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PubMed1975

Surgical disconnection of the medial basal hypothalamus and pituitary function in the rhesus monkey. II. GH and cortisol secretion.

Eighteen female rhesus monkeys subjected to complete or anterior disconnection of the medial basal hypothalamus (MBH) were studied to assess the effects of these deafferentation procedures on GH and cortisol secretion. Basal serum levels of GH were not disturbed or were slightly elevated following complete or anterior MBH disconnection. GH secretion in response to vasopressin administration or insulin hypoglycemia, however, was abolished by complete isolation of the MBH. In contrast, the elevations in serum cortisol concentrations observed in response to these noxious stimuli were not noticeably affected. The normal diurnal rhythm in cortisol secretion remained fully evident following anterior deafferentation, but was severely attenuated or abolished when all neuronal inputs to the MBH were transected. Such observations suggest that the central components of the neuroendocrine systems which regulate basal GH secretion and which subserve stress-induced elevations in cortisol secretion are resident within the MBH-hypophysial unit. In addition, these data indicate that the mechanisms underlying the diurnal rhythm in cortisol secretion, as well as those mediating the discharges of GH in response to vasopressin administration and insulin hypoglycemia, are dependent on the integrity of neuronal connections between the MBH and other hypothalamic and/or extrahypothalamic areas.

Animals↗
PubMed2002

Anatomical analysis of different hemispherotomy procedures based on dissection of cadaveric brains.

OBJECT: Functional hemispherectomy, itself a modification of anatomical hemispherectomy, has been further modified to a less invasive method (hemispherotomy), in which cortical resection is minimized and the rest of the affected hemisphere is functionally isolated by transecting its projection and commissural fibers. Although descriptions of three different types of hemispherotomy procedures have been published, the authors believe that it is important to develop a common and universally acceptable method based on a systematic analysis of topographic anatomy and neuronal connections. To this end, they have analyzed the three aforementioned procedures on the basis of meticulous fiber dissections in previously frozen formalin-fixed human brains. METHODS: The brain anatomy pertinent to surgical hemispherotomy is described in conjunction with dissection studies in 14 previously frozen, formalin-fixed human brains. The anatomical landmarks necessary for performing particular neuronal fiber resections are identified, and their relationships with operative methods are discussed, with an emphasis on commonalities among the three hemispherotomy procedures. CONCLUSIONS: In this analysis the authors confirmed that hemispherotomy typically consists of four common procedures: 1) interruption of the internal capsule and corona radiata; 2) resection of the medial temporal structures; 3) transventricular corpus callosotomy; and 4) disruption of the frontal horizontal fibers. After meticulous dissection of cadavers, the authors have designated a reliable method for performing these four operations that may be applicable as a commonly used procedure.

Adult↗
PubMed2006

Tracing neural circuits in vivo with Mn-enhanced MRI.

The application of MRI-visible paramagnetic tracers to reveal in vivo connectivity can provide important subject-specific information for multisite, multielectrode intracortical recordings in combined behavioral and physiology experiments. To establish the use of such tracers in the nonhuman primate, we recently compared the specificity of the anterograde tracer Mn2+ with that of wheat-germ-agglutinin conjugated to horseradish peroxidase (WGA-HRP) in experiments tracing the neuronal connections of the basal ganglia of the monkey. It was shown that Mn2+ and WGA-HRP yield the same projection patterns and that the former tracer crosses at least two synapses, for it could be found in thalamus following injections into the striatum. Here we provide evidence that Mn2+ reaches the cortex following striatum injections and, thus, is transferred even further than previously shown. In other words, used as a paramagnetic MRI tracer, Mn2+ can permit the visualization of neural networks covering at least four processing stages. Moreover, unilateral intravitreal injections show that Mn2+ is sufficiently synapse specific to permit visualization of the lamina of the dorsal lateral geniculate nucleus (dLGN). Interestingly, the transfer rate of the substance reflected the well-known axonal size differences between the parvocellular and magnocellular layers of dLGN. After intravitreal injections, we were able to demonstrate transfer of Mn2+ into several subcortical and cortical areas, including the inferotemporal cortex. The specificity of the transsynaptic transfer of manganese that we report here indicates the value of this tracer for chronic studies of development and plasticity, as well as for studies of brain pathology.

Animals↗
PubMed2001

Early Neurodegeneration after Hypoxia-Ischemia in Neonatal Rat Is Necrosis while Delayed Neuronal Death Is Apoptosis.

We used silver staining to demonstrate neuronal cell body, axonal, and terminal degeneration in brains from p7 rat pups recovered for 0, 1.5, 3, 6, 24, 48, 72 h, and 6 days following hypoxia-ischemia. We found that initial injury is evident in ipsilateral forebrain by 3 h following hypoxia-ischemia, while injury in ventral basal thalamus develops at 24 h. A secondary phase of injury occurs at 48 h in ipsilateral cortex, but not until 6 days in basal ganglia. Initial injury in striatum and cortex is necrosis, but in thalamus the neurodegeneration is primarily apoptosis. Degeneration also occurs in bilateral white matter tracts, and in synaptic terminal fields associated with apoptosis in regions remote from the primary injury. These results show that hypoxia-ischemia in the developing brain causes both early and delayed neurodegeneration in specific systems in which the morphology of neuronal death is determined by time, region, and potentially by patterns of neuronal connectivity.

Animals↗
PubMed1981

Visuocortical epileptiform discharges in rabbits: differential effects on neuronal development in the lateral geniculate nucleus and superior colliculus.

We have studied the effects of interictal epileptiform discharges originating from the striate cortex on the development of the receptive field characteristics of neurons in the lateral geniculate nucleus (LGNd) and superior colliculus (SC) in neonatal rabbits. The paroxysmal discharges were generated by twice-daily injections of penicillin into an implanted cannula. Control injections of penicillin + penicillinase were given to the other striate cortex of the same animal. Similar experimental procedures were used to study the effect of such projected discharges on the LGNd neurons in adult rabbit. The results of the first experiment show that cortical epileptiform discharges, initiated in neonatal rabbits 7--9 days of age and continuing to 20--25 days of age, retard the normal development of LGNd cells. There was an abnormal increase of indefinite cells, cells failing to respond to any light stimulation, and a concurrent decrease of cells with concentric cells was still present in adult rabbits which had interictal discharges in the striate cortex limited to the period of 7--9 days to 21--25 days of age. The fourth experiment shows that the interictal discharges in neonatal rabbits do not affect the normal receptive field development of neurons in the SC. The present results demonstrate that asymptomatic interictal epileptiform discharges, produced without focal structural damages in immature brain, can affect the development of neuronal connectivity. These results may have some clinical implications in relation to our understanding about the learning and developmental disabilities exhibited in children who had episodic seizure discharges.

Aging↗
PubMed1992

Inhibitory neuron produces heterosynaptic inhibition of the sensory-to-motor neuron synapse in Aplysia.

We have identified an inhibitory neuron (RPL4) in the right pleural ganglion of Aplysia, which produced hyperpolarization of the sensory and motor neurons involved in the tail withdrawal reflex. Activation of RPL4 significantly reduced the amplitude of excitatory postsynaptic potentials produced in tail motor neurons by action potentials triggered in sensory neurons. This example of heterosynaptic inhibition was due, at least in part, to an increase in membrane input conductance in the motor neuron. Since the synaptic strength of the sensory-to-motor neuron connection has been associated with the strength of the tail withdrawal reflex, RPL4 may contribute to modulation of that reflex.

Action Potentials↗
PubMed1988

Distorted development of intracerebral grafts: long-term maintenance of tyrosine hydroxylase-containing neurons in grafts of cortical tissue.

Cortical cells obtained from rat embryos (ED14 to ED20) were implanted in various regions of rat brain and the presence of tyrosine hydroxylase (TH)-, neuropeptide Y (NPY)- and Met-enkephalin (ENK)-immunoreactive neurons within the grafts were tested using an immunohistochemical approach. TH-like immunoreactive (TH-LI) neurons were present within the implants obtained from ED14, but not ED18 or ED20, embryos up to 10 months post-implantation and their presence was not dependent on the age of the host (adult or neonate) at the time of implantation. Furthermore, the density of such cells varied with the site of implantation, being the highest in the dorsomedial corner of the striatum. This distorted development seems to affect also other cell populations, such as NPY-LI neurons which could be observed within the implants in a density much higher than that found in the normal cortex and which presented generally a rather immature morphology. It has been described that the rat cortex contains TH-LI neurons only during a limited period of development. The survival of such neurons within intracerebral grafts of cortical tissue indicates that their disappearance during normal cortical development is dependent upon environmental cues. The survival of TH-LI cells in grafts implanted to neonatal hosts suggests that these cues are not some humoral factors appearing postnatally. On the other hand, the present observations are compatible with several other hypothesis concerning the nature of such cues: humoral factors present during the late embryonic period, signals dependent on neuronal connectivities (input and/or outputs) established during embryonic or postnatal life.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1992

Monoclonal antibodies reveal molecular differences between terminal fields in the rat dentate gyrus.

We have derived a number of monoclonal antibodies which detect molecular differences correlating with the afferent inputs to the molecular layer of the adult rat hippocampal dentate gyrus. One group, dubbed OM-1 to OM-4, strongly stain the outer zone of the molecular layer, which receives its major innervation from the ipsilateral entorhinal cortex. A second group, IM-1 and IM-2, show a complementary pattern and preferentially stain the inner molecular layer, which receives inputs from the ipsilateral and contralateral hippocampus. These antigens are not, however, restricted to these layers, being found outside the hippocampus in several other areas of neuropil in the adult brain. In the developing brain the IM-1 antigen appears ubiquitously from the earliest age studied, embryonic day 12. Within the dentate gyrus, its restriction to the inner terminal field of the molecular layer only occurs during the second postnatal week. In contrast, OM staining appears only sparsely and late in the prenatal brain, appearing in developing cortical white matter between embryonic days 18 and 20. The outer dentate molecular layer becomes OM-positive from birth onwards, corresponding to the time of arrival of entorhinal axons during the first postnatal week. These two groups of monoclonal antibodies recognize a number of different glycoproteins. Ultrastructural immunohistochemistry shows they are cell surface molecules, and as such may be involved in the recognition events required for the establishment of specific patterns of neuronal connectivity.

Animals↗
PubMed1999

Neurotrophins and hippocampal synaptic transmission and plasticity.

Neurotrophins are traditionally thought to be secretory proteins that regulate long-term survival and differentiation of neurons. Recent studies have revealed a previously unexpected role for neurotrophins in synaptic development and plasticity in diverse neuronal populations. In this review, we focus on the synaptic function of brain-derived neurotrophic factor (BDNF) in the hippocampus. Although a variety of in vitro experiments have shown the ability of BDNF to acutely modulate synaptic transmission, whether BDNF truly potentiates basal synaptic transmission in hippocampal neurons remains controversial. More consistent evidence has been obtained for the role of BDNF in long-term potentiation (LTP), a cellular model for learning and memory. BDNF also potentiates high frequency transmission by modulating the number of docked vesicles and the levels of the vesicle protein synaptobrevin and synaptophysin at the CA1 synapses. Both pre- and postsynaptic effects of BDNF have been demonstrated. Recent studies have begun to address the role of BDNF in late-phase LTP and in the development of hippocampal circuit. BDNF and other neurotrophins may represent a new class of neuromodulators that regulate neuronal connectivity and synaptic efficacy. J. Neurosci. Res. 58:76-87, 1999. Published 1999 Wiley-Liss, Inc.

Animals↗
PubMed1987

Neuroendocrinology of pituitary hormone regulation.

Hormone secretion from the pituitary gland is dependent on the intimate association between the hypothalamus and pituitary by vascular and neuronal connections. The anatomic organization of these networks and their specific peptide and/or amide mediators are described in detail. Pertinent factors governing hypothalamic regulation of anterior pituitary secretion are also discussed.

Humans↗
PubMed1999

Catecholaminergic neurons in the diencephalon and basal ganglia of SIDS.

The catecholaminergic systems of sudden infant death syndrome victims were examined in the diencephalon and basal ganglia, in addition to the midbrain, pons, and medulla oblongata, using the immuno-histochemical method involving tyrosine hydroxylase. A significant decrease in tyrosine hydroxylase immunoreactivity was demonstrated in the basal ganglia of sudden infant death syndrome victims between 2 to 12 months of age compared with age-matched control subjects. This change in the basal ganglia may be a secondary finding induced by chronic hypoxia or repeated ischemia in sudden infant death syndrome but suggests impairment of the development of the neuronal connection from the brainstem to the upper cardiorespiratory control in sudden infant death syndrome.

Basal Ganglia↗
PubMedDate not supplied

Transcallosal circuitry revealed by blocking and disinhibiting callosal input in the cat.

The purpose of this study was to obtain quantitative measures of the influence of callosal input to cells at the area 17/18 border region where transcallosal axons terminate most densely. Single-cell recordings were performed at the area 17/18 border region of the right hemisphere, while gamma-aminobutyric acid (GABA) or its antagonist, bicuculline, were applied to the transcallosal projecting regions of the left hemisphere to either block or overactivate the cells which projected to the neurons at the recording site. The results showed that visually evoked responses of the cells at the area 17/18 border were affected by administration of GABA or bicuculline to the contralateral hemisphere. Blockade of transcallosal input by application of GABA in the left hemisphere diminished the visually evoked responses of 51% of the neurons in the right hemisphere, and led to an increase in response magnitude for 17% of the neurons. Disinhibition of transcallosal input by application of bicuculline increased the evoked activity of 40% of the neurons and diminished the response magnitude of 20% of the neurons in the right hemisphere. GABA and bicuculline failed to show antagonistic effects on some cells. Thirty-two percent of the cells were affected by only one type of drug administration, and 13% of the cells showed either an increase or a decrease in responses after both GABA and then bicuculline administration. This study demonstrated complex interactions between neurons connected by the transcallosal pathway. A model of the transcallosal circuitry was proposed to explain the results.

Animals↗
PubMedDate not supplied

Analysis of two types of cone bipolar cells in the retina of a New World monkey, the marmoset, Callithrix jacchus.

Two types of cone bipolar cells, the blue cone bipolar cell and the diffuse bipolar cell (DB3), were labelled immunohistochemically and investigated in the retina of a New World monkey, the marmoset. Blue cone bipolar cells were labelled with an antiserum against cholecystokinin. Short-wavelength-sensitive (SWS) cones were labelled with an antiserum against the SWS cone opsin. The DB3 cells were labelled with antibodies to calbindin. Blue cone bipolar cells in marmoset do not form a regular mosaic but instead follow the random distribution of the SWS cones. Nevertheless, the SWS cone to blue cone bipolar cell connectivity in marmoset is very similar to that previously described for macaque. In contrast to the blue cone bipolar cells, the DB3 cells form a regular mosaic. The synaptic connectivity of DB3 cells in the inner plexiform layer was analyzed. They make output synapses onto ganglion cells and amacrine cells, and gap junctions with each other. Our results provide further evidence for the existence of parallel bipolar cell pathways in the primate retina and support the view that the retinae of Old World and New World primates have common neuronal connectivity. The random distribution of SWS cones and blue cone bipolar cells is an exception to the general rule of a regular mosaic distribution of cell populations in the retina.

Animals↗
PubMed2005

Rostral ganglia are required for induction but not expression of crayfish escape reflex habituation: role of higher centers in reprogramming low-level circuits.

It is widely assumed that learning results from alterations in the strength of synapses within the neural pathways that mediate a learned behavioral response and that these alterations are directly caused by training-induced activity of neurons connected by the changing synapses. Initial evidence for this view came from studies of habituation of defensive reflexes in several invertebrate species. However, more recent studies of habituation of the escape reflex in one of these species, the crayfish, have shown that habituation is substantially caused by tonic inhibitory input from cephalic ganglia; this descending inhibition suppresses the activity of neurons within the escape circuit, which reside in caudal ganglia. Such control by descending inhibition indicates that animals with encephalized nervous systems do not entirely abdicate to low-level circuitry the important decision of whether to habituate to stimuli that might warn of danger. Higher centers in fact play a major role in controlling the habituation of this potentially life-saving protective response. Another way for higher centers to control lower ones would be to induce alteration of the lower center's intrinsic properties. Here, we show that, whereas descending input from higher ganglia is needed to induce habituation, once established, habituation persists even after rostral ganglia are disconnected. This provides evidence that lower-level neural circuits can be reprogrammed through transient interaction with higher ganglia to decrease their intrinsic tendency to produce escape.

Animals↗
PubMed1990

Thalamic midline cell populations projecting to the nucleus accumbens, amygdala, and hippocampus in the rat.

The organization of the thalamic midline efferents to the amygdaloid complex, hippocampal formation, and nucleus accumbens was investigated in the rat by means of multiple retrograde fluorescent tracing. The present findings indicate that these connections derive from separate cell populations of the thalamic midline, with a low degree of divergent collateralization upon more than one of the targets examined. The neural populations projecting to the amygdala, hippocampus, or accumbens are highly intermingled throughout the thalamic midline, but display some topographical prevalence. Midline thalamo-hippocampal cells are concentrated in the nucleus reuniens; thalamo-accumbens neurons prevail in the ventral portion of the paraventricular nucleus, and in the central medial nucleus. Thalamo-amygdaloid cells display a topographical prevalence in the rostral third of the thalamic midline and are concentrated in the dorsal part of the paraventricular nucleus and in the medial part of the nucleus reuniens. Both dorsally in the paraventricular nucleus and ventrally in the nucleus reuniens, thalamo-amygdaloid cells are located closer to the ependymal lining than the neurons projecting to the hippocampus or nucleus accumbens. Further, thalamo-amygdaloid cells, especially in the paraventricular nucleus, extend their dendritic processes in the vicinity of the ependymal lining, where they arborize profusely. These features indicate a close topographical relationship of neurons projecting to the amygdala with ependymal cells. The fairly discrete origin of midline outputs to the amygdala, hippocampus, and accumbens indicates that the flow of information is conveyed through separate channels from the thalamic midline to limbic and limbic-related targets. Together with the literature on the limbic afferents to the thalamus, these findings emphasize the relationships between the thalamus and the limbic system subserved by parallel input-output routes. However, because of the overlap of the projection cell populations, the thalamic midline may represent a locus of interaction among neurons connected with different parts of the limbic system. The functional implications of these findings are discussed in relation to the "nonspecific" thalamic system, as well as to the circuits involved in memory formation.

Amnesia↗
PubMed2004

TrkB regulates neocortex formation through the Shc/PLCgamma-mediated control of neuronal migration.

The generation of complex neuronal structures, such as the neocortex, requires accurate positioning of neurons and glia within the structure, followed by differentiation, formation of neuronal connections, and myelination. To understand the importance of TrkB signaling during these events, we have used conditional and knockin mutagenesis of the TrkB neurotrophin receptor, and we now show that this tyrosine kinase receptor, through docking sites for the Shc/FRS2 adaptors and phospholipase Cgamma (PLCgamma), coordinates these events in the cerebral cortex by (1) controlling cortical stratification through the timing of neuronal migration during cortex formation, and (2) regulating both neuronal and oligodendrocyte differentiation. These results provide genetic evidence that TrkB regulates important functions throughout the formation of the cerebral cortex via recruitment of the Shc/FRS2 adaptors and PLCgamma.

Adaptor Proteins, Signal Transducing↗
PubMed1997

Developmental synaptic depression underlying reorganization of visceral reflex pathways in the spinal cord.

During development, neuronal connectivity has a remarkable plasticity. Synaptic refinement in the spinal autonomic nucleus might be involved in the elimination of primitive segmental reflexes and the emergence of mature spinobulbospinal reflexes, which occurs a few weeks after birth. To address this possibility, we examined the postnatal changes of segmental excitatory synaptic transmission by applying the whole-cell recording technique to parasympathetic preganglionic neurons in slice preparations of the rat lumbosacral spinal cord. The mean magnitude of unitary excitatory synaptic currents evoked in preganglionic neurons by stimulation of single interneurons remained unchanged during the first two postnatal weeks but was reduced by 50% during the third postnatal week. This reduction in synaptic efficacy was associated with a decrease in the amount of transmitter release from interneurons. Moreover, this developmental depression of segmental synaptic transmission was prevented by spinal cord transection at the thoracic level on postnatal day 14. Thus, developmental modification of excitatory synapses on preganglionic neurons appears to be attributable to competition between segmental interneuronal and descending bulbospinal inputs, which results in the developmental reorganization of parasympathetic excretory reflex pathways.

Afferent Pathways↗
PubMed1982

Postnatal changes in the number of neurons and synapses in the visual cortex (area 17) of the macaque monkey: a stereological analysis in normal and monocularly deprived animals.

The surface area of the striate cortex and the thickness of its laminae were measured in a series of newborn, 3-month, 6-month, and adult macaque monkeys. The numerical densities (Nv) of neurons and synapses were measured in individual laminae. The total numbers of neurons and synapses in the striate cortex of one hemisphere were derived from these measures. Normal monkeys were compared at 3 months and 6 months of age to animals having been reared from birth with a monocular eyelid suture. No significant differences were observed between normal and monocularly deprived monkeys. The perceptual deficits and physiological abnormalities that have been reported in monocularly deprived monkeys do not appear to result from a reduction in the amount of neural circuitry in the striate cortex. The combined data from these groups, however, demonstrated several developmental changes. Cortical thickness increased from birth to 6 months and diminished to near-newborn values in the adult. The 6-month cortex was 19% thicker than that of the adult. This overshoot was greatest in layers II and III, which were 43% thicker at 6 months. Cortical surface area demonstrated a similar trend, being 23% greater at 6 months, but the differences were not statistically significant. The Nv of neurons decreased from birth to 6 months and increased to near-newborn values in the adult. The 6-month Nv was 30% less than that of adults and the greatest changes were seen in layers II and III where the Nv was 38% less than adult values. The total number of neurons in the striate cortex of one hemisphere was 16% less in adults than in newborn animals, but statistically significant neuron losses were limited to layers I, II, IVC alpha, V, and VI. The Nv of synapses increased from birth to 6 months and diminished to near-newborn values in the adult. The 6-month overshoot was 34% for the total cortex and 41% for layers I-III. The total number of synapses in the striate cortex was 95% greater at 6 months than in the adult. In layers I-III the synapses were 130-155% more numerous at 6 months. These data demonstrate an increase in neuronal connectivity in the striate cortex from birth to 6 months, especially in layers I-III, and a subsequent decrease in the adult.

Aging↗