Search PubMed⌕ Search

Biomedical subjects

B W Connors

Publications and source records attributed to B W Connors.

At least 55 records · Page 3Linked to original sources
PubMed1989

Repetitive burst-firing neurons in the deep layers of mouse somatosensory cortex.

Intracellular recordings were made from neurons of the mouse somatosensory cortex isolated in vitro. Two physiologically distinct classes of pyramidal cells were observed: regular-spiking cells were the majority, and generated accommodating trains of single spikes; bursting cells generated clusters of 2-5 action potentials, and clusters were separated by prolonged afterhyperpolarizations. The bursting cells of the mouse neocortex were unusual in producing repetitive bursting during sustained current pulses, and in being localized to a laminar zone straddling layers V and VI.

Animals↗
PubMed1989

Horizontal spread of synchronized activity in neocortex and its control by GABA-mediated inhibition.

1. Suppression of GABAA receptor-mediated inhibition disrupts the neural activity of neocortex and can lead to synchronized discharges that mimic those of partial epilepsy. We have studied the role of GABAA-mediated inhibition in controlling the synchronization and horizontal (tangential) spread of cortical activity. 2. Slices of rat SmI were maintained in vitro and focally stimulated in layer VI while recording with a horizontal array of extracellular electrodes. Inhibition was slightly suppressed by adding low concentrations of the GABAA antagonists bicuculline or bicuculline methiodide to the bathing medium. Under control conditions neural activity was narrowly confined to a vertical strip of cortex. The horizontal spread of activity expanded about twofold in the presence of antagonist concentrations (less than or equal to 0.5 microM) that were expected to suppress GABAA function by no more than 10-20%. 3. At antagonist concentrations between 0.4 and 1.0 microM, evoked epileptiform activity appeared. These threshold-dose epileptiform events showed wide variations in size and duration (even at the same recording site), very variable distances of horizontal propagation, specific sites of propagation failure, reversals of propagation direction, and directional asymmetries in their probability of propagation. This contrasts with activity observed previously (Ref. 9) in high bicuculline concentrations (greater than or equal to 10 microM): large, stereotyped events that propagate reliably without decrement or reflection. 4. Intracellular recordings were obtained from pyramidal neurons in layers II/III in the presence of less than or equal to 1 microM bicuculline. Inhibitory postsynaptic potentials (IPSPs) were observed during both primary evoked responses and propagating epileptiform events and were often comparable in size and duration to those in untreated cortex. Epileptiform field potentials were always correlated with synaptic activity in single cells, but the pattern and type of PSPs varied with the form of the field potentials. Large amplitude epileptiform events coincided with an overwhelming inhibition of upper layer neurons. 5. We conclude that 1) the horizontal spread of normal cortical activity is strongly constrained by GABAA-mediated IPSPs, 2) a relatively small reduction in the efficacy of inhibition leads to a large increase in the spread of excitation, 3) initiation and propagation of synchronized epileptiform activity can occur even in the presence of robust cortical inhibition, and 4) the character of epileptiform activity is strongly affected by the influences of inhibition.

Animals↗
PubMed1989

Synchronized excitation and inhibition driven by intrinsically bursting neurons in neocortex.

1. The cellular mechanisms of synchronous synaptic activity were studied in isolated slices of rat SmI neocortex in which gamma-aminobutyric acid (GABA)-mediated inhibition was slightly suppressed. Intracellular measurements were made from single neurons, and extracellular recordings monitored the timing and intensity of population events. 2. Neurons in cortical layers II-VI were classified by the attributes of their single action potentials and repetitive firing patterns during injection of intracellular current pulses. Regular-spiking (RS) cells occurred in all layers and had relatively long-duration spikes and strong frequency adaptation. Intrinsically bursting (IB) cells occurred only in layers IV and V and generated bursts of greater than or equal to 3 spikes; some IB cells of lower-layer V produced repetitive bursts during long depolarizing pulses. Fast-spiking (FS) cells had brief spikes and little or no adaptation and fired at high frequencies. 3. When GABAA-mediated inhibition was slightly reduced with low doses of bicuculline methiodide (BMI, 0.8-1.0 microM), synchronous events were evoked by stimulating layer VI with single shocks. Synchronous events were characterized by prominent, often all-or-none extracellular field potentials that propagated horizontally for variable distances up to several millimeters. Large field potentials were invariably correlated with excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) in single neurons. Both PSPs and field potentials often had long (up to 250 ms) and variable latencies, and sometimes two or more events were generated by single stimuli. In all cases the PSPs and field potentials were synchronous. Both field potentials and single cells sometimes generated short epochs (3-7 peaks) of rhythmic events at 20-50 Hz. 4. The physiological class of single neurons was correlated with the relative dominance of excitation and inhibition during each synchronous event. In phase with each synchronous event, most RS cells were very strongly inhibited with only small amounts of concurrent excitation. By contrast, IB cells were strongly and consistently excited, with relatively little inhibition. FS cells were also phasically excited. 5. Anatomic studies have identified RS and IB cells as pyramidal cells and FS cells as GABAergic nonpyramidal cells. This implies that, during the synchronous events of the present study, the majority of pyramidal cells were dominated by IPSPs. Synchronous excitation of FS cells, the presumed inhibitory interneurons, is consistent with this. Only a subset of the pyramidal neurons, almost all of them IB cells of the middle layers, displayed strong, synchronous excitation and clusters of action potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Two inhibitory postsynaptic potentials, and GABAA and GABAB receptor-mediated responses in neocortex of rat and cat.

1. Pyramidal neurones from layers II and III of the rat primary somatosensory cortex and cat primary visual cortex were studied in vitro. Inhibitory postsynaptic potentials (IPSPs) and responses to exogenously applied gamma-aminobutyric acid (GABA) and its analogue baclofen were characterized. The results from rats and cats were very similar. 2. Single electrical stimuli to deep cortical layers evoked a sequence of PSPs in the resting neurone: (a) an initial, brief excitation (EPSP), (b) a short-latency, fast inhibition (the f-IPSP) and (c) a long-latency, more prolonged inhibition (the l-IPSP). The f-IPSP was accompanied by a large conductance increase (about 70-90 nS) and reversed polarity at -75 mV; the l-IPSP displayed a relatively small conductance increase (about 10-20 nS) and reversed at greater than -90 mV. 3. Focal application of GABA near the soma evoked a triphasic response when measured near the threshold voltage for action potentials: (a) the GABAhf (hyperpolarizing, fast) phase was very brief and was generated by a large conductance increase with a reversal potential of -78 mV, (b) the GABAd (depolarizing) phase also had a high conductance but reversed at -51 mV, (c) the GABAhl (hyperpolarizing, long-lasting) phase had a relatively low conductance and reversed at -70 mV. The GABAhf response was specifically localized to the soma, whereas the apical or basilar dendrites generated predominantly GABAd responses. 4. Baclofen, a selective GABAB receptor agonist, caused a small (about 2 mV), slow hyperpolarization of the resting potential, which reversed at -90 mV. Saturating baclofen doses increased membrane conductance by a maximum of about 12 nS. Baclofen depressed the amplitude and conductance of PSPs; when baclofen was focally applied near the soma. IPSPs were selectively depressed. 5. The GABAA receptor antagonists bicuculline methiodide or picrotoxin (10 microM) greatly depressed f-IPSPs, but either enhanced or did not affect l-IPSPs. Concomitantly, GABAhf and GABAd responses were antagonized, leaving a more prominent GABAhl response that reversed polarity at a more negative level of -87 mV. Baclofen responses were unaffected by bicuculline and picrotoxin. Extracellular barium abolished the baclofen response, and shifted the reversal potentials of the GABAd and GABAhl responses in the positive direction; the GABAhf response was unaffected. 6. Both focal GABA and f-IPSPs strongly depressed the intrinsic excitability of pyramidal neurones. Each greatly increased spike threshold and abolished or vastly reduced the capacity of the cells to fire repetitively during intense stimuli.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1988

Periodicity and directionality in the propagation of epileptiform discharges across neocortex.

1. The horizontal propagation of epileptiform discharges has been studied in slices of neocortex treated with high concentrations of bicuculline methiodide, an antagonist of the inhibitory transmitter gamma-aminobutyric acid (GABA). The cortical areas examined were: primary somatosensory (SmI) and motor (MI), and primary (area 17) and secondary (area 18) visual areas of rats, and area 17 of cats. In all of these areas an electrical stimulus evoked single, all-or-none paroxysmal field potentials (PFPs) that propagated across the entire width of the slice without decrement. 2. The velocity of PFP propagation was approximately 0.06-0.09 m/s when averaged over cortical distances of several millimeters. PFP propagation occurred equally well in both directions across a slice. 3. Measurement of PFP propagation at higher spatial resolution (100-180 micron intervals) revealed that velocity was not homogeneous within rat SmI, rat area 18 and cat area 17, but instead varied manyfold as horizontal position changed. In these areas of cortex, propagation patterns were spatially periodic; power spectra reveal that the dominant spatial frequencies were centered about 1 mm-1, with negligible contributions above 2 mm-1. Occasionally PFP propagation was discontinuous, skipping over a small region of cortex and arriving distally before propagating into the more proximal region. 4. In those cortices with periodic propagation patterns, PFP velocity was also strongly direction-dependent. Propagation patterns measured in opposite directions across the same strip of cortex displayed similar periodicities, but in many slices they were negatively correlated, i.e., the propagation pattern in one direction was antiphasic compared to that in the other direction. 5. In contrast, propagation velocity across the center of area 17 of the rat was relatively constant and not directional. Near the boundaries of areas 17 and 18, however, PFP velocity changed abruptly and became periodic within area 18. Similarly, velocity within rat MI was more constant and less directional than in the adjacent SmI. 6. The patterns of PFP propagation velocity are often spatially periodic, directionally asymmetric, and depend upon cortical area. We suggest that the periodic patterns reflect systematic variations in the length or density of horizontal excitatory connections. Alternatively, or concurrently, periodicities could arise from the patchy distributions of intrinsic connections that have been observed anatomically in many areas of neocortex.

Animals↗
PubMed1987

Electrophysiological properties of ependymal cells (radial glia) in dorsal cortex of the turtle, Pseudemys scripta.

1. We have investigated the electrophysiological properties of ependymal cells in the isolated dorsal cortex of the turtle, Pseudemys scripta. The cell bodies of these radial glia form an epithelium at the ventricular surface, and each cell sends one or more branching processes through the cortex to the pial surface. Very few non-ependymal glia exist in the dorsal cortex. 2. Ependymal cells had high resting membrane potentials (-90 mV), very fast time constants and a lack of intrinsic excitability or synaptic potentials. 3. Changes in the K+ concentration ([K+]) of the bathing solution caused near-Nernstian changes of ependymal membrane potentials. When local neuronal pathways were activated, ependymal cells slowly depolarized while extracellular voltage shifted negatively. Simultaneous measurements of extracellular [K+] ([K+]o) near the impaled ependymal cell body showed that these slow depolarizations were fully accounted for by activity-dependent increases in [K+]o. Similar measurements during focal pressure applications of solutions with high [K+] suggested that intrasomatic recordings reflect predominantly the [K+]o adjacent to the cell body, and not the intracortical process. 4. Intracellular injections of the fluorescent dye Lucifer Yellow CH, and simultaneous recordings from neighbouring cells, indicated that ependymal cells are chemically and electrically coupled to one another. Increasing the ambient CO2 level from 5 to 40% depolarized cells, increased their input resistance, and abolished interglial dye coupling. 5. The physiological properties of ependymal cells are very similar to those of a variety of glial cell types in a range of vertebrate and invertebrate species. In the absence of other types of glia, radial glia may function as the sole cellular mediators of K+ redistribution (i.e. K+ spatial buffering) following neural activity, as well as the generators of slow extracellular potentials.

Action Potentials↗
PubMed1986

Brain extracellular space: developmental studies in rat optic nerve.

Analysis of neural activity-dependent fluctuations in K+, H+, and ECS dimensions in the developing RON has revealed major changes during the first two to three postnatal weeks. The emergence of the adult ceiling level for evoked extracellular K+ (10 to 12 mM) and significant ECS shrinkage are roughly correlated in time with the proliferation and maturation of glial cells in this structure. This observation and others have led to the hypothesis that ECS shrinkage depends upon electrolyte and water transport into glial cells with subsequent swelling. Development of the adult K+ ceiling level may also depend upon glial cells, but it is likely that other factors contribute to this homeostatic mechanism. Marked alterations in activity-dependent pHo shifts were seen with development and may be related to changes in the activity of carbonic anhydrase in this structure. The technological means are at hand to pursue these questions vigorously in an effort to provide further insight into the mechanisms of ionic and fluid homeostasis of brain ECS, and the developing RON appears to be a useful model system in this regard.

Aging↗
PubMed1986

Cellular physiology of the turtle visual cortex: synaptic properties and intrinsic circuitry.

We have examined the synaptic physiology of the isolated dorsal cortex of the turtle, Pseudemys scripta elegans. Electrical stimulation of afferent pathways elicited distinct, stereotyped responses in pyramidal and stellate neurons. Single shocks evoked a long-lasting barrage of excitatory postsynaptic potentials (EPSPs) in stellate cells, and led to a burst of several action potentials. Under the same circumstances, pyramidal cells displayed a small amount of short-latency excitation, but this was accompanied by a profound and prolonged set of inhibitory post-synaptic potentials (IPSPs). Synaptic excitation of the distal dendrites of pyramidal cells could evoke dendritic action potentials that were visible at the soma as small all-or-none spikes rising from the hyperpolarized level of the IPSP. There appeared to be two mechanistically different types of IPSPs in pyramidal cells. The first occurred at short latency, could produce a very large conductance increase, reversed polarity at -71 mV, and was chloride-dependent. The second was generally smaller and more protracted, had a relatively negative reversal potential of -85 to -95 mV, and was insensitive to chloride injection. Focal application of small doses of the putative inhibitory neurotransmitter gamma-aminobutyric acid (GABA) onto the somata of pyramidal cells caused a conductance increase and hyperpolarization. This response had features in common with the short-latency IPSP, including an identical reversal potential. Application of large doses of GABA to the somata of pyramidal cells or smaller doses to their dendrites elicited multiphasic or purely depolarizing responses that were at least partly due to time- or space-dependent shifts of the equilibrium potential of the response. Bicuculline methiodide, a potent GABA antagonist, depressed both the responses to GABA and the short-latency IPSP, but not the long-latency IPSP; synchronized epileptiform burst discharges also resulted. These findings, together with responses to locally applied electric shocks and the excitatory amino acid glutamate, suggested that inhibition of pyramidal cells was generated intrinsically by stellate cells, and that the cortical circuit provides pathways for both feedforward and feedback GABAergic inhibition. The data also suggest that pyramidal cells are mutually excitatory. These features are similar to the basic intrinsic circuitry in the telencephalic cortices of mammals.

Animals↗
PubMed1986

Mechanisms of interictal epileptogenesis.

The interictal discharge is a brief epileptiform event that provides the simplest experimental system available for investigating some of the basic mechanisms of epilepsy. Interictal discharges are characterized by two major abnormal properties: each involved neuron exhibits a transient large amplitude depolarization (the "depolarization shift") associated with repetitive spike generation, and this excitation arises with virtual synchrony in the majority of cells in a local population. Recent studies have attempted to define the cellular properties that predispose a cortical circuit to this pathological behavior. There appear to be three general factors that interactively determine cortical susceptibility to epilepsy: Intrinsic membrane properties of neurons. The intrinsic excitability of individual cells may vary greatly within a cortical area; the initiation of a synchronous discharge usually occurs in the subpopulation of cells that has the endogenous ability to generate bursts of action potentials. Efficacy of local inhibitory synaptic mechanisms. Normal integrative functions of the cortex require robust inhibition; depression of inhibition is one of the most reliable ways to trigger a seizure. Effectiveness of excitatory synaptic connections and other synchronizing mechanisms. Highly synchronized discharge among a large number of neurons requires widely divergent excitatory interactions. Differences in these factors for different cortical areas can confer relative susceptibility or resistance to development of epileptiform discharge. Pharmacologic, pathologic, developmental, and genetic processes can presumably mitigate or aggravate focal cortical epileptogenesis by affecting any of these three general factors.

Animals↗
PubMed1986

Cellular physiology of the turtle visual cortex: distinctive properties of pyramidal and stellate neurons.

The electrophysiological properties of neurons in the three-layered dorsal cortex of the turtle, Pseudemys scripta elegans, have been studied in vitro. Intracellular recordings suggested two distinct classes of neuronal behavior. Cell labeling with either Lucifer Yellow or horseradish peroxidase revealed that these behaviors correlated with the two morphological classes of cortical neurons: pyramidal cells and stellate cells. Examination of Golgi-stained neurons of dorsal cortex did not uncover any other obvious classes. Pyramidal cells had their somata in the cell layer, and extended several densely spined apical dendrites through the molecular layer to the pia. They also had spiny basilar dendrites directed through the subcellular layer toward the ependymal border. Physiologically, pyramidal cells had relatively prolonged action potentials that showed marked frequency adaptation during a sustained suprathreshold current pulse. Their most striking characteristic was a tendency to fire two discrete sizes of action potential, one small (mean = 34 mV) and of relatively low threshold, the other large (mean = 76 mV) and of higher threshold. We hypothesize that at least some small spikes arise from distal dendritic sites, whereas large spikes are somatically generated. Both spikes were tetrodotoxin-sensitive, although calcium-dependent electrogenesis occurred when potassium channels were blocked. In contrast to pyramidal cells, the somata of stellate cells were found in the molecular and subcellular zones. Their dendrites tended to be horizontally oriented and spine-free. Stellate cells had relatively brief action potentials, each of which was followed by a large but short-lasting undershoot of membrane potential. Stellate cells showed little or no spike frequency adaptation. Spike amplitudes were always relatively uniform and large (mean = 73 mV). Thus, in the dorsal cortex of turtles, the pyramidal cells, which are projection neurons, and stellate cells, which are local GABAergic inhibitory neurons, have distinctly different membrane characteristics. The physiological properties of the two types of turtle cortical neurons are very similar to their counterparts in cortical structures of the mammalian telencephalon.

Action Potentials↗
PubMed1985

Comparative electrophysiology of pyramidal and sparsely spiny stellate neurons of the neocortex.

Slices of sensorimotor and anterior cingulate cortex from guinea pigs were maintained in vitro and bathed in a normal physiological medium. Electrophysiological properties of neurons were assessed with intracellular recording techniques. Some neurons were identified morphologically by intracellular injection of the fluorescent dye Lucifer yellow CH. Three distinct neuronal classes of electrophysiological behavior were observed; these were termed regular spiking, bursting, and fast spiking. The physiological properties of neurons from sensorimotor and anterior cingulate areas did not differ significantly. Regular-spiking cells were characterized by action potentials with a mean duration of 0.80 ms at one-half amplitude, a ratio of maximum rate of spike rise to maximum rate of fall of 4.12, and a prominent afterhyperpolarization following a train of spikes. The primary slope of initial spike frequency versus injected current intensity was 241 Hz/nA. During prolonged suprathreshold current pulses the frequency of firing adapted strongly. When local synaptic pathways were activated, all cells were transiently excited and then strongly inhibited. Bursting cells were distinguished by their ability to generate endogenous, all-or-none bursts of three to five action potentials. Their properties were otherwise very similar to regular-spiking cells. The ability to generate a burst was eliminated when the membrane was depolarized to near the firing threshold with tonic current. By contrast, hyperpolarization of regular-spiking (i.e., nonbursting) cells did not uncover latent bursting tendencies. The action potentials of fast-spiking cells were much briefer (mean of 0.32 ms) than those of the other cell types.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1985

Activity-dependent shrinkage of extracellular space in rat optic nerve: a developmental study.

Activity-dependent shrinkage of extracellular space (ECS) is described in a simple model of the mammalian central nervous system, the rat optic nerve. In response to neural activation, the ECS of the mature nerve rapidly and reversibly decreases by as much as 20%. Activity-dependent ECS shrinkage is not present in neonatal nerves but develops over the first 2 weeks of life, roughly coincident with the appearance of glial cells in this structure. These and other observations suggest that activity-dependent ECS shrinkage results from fluid and electrolyte movements into glial cells.

Aging↗
PubMed1984

Mechanisms of epileptogenesis in cortical structures.

Studies of the mechanisms of epileptogenesis in brain-slice model systems have emphasized the role of three interacting processes in the development of interictal discharge. These processes are intrinsic burst activity, disinhibition, and excitatory synaptic coupling. Intrinsic membrane excitability may be altered by neuromodulators, injury, genetic mutations, and other factors. Disinhibition releases intrinsic burst-generating capacities in subpopulations of neurons and may become an important factor following cortical injury or repetitive activation of inhibitory circuits. Excitatory synaptic coupling is required in order to synchronize populations of neurons. Synaptic currents also serve as a major generator of slow depolarization shifts in individual neurons. The contribution of each of these factors to epileptogenesis may vary with the type of pathological process and the properties of the specific neuronal population.

Animals↗
PubMed1984

Chloride conductance and extracellular potassium concentration interact to modify the excitability of rat optic nerve fibres.

The excitability of developing rat optic nerves has been studied under conditions in which extracellular Cl- was replaced with other anions. In nerves younger than 3 days old, replacing Cl- with propionate or SO4(2-) usually led to spontaneous and repetitive cycling of extracellular K+ concentration ([K+]o). [K+]o reached peaks of 8-12 mM and then fell transiently below the base-line level of 5 mM before increasing again. This cycling behaviour continued, with a wave-length of 1-2 min, for as long as 2 h. Nerves older than 5 days either did not cycle or did so only transiently. Substitution of ten different anions for Cl- indicated that a minimum hydrated radius, between that of BrO3- and HCO3-, was necessary to induce cycling behaviour. Cycling behaviour was abolished by the Na+-channel blocker tetrodotoxin. Reduction of the bath [K+] to 2.5 mM slowed the frequency of spontaneous cycles; a bath [K+] of 1 mM abolished them. When the temperature was lowered, cycle frequency slowed. Substitution of large anions for Cl- enhanced axonal excitability. This was inferred from the prevalence of spontaneous action potentials during cycling behaviour, and from the generation of relatively large evoked increases of [K+]o. Cycling behaviour is hypothesized to result from a repetition of the following three processes: (i) spontaneous axonal firing elicits a gradual increase in [K+]o which increases axonal excitability and facilitates further K+ release, (ii) axonal firing and K+ release are eventually halted by a combination of depolarization block, intracellular Na+ accumulation and hyperpolarization from electrogenic pumping, (iii) recovery of [K+]o to its minimal value depends on active K+ reuptake mediated by a highly stimulated axonal Na+-K+-ATPase. We conclude that a large proportion of the resting membrane conductance of optic nerve fibres is Cl- specific. A high Cl- conductance may stabilize fine central axons against the depolarizing effects of [K+]o increases.

Action Potentials↗
PubMed1984

Carbon dioxide sensitivity of dye coupling among glia and neurons of the neocortex.

Among neocortical astrocytes and neurons, intracellular injection of the fluorescent dye Lucifer Yellow CH into single cells will often label multiple adjacent cells. It is possible that this intercellular dye movement occurs through gap junctions, which in several systems are sensitive to cytoplasmic acidification. In the present study we tested the effect of increased CO2 levels, a treatment expected to decrease intracellular pH (pHi), on the prevalence of glial and neuronal dye coupling in neocortical slices. When CO2 levels were raised to 40% or 50%, dye coupling among astrocytes was completely abolished. Under the same conditions, the prevalence of dye coupling among neocortical neurons of adult guinea pigs was significantly reduced to 18.7%, compared to the control level of 32.3%. Dye coupling among immature rat neocortical neurons, which normally occurs at relatively high rates, was not measurably affected by CO2 levels up to 50%. The results suggest that coupling between cortical glia is very sensitive to cytoplasmic acidification. The relative insensitivity of neuronal coupling to CO2 may indicate either that the conductance of neuronal gap junctions is only weakly affected by pHi or that neuron-to-neuron dye passage occurs via other types of intercytoplasmic pathways.

Animals↗
PubMed1983

Coupling between neurons of the developing rat neocortex.

We have estimated the prevalence of coupling between neurons of the rat neocortex during postnatal development. Single intracellular injections of the fluorescent dye Lucifer Yellow CH resulted in dye coupling among 70% of neurons from 1 to 4 days of age. Dye coupling dropped to 30 to 40% by 10 to 18 days and occurred in 20% of injected adult neurons. The number of neurons per dye-coupled aggregate also decreased. Whereas three to seven coupled neurons were common in cortex of 1 to 4 days, aggregates of more than two neurons were exceptionally rare in adults. The frequency of dye coupling did not vary systematically with cortical depth at any age. When chemical synaptic activity was blocked, most 4-day neurons exhibited short latency antidromically evoked depolarizations which were relatively insensitive to repetitive activation and membrane polarization. These depolarizations may represent electrotonically conducted spikes from coupled neurons. No such potentials were found in adult neurons. The results suggest that neuronal coupling is extensive in immature rat neocortex, but that coupling declines at a time just before the numbers of chemical synapses increase most rapidly.

Aging↗
PubMed1982

Activity-dependent K+ accumulation in the developing rat optic nerve.

Potassium-sensitive microelectrodes were used to study activity-dependent changes of extracellular potassium ion concentration ([K+]o) in rat optic nerves of different postnatal ages (1 day to adulthood). The maximum level to which [K+]o rose with optimal frequencies of stimulation depended on age: mean maximum evoked [K+]o was 17.2 microM in 1- to 3-day-old optic nerves and 9.8 microM in adult nerves. The ceiling [K+]o seen in immature optic nerves, which is uniquely large for a mammalian central nervous system structure, may result from a relatively enhanced rate of evoked K+ release.

Aging↗