic burst discharges and another generated regular trains of single spikes. Burst responses were triggered in an all-or-none manner from depolarizing afterpotentials in most bursting neurons. Regular spiking cells responded to electrical stimulation of ascending afferents with a typical EPSP-IPSP sequence, whereas IPSPs were hard to detect in bursting cells. Orthodromic activation of the latter evoked a prominent voltage-dependent depolarization that could trigger a burst response. Intracellularly labelled bursting and regular spiking cells were located in layer 5b, but had distinctly different morphologies. Bursting neurons had a large pyramidal soma, a gradually emerging apical dendrite, and an extensive apical and basal dendritic tree. Their axonal collateral arborization was predominantly limited to layers 5/6. In contrast, regular spiking cells had a more rounded soma with abruptly emerging apical dendrite, a smaller dendritic arborization, and 2 to 8 ascending axonal collaterals that arborized widely in the supragranular layers. Both bursting and regular spiking cells had main axons that entered the subcortical white matter. These data show that some subgroups of pyramidal neurons within the deeper parts of layer 5 of rat cortex are morphologically and physiologically distinct and have different intracortical connections. Bursting cells presumably function to amplify and synchronize cortical outputs, whereas regular spiking output neurons provide excitatory feedback to neurons at all cortical levels and receive a more effective orthodromic inhibitory input. These data support the hypothesis that differences in gross neuronal structure, perhaps even the subtle differences that distinguish subclasses of neurons in a given lamina, are predictive of underlying differences in the type and distribution of ion channels in the nerve cell membrane and connections of cells within the cortical circuit.

Animals↗
PubMed1990

Transient expression of polysynaptic NMDA receptor-mediated activity during neocortical development.

During a restricted period of early postnatal development, rat neocortical neurons receive a powerful N-methyl-D-aspartate (NMDA) receptor-mediated synaptic input of variable onset latency and duration. These large-amplitude excitatory postsynaptic potentials are especially pronounced in supragranular layers and are generated by activities in polysynaptic circuits. Their occurrence in cortical slices from juvenile (postnatal (P) days 11-20), but not neonatal (P5-10) or adult (greater than or equal to P28) animals, appears to be in part a consequence of the relative immaturity of gamma-aminobutyric acid (GABA)-mediated inhibition, at a time when the requisite functional excitatory circuitry has been established. The transient manifestation of strong NMDA receptor-mediated potentials coincides temporally with a 'developmental window' within which there is enhanced sensitivity for epileptogenesis and for induction of long-term synaptic modifications in rat cortex.

2-Amino-5-phosphonovalerate↗
PubMed1988

Pharmacological induction of use-dependent receptive field modifications in the visual cortex.

Lasting modifications of the receptive fields of neurons in the visual cortex can be induced by pairing visual stimuli with iontophoretic application of the neuromodulators acetylcholine and noradrenaline or the excitatory amino acids N-methyl-D-aspartate (NMDA) and L-glutamate. The modifications are obtained in less than 1 hour and persist for more than 40 minutes. Thus, acetylcholine and norepinephrine have a permissive role in use-dependent neuronal plasticity. These results support the notion of a postsynaptic threshold for neuronal malleability that differs from that of sodium-dependent action potentials.

Acetylcholine↗
PubMed1987

Evidence for a threshold in experience-dependent long-term changes of kitten visual cortex.

In order to determine the role of unstructured and of spontaneous activity in the developmental plasticity of the visual cortex, we blocked in 7 kittens the retinal activity of one eye completely by intraocular injections of tetrodotoxin (TTX) while the other eye was left open. Littermates of these kittens were monocularly deprived by lid suture and served as controls. In 3 additional kittens one eye was inactivated with TTX and the other closed by lid suture to assess whether mere asymmetries in the activation levels of the two eyes were sufficient to induce ocular dominance changes. Despite some variability between the matched pairs, the ocular dominance shift towards the normal eye did not differ significantly in the kittens with monocular lid suture and monocular TTX injection (P greater than 0.3/chi 2). In the TTX-treated kittens there was a trend for neurones to be less sharply tuned for orientation but it was not significant (P greater than 0.08/chi 2). In the kittens which had one eye injected with TTX and the other sutured closed no shift of ocular dominance was apparent. Separate analysis of both hemispheres revealed only a small bias towards the respective contralateral eye. We conclude that the process mediating activity-dependent long-term changes of ocular dominance has a threshold. Afferent activity that fails to excite the postsynaptic neuron above this threshold plays neither a significant role in the stabilization nor in the disruption of functional connections.

Animals↗
PubMed1987

Functional and neuronal binocularity in kittens raised with rapidly alternating monocular occlusion.

1. In order to determine the degree of synchrony of binocular activation required for the development of binocularity we reared 11 kittens with rapidly alternating monocular occlusion. Alternating occlusion was achieved with microprocessor-controlled electrooptic solid-state shutters, which were fitted to individually moulded goggles. The intervals of alternating occlusion were varied from 50 to 1,000 ms. Two normally reared kittens and three kittens that were reared with the shutters operating synchronously with open/close intervals of 50/50 ms, 200/200 ms, and 400/100 ms, respectively, were used as controls. Toward the end of the critical period we examined the kittens' ability for binocular depth discrimination and tested binocular luminance summation of the pupillary light reflex. Single-cell recordings were made from the visual cortex in order to determine the percentages of binocularly excitable neurons. 2. There was a good correlation between the degree of asynchrony of binocular experience, the impairment of depth discrimination, and the percentage of binocular neurons. Kittens reared with alternation rates of 200, 330, and 400 ms, respectively, had developed normal binocularity and were indistinguishable from the controls. Alternation rates of 500 ms or longer prevented the development of normal depth discrimination and luminance summation and resulted in reduced cortical binocularity. 3. A linear relationship between depth discrimination, binocular luminance summation, and percentages of binocular neurons was found. 4. Our findings indicate that an asynchrony of binocular activation of several hundred milliseconds is compatible with the development of normal binocularity in the kitten visual system.

Animals↗
PubMed1986

Development of horizontal intrinsic connections in cat striate cortex.

Intracortical injections of horseradish peroxidase conjugated with wheat-germ agglutinin (WGA-HRP) reveal a characteristic patchy staining pattern within the superficial layers of cat striate cortex. The patches consist of a dense accumulation of labeled neurons and axonal arborizations. We have investigated the tangential organization and the development of these intrinsic cortical connections by using a flat-mount preparation of area 17. The diameter of the patches varied from 200 to 400 micron, the center-to-center distance ranged from 400 to 800 micron, and the spread of patches extended further in the anterior-posterior than in the medial-lateral direction. The expression of these horizontal patchy connections is age- and experience-dependent. From ten days to six weeks of age patches are exuberant and on occasion fuse to beaded bands extending radially from the injection site. From 6 weeks onwards the number and the tangential spread of the patches decreases to one or two rows of isolated clusters. Long-term binocular deprivation disrupts this pattern of intrinsic connections nearly completely. We infer from these results that there is an inborn pattern of discrete horizontal connections in striate cortex which is shaped by visual experience and requires contour vision for its maintenance.

Animals↗