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PubMed1979

Participation of adrenergic and noradrenergic neurones in central connections of arterial baroreceptor reflexes in the rat.

We examined activities of tyrosine hydroxylase (TH) and phenylethanolamine-N-methyl transferase (PNMT) and concentrations of norepinephrine (NE) in seven brain regions and the spinal cord of Wistar rats with elevated blood pressures 1 week and 4 weeks after denervation of carotid and aortic baroreceptors, and compared them to values in sham-operated control rats. TH activity was increased in the solitary tract nucleus (to 188% of control), parahypoglossal nucleus (to 254%), locus ceruleus (to 191%), and posterior hypothalamus (to 225%) at 1 week but not at 4 weeks after denervation. Similarly, NE concentrations were significantly altered in a number of brain regions at 1 week but not at 4 weeks after denervation. The only change in NE concentration at 4 weeks was in spinal cord where the level was reduced to 80% of control in the denervated rats. In contrast, the only change in PNMT activity 1 week after denervation was in posterior hypothalamus (to 59% of control), whereas at 4 weeks there was in increase in the spinal cord (to 159%) and a decrease in both the anterior and posterior hypothalamus (to 59% and 64% of control, respectively). The experiments suggest that increased activity of noradrenergic neurones in the brain may play a significant role in initiating the increase in pressure produced by baroreceptor denervation, whereas decreased activity of hypothalamic adrenergic neurones may be more important in maintaining the raised pressure. An increase in the activity of both adrenergic and noradrenergic nerves in the spinal cord, however, could contribute to maintaining the increase in blood pressure 4 weeks after denervation.

Adrenergic Fibers↗
PubMed2006

Neuronal networks and synaptic plasticity: understanding complex system dynamics by interfacing neurons with silicon technologies.

Information processing in the central nervous system is primarily mediated through synaptic connections between neurons. This connectivity in turn defines how large ensembles of neurons may coordinate network output to execute complex sensory and motor functions including learning and memory. The synaptic connectivity between any given pair of neurons is not hard-wired; rather it exhibits a high degree of plasticity, which in turn forms the basis for learning and memory. While there has been extensive research to define the cellular and molecular basis of synaptic plasticity, at the level of either pairs of neurons or smaller networks, analysis of larger neuronal ensembles has proved technically challenging. The ability to monitor the activities of larger neuronal networks simultaneously and non-invasively is a necessary prerequisite to understanding how neuronal networks function at the systems level. Here we describe recent breakthroughs in the area of various bionic hybrids whereby neuronal networks have been successfully interfaced with silicon devices to monitor the output of synaptically connected neurons. These technologies hold tremendous potential for future research not only in the area of synaptic plasticity but also for the development of strategies that will enable implantation of electronic devices in live animals during various memory tasks.

Animals↗
PubMed1996

Networks with lateral connectivity. II. Development of neuronal grouping and corresponding receptive field changes.

1. Using a three-layered network model defined in the previous paper, we studied the basic features of neurons in the cortical layer while the synaptic strengths of lateral excitatory connections were made modifiable by a Hebbian learning rule and a normalization process. 2. We found that neurons in the cortical layer formed groups through their lateral excitatory connections after the network was trained with sequential random dot stimulations. Neurons within a group connected tightly; neurons in different groups connected weakly. 3. The effects of model parameters and input parameters on the formation of neuronal groups were investigated. Results showed that the average size and rough shapes of groups were mainly determined by the spatial distribution of lateral connections within the cortical layer, irrespective of input parameters and training methods. Thus groups are structure dependent. 4. Lateral inhibition in the network is the only key factor that affects the grouping of neurons. Without an appropriate amount of distant inhibition, group formation does not occur. Group formation is very robust to all other parameters we tested. On the other hand, group locations are very easily disturbed by inputs or changes of parameters, suggesting that such neuronal groups are dynamically maintained. 5. With the development of neuronal groups, neurons can be divided into two response types. TN-1 neurons respond weakly to inputs and have small receptive fields or do not respond at all (silent); TN-II neurons, approximately 30-40% of all, respond strongly to inputs and have large receptive fields. The two types of neurons also differ with respect to response threshold and temporal firing patterns. After groups formed, receptive fields of TN-II neurons within the same group clustered spatially with high overlap, whereas receptive fields of TN-I neurons with detectable responses shifted systematically with the neuron's spatial location. 6. The two types of neurons are homogeneously distributed across the cortical layer. The population of each type of neuron produces a full representation of the input layer with weak or strong responses, respectively. 7. We concluded that neurons in the cortical network naturally assembled into functional groups. Such groups are dynamic and amenable to change by input stimuli. A fraction of neurons (30-40%) within the same group shares a similar receptive field and strongly respond together to stimuli, so that the network has more robust response to inputs. On the other hand, the responses of a large portion (60-70%) of neurons become weak or silent: these neurons are available for other (unknown) functional purposes.

Afferent Pathways↗
PubMed2003

Postnatal development of pre- and postsynaptic GABA markers at chandelier cell connections with pyramidal neurons in monkey prefrontal cortex.

The protracted postnatal maturation of the primate prefrontal cortex (PFC) is associated with substantial changes in the number of excitatory synapses on pyramidal neurons, whereas the total number of inhibitory synapses appears to remain constant. In this study, we sought to determine whether the developmental changes in excitatory input to pyramidal cells are paralleled by changes in functional markers of inhibitory inputs to pyramidal neurons. The chandelier subclass of gamma-aminobutyric acid (GABA) neurons provides potent inhibitory control over pyramidal neurons by virtue of their axon terminals, which form distinct vertical structures (termed cartridges) that synapse at the axon initial segment (AIS) of pyramidal neurons. Thus, we examined the relative densities, laminar distributions, and lengths of presynaptic chandelier axon cartridges immunoreactive for the GABA membrane transporter 1 (GAT1) or the calcium-binding protein parvalbumin (PV) and of postsynaptic pyramidal neuron AIS immunoreactive for the GABA(A) receptor alpha(2) subunit (GABA(A) alpha(2)) in PFC area 46 of 38 rhesus monkeys (Macaca mulatta). From birth through 2 years of age, the relative densities and laminar distributions of these three markers exhibited different trajectories, suggesting developmental shifts in the weighting of at least some factors that determine inhibition at the AIS. In contrast, from 2 to 4 years of age, all three markers exhibited similar declines in density and length that paralleled the periadolescent pruning of excitatory synapses to pyramidal neurons. Across development, the predominant laminar location of PV-labeled cartridges and GABA(A) alpha(2)-immunoreactive AIS shifted from the middle to superficial layers, whereas the laminar distribution of GAT1-positive cartridges did not change. Together, these findings suggest that the maturation of inhibitory inputs to the AIS of PFC pyramidal neurons is a complex process that may differentially affect the firing patterns of subpopulations of pyramidal neurons at specific postnatal time points.

Animals↗
PubMed1995

Lamina-specific synaptic connections of hippocampal neurons in vitro.

By using slice cultures as a model, we demonstrate here that different target selectivities exist among the various afferent fibers to the hippocampus. As in intact animals, septohippocampal cholinergic fibers, provided by a slice culture of septum, innervate a co-cultured slice of hippocampus diffusely, that is, without forming distinct layers of termination. As in vivo, the septal cholinergic fibers establish synapses with a variety of target cells. Conversely, fibers from an entorhinal slice co-cultured to a hippocampal slice display their normal laminar specificity. They preferentially terminate in the outer molecular layer of the fascia dentata, thereby selectively contacting peripheral dendrites of the granule cells. This preferential termination on peripheral dendritic segments is remarkable, since these fibers do not have to compete with commissural fibers, hypothalamic fibers, and septal afferents for dendritic space under these culture conditions. Moreover, in triplet cultures in which first two hippocampal slices were co-cultured and then, with a delay of 5 days, an entorhinal slice was added, the fibers from the entorhinal slice and those from the hippocampal culture terminated in their appropriate layers in the hippocampal target culture. However, in this approach the normal sequence of ingrowth of these two afferents was reversed. In normal ontogenetic development, entorhinal afferents arrive in the hippocampus before the commissural fibers. The results show that there are different degrees of target selectivity of hippocampal afferents and that the characteristic lamination of certain afferent fibers in the hippocampus is not determined by their sequential ingrowth during development.

Afferent Pathways↗
PubMed1998

Efferent synaptic connections of dopaminergic neurons grafted into the caudate nucleus of experimentally induced parkinsonian monkeys are different from those of control animals.

This study investigated the question of whether grafted dopamine cells in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys form synapses and, if they do, whether their postsynaptic targets were the same as those in control monkeys or in previous studies in rats. Electron-microscopic single immunostaining was performed for tyrosine hydroxylase on vibratome sections prepared from the head of the caudate nucleus of controls and MPTP-treated African green monkeys (Cercopithecus aethiops sabaeus) that received a graft. Furthermore, correlated light- and electron-microscopic double immunostaining was carried out for tyrosine hydroxylase and calbindin in the same brain area of MPTP-treated plus grafted animals. In control monkeys, the majority (97%) of dopamine boutons terminate on spines that were also synaptic targets of immunonegative boutons forming asymmetric synaptic contacts: synaptic triads. In MPTP-treated, grafted animals, the majority of transplanted dopamine cells terminate on dendritic shafts (67%) and somata (32%), and only a few (1.33%) form axospine synapses. The results of the double immunostaining experiments indicated that these newly formed axosomatic and axodendritic synapses are associated with calbindin-immunoreactive, medium-sized, spiny striatonigral projection neurons. These observations indicate that: (1) dopamine from transplanted embryonic tissue acts via synaptic contacts on host neurons; (2) the primary synaptic targets of transplanted dopamine cells are not spines but dendrites and somata of host neurons; (3) these target neurons are the same as in control animals; and (4) comparing these observations with results of control and grafted rats, there are major species differences between rats and monkeys in the dopamine innervation of both control and transplanted animals.

Animals↗
PubMed1986

Inhibitory connections between motor neurons modify a centrally generated motor pattern in the leech nervous system.

Both excitatory and inhibitory motor neurons innervate longitudinal body wall muscles in the leech Hirudo medicinalis. Each inhibitory motor neuron also centrally inhibits the excitatory motor neurons that innervate its same muscle field. This central inhibition is strong, probably monosynaptic, and largely a function of graded membrane potential changes in the inhibitory motor neurons. During leech swimming, both the excitatory and inhibitory motor neurons are rhythmically active. Here, we present evidence that the inhibitory motor neurons phasically inhibit the excitatory motor neurons during swimming, thereby augmenting the amplitude of membrane potential oscillations and the burst intensity of the excitors.

Animals↗
PubMed1993

The effect of alpha-latrotoxin on a synaptic connection between identified neurons in the brain of the mollusc Helix pomatia L.

The effect of alpha-latrotoxin on identified monosynaptic peptidergic contacts between identified neurons from the brain of the snail Helix pomatia L. was studied. It was found that, after extracellular application, toxin evoked an increase in the amplitude of the postsynaptic response. Neither amplitude nor duration of the action potential in a presynaptic neuron was affected. Intracellular injection of toxin into the soma of a presynaptic neuron led to a decrease in the postsynaptic current amplitude. The current induced by intracellular injection of cAMP into a postsynaptic neuron was also inhibited by extracellular or intracellular application of toxin. These data indicate that toxin evokes both an increase of transmitter release from a presynaptic neuron and a decrease in amplitude of the postsynaptic response.

Action Potentials↗
PubMed2006

A monosynaptic connection between baroinhibited neurons in the RVLM and IML in Sprague-Dawley rats.

To date, few studies have examined the relationship between the firing rate of neurons in the rostral ventrolateral medulla (RVLM) and neurons in the intermediolateral cell column (IML) of the spinal cord. In 19 Sprague-Dawley rats, the relationship between 20 pairs of baroinhibited RVLM and IML units was analyzed by cross-correlation. Three criteria were applied before acceptance that the firing rate of a pair of neurons was correlated. First, at an appropriate latency following the firing of an RVLM neuron, as judged from previous studies (4-200 ms), the peak in the firing rate of an IML neuron was approximately double that of the averaged surrounding bin counts. Secondly, the peak grew steadily in the examined period. Thirdly, the peak was restricted to a 1-ms bin. With this approach, a correlation was found between RVLM and IML neurons in 3 pairs in all. In 2 pairs, a correlation was found at basal arterial pressure (AP). When AP was decreased using a caval snare, a correlation was demonstrated in a further pair. A possible potentiation of synaptic strength during hypotensive stimuli is discussed.

Action Potentials↗
PubMed1999

Nanomolar concentrations of lead inhibit glutamatergic and GABAergic transmission in hippocampal neurons.

To investigate whether lead (Pb2+) affects the tetrodotoxin (TTX)-sensitive release of neurotransmitters, the whole-cell mode of the patch-clamp technique was applied to cultured hippocampal neurons. Pb2+ (>/=10 nM) reversibly blocked the TTX-sensitive release of glutamate and gamma-aminobutyric acid (GABA), as evidenced by the reduction of the amplitude and frequency of glutamate- and GABA-mediated postsynaptic currents (PSCs) evoked by spontaneous neuronal firing. This effect of Pb2+, which occurred 2-3 s after exposure of the neurons to Pb2+-containing external solution, was not related to changes in Na+-channel activity, and was quantified by measurements of changes in the amplitude of PSCs evoked when a 50-micros, 5-V stimulus was applied via a bipolar electrode to a neuron synaptically connected to the neuron under study. With an IC50 of approximately 68 nM, Pb2+ blocked the evoked release of glutamate and GABA. This effect was most likely mediated by Pb2+'s actions on extracellular targets, because there was a very short delay (<3 s) for its onset, and it could be completely reversed by the chelator ethylene diaminetetraacetic acid (EDTA). Given that Pb2+-induced blockade of evoked transmitter release could be reversed by 4-aminopyridine, it is suggested that the effect on release was mediated via the binding of Pb2+ to voltage-gated Ca2+ channels. Thus, it is most likely that the neurotoxic effects of Pb2+ in the mammalian brain involve a decrease of the TTX-sensitive, Ca2+-dependent release of neurotransmitters.

4-Aminopyridine↗