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PubMed1986

Functional characterization of preganglionic neurons projecting in the lumbar splanchnic nerves: vasoconstrictor neurons.

Lumbar preganglionic neurons, which project in the lumbar splanchnic nerves and which probably have a vasoconstrictor function (visceral vasoconstrictor, VVC neurons), were analyzed for their discharge patterns. The responses of these neurons to the following natural stimuli were tested: stimulation of arterial baroreceptors, arterial chemoreceptors and visceral afferents from the urinary bladder, the colon and the mucosal skin of the anus. Forty-nine preganglionic neurons were classified as VVC neurons. They showed the following characteristics: the ongoing activity of the VVC neurons exhibited pronounced cardiac rhythmicity and correlated with the cycle of the artificial ventilation. Stimulation of arterial baroreceptors, produced by increase of blood pressure or by increase of pressure in an isolated carotid blind sac, led to inhibition of activity in VVC neurons. Unloading of arterial baroreceptors, produced by decrease of blood pressure, led to an increase in VVC neuron activity. Stimulation of arterial chemoreceptors by bolus injections of CO2-enriched saline solution, close to a carotid glomus, led to a weak excitation of VVC neurons. Stimulation of arterial chemoreceptors by systemic hypoxia led to weak excitation and/or to depression of activity in VVC neurons. Stimulation of visceral afferents from urinary bladder and colon by isovolumetric contractions and distensions of the organs had no effect on most VVC neurons. Anal stimulation also did not induce reflexes in the majority of the VVC neurons. Some 14% of the VVC neurons (7 from 49) were excited by at least one of the visceral stimuli in the same manner as the motility-regulating (MR) neurons. This investigation shows that preganglionic neurons, probably involved in regulation of vascular resistance in colon and pelvic organs, are functionally a distinct population of neurons with some interesting functional overlap with the motility-regulating neurons.

Animals↗
PubMed1984

Transmitter identification of pyloric neurons: electrically coupled neurons use different transmitters.

The neurotransmitters mediating the synaptic interactions among the neurons of the pyloric system of the stomatogastric ganglion (STG) of the lobster, Panulirus interruptus, were examined using a combination of electrophysiological, pharmacological, and biochemical techniques. Iontophoretically applied L-glutamate inhibited all motor neurons of the pyloric system. This inhibitory response was blocked by low concentrations of picrotoxin but unaffected by atropine. The anterior burster (AB) interneuron, pyloric dilator (PD) motor neurons, and ventricular dilator (VD) motor neuron were depolarized and excited by iontophoretically applied acetylcholine (ACh). The lateral pyloric (LP) and pyloric (PY) constrictor motor neurons were inhibited by ACh and by the cholinergic agonist, carbachol. These inhibitory cholinergic responses were blocked by atropine but not by picrotoxin. The inhibitory postsynaptic potentials (IPSPs) evoked by the constrictor motor neurons were blocked by picrotoxin but not by atropine. Taken together with previously published data (15, 18), this suggests that the constrictor motor neurons release glutamate at both their excitatory neuromuscular junctions and their inhibitory intraganglionic junctions. The lucifer yellow photoinactivation technique (27) was used to study separately the neurotransmitters released by the electrically coupled PD and AB neurons. The AB-evoked IPSPs were blocked by picrotoxin but not by atropine. The PD-evoked IPSPs were blocked by atropine and other muscarinic antagonists but not by picrotoxin. Somata of PD neurons contained choline acetyltransferase (CAT) activity, but somata of AB neurons contained no detectable CAT activity. On the basis of the data in this paper and previously published data (17, 18), we conclude that the PD neurons release ACh at both their excitatory neuromuscular junctions and their inhibitory intraganglionic connections. Although the AB neuron is electrically coupled to the PD neurons, the AB neuron is not cholinergic. Glutamate is a likely transmitter candidate for the AB neuron. These data show that electrically coupled neurons can release different transmitters. Furthermore, these data show that an IPSP can be the result of the combined actions of two different neurotransmitters, each released from a different neuron. The functional consequences of these conclusions are explored in the following papers (9, 22).

Acetylcholine↗
PubMed1987

Corticogeniculate neurons, corticotectal neurons, and suspected interneurons in visual cortex of awake rabbits: receptive-field properties, axonal properties, and effects of EEG arousal.

The intrinsic stability of the rabbit eye was exploited to enable receptive-field analysis of antidromically identified corticotectal (CT) neurons (n = 101) and corticogeniculate (CG) neurons (n = 124) in visual area I of awake rabbits. Eye position was monitored to within 1/5 degrees. We also studied the receptive-field properties of neurons synaptically activated via electrical stimulation of the dorsal lateral geniculate nucleus (LGNd). Whereas most CT neurons had either complex (59%) or motion/uniform (15%) receptive fields, we also found CT neurons with simple (9%) and concentric (4%) receptive fields. Most complex CT cells were broadly tuned to both stimulus orientation and velocity, but only 41% of these cells were directionally selective. We could elicit no visual responses from 6% of CT cells, and these cells had significantly lower conduction velocities than visually responsive CT cells. The median spontaneous firing rates for all classes of CT neurons were 4-8 spikes/s. CG neurons had primarily simple (60%) and concentric (9%) receptive fields, and none of these cells had complex receptive fields. CG simple cells were more narrowly tuned to both stimulus orientation and velocity than were complex CT cells, and most (85%) were directionally selective. Axonal conduction velocities of CG neurons (mean = 1.2 m/s) were much lower than those of CT neurons (mean = 6.4 m/s), and CG neurons that were visually unresponsive (23%) had lower axonal conduction velocities than did visually responsive CG neurons. Some visually unresponsive CG neurons (14%) responded with saccadic eye movements. The median spontaneous firing rates for all classes of CG neurons were less than 1 spike/s. All neurons synaptically activated via LGNd stimulation at latencies of less than 2.0 ms had receptive fields that were not orientation selective (89% motion/uniform, 11% concentric), whereas most cells with orientation-selective receptive fields had considerably longer synaptic latencies. Most short-latency motion/uniform neurons responded to electrical stimulation of the LGNd (and visual area II) with a high-frequency burst (500-900 Hz) of three or more spikes. Action potentials of these neurons were of short duration, thresholds of synaptic activation were low, and spontaneous firing rates were the highest seen in rabbit visual cortex. These properties are similar to those reported for interneurons in several regions in mammalian central nervous system. Nonvisual sensory stimuli that resulted in electroencephalographic arousal (hippocampal theta activity) had a profound effect on the visual responses of many visual cortical neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Lateral tegmental field neurons of cat medulla: a source of basal activity of raphespinal sympathoinhibitory neurons.

1. We tested the hypothesis that sympathoinhibitory (SI) neurons in the lateral tegmental field (LTF) of the cat medulla exert their actions over a pathway that includes raphe neurons whose axons innervate the thoracic intermediolateral nucleus (IML). 2. We recorded from 32 LTF neurons with sympathetic nerve-related activity [as demonstrated with spike-triggered averaging of inferior cardiac sympathetic nerve discharge (SND)] whose firing rate increased during the inhibition of SND produced by baroreceptor reflex activation. These neurons were classified as SI in function. 3. Twenty-three of these 32 LTF-SI neurons were antidromically activated by microstimulation of the raphe nuclei, 2-4 mm rostral to the obex and 3-4.5 mm below the dorsal surface of the medulla. The threshold current for eliciting the longest-latency antidromic responses [18.9 +/- 2.4 (SE) ms] was increased when the stimulating microelectrode was moved more dorsally in the midline. With one exception, these neurons could not be antidromically activated by stimulation of sites either 1.5-2.0 mm lateral to the midline, contralateral to the site of unit recording or raphe sites caudal to the obex. Threshold stimuli applied 2-4 mm rostral to the obex and 1 mm lateral to the midline, ipsilateral to the site of unit recording, elicited antidromic responses whose onset latencies were shorter than those produced by raphe stimulation. These data support the view that the axons of LTF-SI neurons terminated in the region of the raphe that contains SI neurons whose axons innervate the IML. 4. We recorded from 32 raphe neurons with sympathetic nerve-related activity whose firing rate increased during baroreceptor reflex activation. These neurons were classified as SI in function. Twenty-five of the 32 raphe-SI neurons were antidromically activated by microstimulation of the third thoracic (T3) IML. Seven (including 5 with spinal axons) of 24 raphe-SI neurons tested were synaptically activated by microstimulation of the region of the LTF containing SI neurons. The modal onset latency of synaptic activation was 22.8 +/- 8.4 ms. This value is close to the difference in spontaneous firing times (26 ms on the average) of LTF-SI and raphe-SI neurons, relative to the peak of the cardiac-related burst of SND. 5. Taken together, these data are consistent with the hypothesis that LTF-SI neurons are a source of the background discharges of raphespinal-SI neurons. 6. Thirteen raphe-SI neurons were antidromically activated by stimulation of both the medulla and T3 IML.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1999

Cellular localization of huntingtin in striatal and cortical neurons in rats: lack of correlation with neuronal vulnerability in Huntington's disease.

Immunohistochemistry and single-cell RT-PCR were used to characterize the localization of huntingtin and/or its mRNA in the major types of striatal neurons and in corticostriatal projection neurons in rats. Single-label immunohistochemical studies revealed that striatum contains scattered large neurons rich in huntingtin and more numerous medium-sized neurons moderate in huntingtin. Double-label immunohistochemical studies showed that the large huntingtin-rich striatal neurons include nearly all cholinergic interneurons and some parvalbuminergic interneurons. Somatostatinergic striatal interneurons, which are medium in size, rarely contained huntingtin. Calbindin immunolabeling showed that the vast majority of the medium-sized striatal neurons that contain huntingtin are projection neurons, but only approximately 65% of calbindin-labeled projection neurons (localized to the matrix compartment of striatum) were labeled for huntingtin. Calbindin-containing projection neurons of the matrix compartment and calbindin-negative projection neurons of the striatal patch compartment contained huntingtin with comparable frequency. Single-cell RT-PCR confirmed that striatal cholinergic interneurons contain huntingtin, but only approximately 65% of projection neurons contained detectable huntingtin message. The finding that huntingtin is not consistently found in striatal projection neurons [which die in Huntington's disease (HD)] but is abundant in striatal cholinergic interneurons (which survive in Huntington's disease) suggests that the mutation in huntingtin that causes HD may not directly kill neurons. In contrast to the heterogeneous expression of huntingtin in the different striatal neuron types, we found all corticostriatal neurons to be rich in huntingtin protein and mRNA. One possibility raised by our findings is that the HD mutation may render corticostriatal neurons destructive rather than render striatal neurons vulnerable.

Animals↗
PubMed1987

Extension and retraction of axonal projections by some developing neurons in the leech depends upon the existence of neighboring homologues. II. The AP and AE neurons.

To assess the generality of our previous finding (Gao and Macagno, 1987) that segmental homologues play a role in the establishment of the pattern of axonal projections of the heart accessory HA neurons, we have extended our studies to two other identified leech neurons: the anterior pagoda (AP) neurons and the annulus erector (AE) motor neurons. Bilateral pairs of AP neurons are found in the first through the twentieth segmental ganglia (SG1 through SG20) of the leech ventral nerve cord. All AP neurons initially extend axonal projections to the contralateral periphery as well as longitudinal projections along the contralateral interganglionic connective nerves toward anterior and posterior neighboring ganglia. Although the peripheral projections are maintained by all AP neurons throughout the life of the animal, the longitudinal projections disappear in all but two segments: the AP neurons in SG1 maintain their anterior projections and extend them into the head ganglion, and those in SG20 maintain their posterior projections and extend them into SG21 and the tail ganglion. When single AP neurons are deleted anywhere along the nerve cord before processes begin to atrophy, however, the longitudinal projections are retained by their ipsilateral homologues in adjacent ganglia. The rescued processes appear to take over the projections of the deleted neurons. In cases where two or more AP neurons on the same side of the nerve cord are deleted from adjacent ganglia, a contralateral homologue sometimes extends projections to the periphery ipsilaterally or on both sides. We obtained similar results when we deleted single AE neurons from midbody ganglia. Thus, our experiments with three different identified neurons consistently show that the initial pattern of projections is the same in all ganglia, but that the existence of homologues in adjacent ganglia leads to the pruning of some of the initial projections. A consequence of this homologue-dependent process retraction is that neurons normally lacking neighboring homologues will have patterns of projections different from those neurons that do have such neighbors. Process loss by the HA, AP, and AE neurons may be the result either of competition for targets, inputs, or growth factors or of direct interactions among homologous cells.

Animals↗
PubMed1990

Extensive monosynaptic inhibition of ventral respiratory group neurons by augmenting neurons in the Bötzinger complex in the cat.

Axonal projections and synaptic connectivity of expiratory Bötzinger neurons with an augmenting firing pattern (Bot-Aug neurons) to neurons in the ipsilateral ventral respiratory group (VRG) were studied in anaesthetized cats. Antidromic mapping revealed extensive axonal arborizations of Bot-Aug neurons (24 of 45) to the rostral or caudal VRG, with some having arbors in both regions. Of 234 pairs of neurons studied with intracellular recording and spike-triggered averaging, monosynaptic inhibitory postsynaptic potentials (IPSPs) were evoked in 49/221 VRG neurons by 38/98 Bot-Aug neurons. The highest incidence of monosynaptic inhibition was found in inspiratory bulbospinal neurons (10 of 23 tested). Evidence was also found for monosynaptic inhibition, by a separate group of Bot-Aug neurons, of expiratory bulbospinal neurons (12/58), while excitatory postsynaptic potentials (EPSPs) were identified in another two of these neurons. In addition, monosynaptic IPSPs were recorded from 13 of 53 identified laryngeal motoneurons, and from 14 of 100 respiratory propriobulbar neurons. Presumptive disynaptic IPSPs were recorded from 11 of the 221 VRG neurons. We conclude that Bot-Aug neurons exert widespread inhibition on all major neuron categories in the ipsilateral VRG, and should be regarded as an important element in shaping the spatiotemporal output pattern of both respiratory motoneurons and premotor neurons.

Animals↗
PubMed1997

Dynamics of neurons controlling movements of a locust hind leg II. Flexor tibiae motor neurons.

Imposed movements of a proprioceptor that monitors the relative position of the tibia about the femur, the femorotibial chordotonal organ (FeCO), evoke resistance reflexes in the motor neurons that control the movements of the tibia of the locust. The response dynamics of one pool of motor neurons, the flexor tibiae motor neurons, which are located in three groups (anterior, lateral, and posterior), have been analyzed by the Wiener kernel method. First- and second-order kernels that represent the linear and nonlinear responses, respectively, were computed by a cross-correlation between the intracellularly recorded synaptic responses in the motor neurons and the white noise stimulus applied to the FeCO, and were used to define the input-output characteristics of the motor neurons. The posterior fast, intermediate, and slow and the anterior fast and intermediate flexor tibiae motor neurons had biphasic first-order kernels with initial negative phases, indicating that they are velocity sensitive. The falling phases of the kernels had distinct shoulders, indicating that the responses of the motor neurons also had delayed low-pass components, i.e., position sensitivity. The anterior slow flexor motor neuron had a monophasic, low-passed, first-order kernel, indicating that it is position sensitive. The linear component of the motor neuron responses, predicted by convolving the first-order kernels with the stimulus signal, strongly resembled the actual response, whereas the second-order nonlinear component was small, particularly at > 10 Hz. The power spectra of the fast motor neurons showed that they had the highest cutoff frequencies (at > 8 Hz), whereas the slow flexor motor neurons had a gradual roll-off at 1 Hz. The intermediate flexor motor neuron had an intermediate cutoff frequency of approximately 2-3 Hz. The linear responses of the flexor motor neurons could be decomposed into low- and high-frequency components. The high-frequency components (> 10 Hz) were velocity dependent and linear, whereas the low-frequency components (< 10 Hz) were position dependent and nonlinear. The nonlinearity was a signal compression (or half-wave rectification). The results show that although the flexor motor neurons receive many common inputs during FeCO stimulation, each individual has specific dynamic response properties. The responses of the motor neurons are fractionated so that a given individual within the pool will respond best to position, whereas others will respond better to velocity. Likewise, some motor neurons respond best at low frequencies, whereas others respond best at higher frequencies of stimulation.

Animals↗
PubMed1998

Passive electrical properties of ventral horn neurons in rat spinal cord slices.

Recordings were made from large neurons located in the ventral horn of transverse spinal cord slices from young rats (7-15 days). Whole cell recordings were made simultaneously with two electrodes from the soma of these neurons, visualized using infra-red differential interference contrast optics. Positive identification of motoneurons could not always be achieved. The response of a neuron to a brief pulse of current delivered by one electrode, and recorded by the other electrode, were matched optimally to responses of a compartmental model of the same neuron with an identical current pulse as input. The compartmental model was based on a reconstruction of the neuron, using Biocytin staining. The compartmental model had three free parameters: specific membrane capacitance (Cm), membrane resistivity (Rm), and cytoplasmatic resistivity (Ri), all assumed to be uniform throughout the neuron. The experimental and model responses could be matched unequivocally for four neurons, giving Cm = 2.4 +/- 0.5 microF/cm2, Rm = 5.3 +/- 0. 9 kOmega/cm2, and Ri = 87 +/- 22 Omega/cm. No somatic shunt was required. For the remaining six neurons, a less perfect fit (but still within 95% confidence limits) was indicative of nonhomogeneous membrane properties. The electrotonic length of uncut dendrites was 0.85 +/- 0.14 lambda. The results resolve the issue of a somatic shunt conductance for motoneurons, relegating it to a microelectrode impalement artifact. They are consistent with previous reports on the electrical compactness of motoneurons to steady state currents and voltages. However, the much higher value of Cm (than the previously assumed 1 microF/cm2) implies much greater dendritic attenuation of fast synaptic potentials, and a much enhanced integrative response of motoneurons to synaptic potentials.

Action Potentials↗
PubMed1992

Fine structure of rat septohippocampal neurons: I. Identification of septohippocampal projection neurons by retrograde tracing combined with electron microscopic immunocytochemistry and intracellular staining.

In this report the normal dendritic organization and fine structure of identified septohippocampal projection neurons is described as a prerequisite for a time course analysis of retrograde changes in these neurons following axotomy (see Naumann et al., J. Comp. Neurol. 325:219-242, 1992). Septohippocampal projection neurons were retrogradely labeled by injection of the fluorescent tracer Fluoro-Gold into the hippocampus. Next, retrogradely labeled cells in Vibratome sections of the medial septum/diagonal band complex were intracellularly stained with the fluorescent dye Lucifer Yellow (LY). Photooxidation of LY resulted in a stable electron-dense reaction product, which allowed us to study these double-labeled neurons by electron microscopy. Another series of sections containing retrogradely labeled neurons were immunostained for choline acetyltransferase (ChAT) or parvalbumin (PARV). In this way the fine structure of two different chemically characterized subpopulations of septohippocampal neurons could be compared with that of the LY-injected neurons. Intracellular filling of retrogradely labeled neurons with LY stained the cell body and the entire dendritic arbor. Essentially, three classes of neurons could be distinguished, i.e., bipolar cells, multipolar neurons, and an intermediate group. All these neurons displayed smooth, often varicose dendrites lacking spines. Mainly located close to the midline, there was a group of cells with only very few if any LY-stained dendrites. In the electron microscope, the double-labeled neurons were easily identified by numerous electron-dense lysosomes associated with transported Fluoro-Gold and the diffuse reaction product resulting from photooxidation. They displayed fine-structural characteristics as previously described for cholinergic neurons. In fact, our fine-structural analysis of ChAT-positive Fluoro-Gold-labeled neurons, but also of back-filled PARV-positive cells, gave very similar results. All these neurons had infolded nuclei, abundant cytoplasmic organelles, and a few axosomatic synapses. Thus, a plain electron microscopic study does not allow one to distinguish between subpopulations of septohippocampal projection neurons.

Animals↗
PubMed1998

Do non-dopaminergic neurons in the ventral tegmental area play a role in the responses elicited in A10 dopaminergic neurons by electrical stimulation of the prefrontal cortex?

It is rapidly becoming apparent that the prefrontal cortex (PFC) plays a major role in controlling the activity of midbrain dopaminergic (DA) neurons. We have previously demonstrated that electrical stimulation of the PFC elicits inhibition-excitation (IE) and excitation (E) activity patterns in DA neurons in the ventral tegmental area (VTA; A10 cell group). Since non-DA neurons in the VTA are cortically innervated, synapse upon DA neurons and appear to have an inhibitory impact, we determined the extent to which the responses of these neurons to stimulation of the PFC could account for the responses seen in DA neurons upon cortical stimulation. Stimulation of the PFC (0.25 mA and 1.0 mA) elicited three categories of response in the majority of VTA non-DA neurons. Types I and II were characterised by a short-to-moderate latency excitation (referred to as "early excitations"), in the latter case preceded by inhibition. Type III responses consisted of inhibition in the absence of an early excitation. Elements of these responses were compared with the temporal characteristics of key elements of responses elicited in DA neurons by PFC stimulation. Although the early excitations in non-DA neurons preceded the inhibitions in DA neurons exhibiting IE responses, the early excitations began approximately 100 ms before the inhibitions in DA neurons and often ended several tens of milliseconds before the inhibitions began, making a causal relationship between these events unlikely. The inhibitions in Type III responses, combined with the inhibitions which followed the early excitations in many Type I and II responses, showed temporal characteristics that suggested a possible causal relationship with the excitations in DA neurons exhibiting E responses, but not those exhibiting IE responses. However, since the excitatory phases of E and IE responses appear to be homologous, the lack of involvement of non-DA neurons in the excitatory phase of IE responses tends to cast doubt on the involvement of non-DA neurons in the excitation during E responses. In fact, the most coherent impression that emerges is that non-DA neurons in the VTA do not influence the activity of A10 DA neurons on a short time-scale (i.e. phasically), but instead may influence activity on a longer time-scale (i.e. tonically).

Action Potentials↗
PubMed1988

Morphological differentiation of embryonic rat sympathetic neurons in tissue culture. I. Conditions under which neurons form axons but not dendrites.

We have examined the morphology of fetal rat sympathetic neurons grown in serum-free medium in the absence of nonneuronal cells. Because cell density can affect phenotypic expression in vitro, the morphological analysis was subdivided into the study of isolated neurons (neurons whose somata were at least 150 micron from their nearest neighbor) and of more highly aggregated neurons. When isolated neurons were injected with intracellular markers, it was found that most (79%) had a single process emanating from their somata and that this unipolar state persisted for at least 8 weeks in vitro. The processes of unipolar sympathetic neurons had the appearance of axons in that they were thin and long, had a constant diameter, and were relatively unbranched. Cytochemical methods revealed that such processes had other axonal characteristics: (1) they were more reactive with a monoclonal antibody against phosphorylated forms of the M and H neurofilament subunits than with an antibody to nonphosphorylated forms of these proteins; (2) they also reacted with antibodies to the tau microtubule-associated protein and to the phosphorylated forms of the H neurofilament subunit; and (3) they contained only small amounts of RNA as determined by [3H]uridine autoradiography. These data indicate that neurons which normally form dendrites in vivo need not express this capacity in vitro and that axonal and dendritic growth can be dissociated under some conditions in culture. While most isolated neurons were unipolar, neurons in regions of high neuronal cell density were usually multipolar. In addition to axons, multipolar neurons had processes with some of the characteristics expected of rudimentary dendrites: they ended locally (usually within 100 micron), were often highly branched, and reacted with an antibody to nonphosphorylated forms of the M and H neurofilament subunits. The effects of density were most prominent when neurons were within aggregates in which the somata were in close apposition. Density-dependent changes in morphology were less frequently observed when neuronal somata were separated by greater distances (30-100 micron). These data indicate that the morphology of sympathetic neurons is subject to environmental regulation and that neuron-neuron interactions can promote the extension of rudimentary dendrites in vitro.

Animals↗
PubMed1982

Preparation and partial characterization of highly purified primary cultures of neurons and non-neuronal (glial) cells from embryonic chick cerebral hemispheres and several other regions of the nervous system.

Purified cultures of neurons and non-neuronal (glial) cells were prepared from the cerebral hemispheres of 10-day chick embryos by a method previously used for embryonic chick sympathetic ganglia 16. This technique separates these cell types on the basis of both: (1) differences in the adhesiveness of neurons and non-neuronal cells to a collagen substrate; and (2) the capacity of neurons to form homotypic aggregates. Purity of the cerebral non-neuronal cultures was determined to be greater than or equal to 99.5% by microscopic examination, while that of the cerebral neuronal cultures was only 92%. Modification of the technique by periodic redissociation of the neuronal aggregates during cell separation increased the purity of the neuronal cultures to greater than or equal to 97% as determined both by microscopic examination and by measurement of levels of butyrylcholinesterase, an enzyme present in the non-neuronal cells. Highly purified cultures of neurons were also prepared from the optic lobes of 10-day chick embryos (greater than or equal to 98%), but attempts to obtain non-neuronal cultures of reasonable density from this tissue were unsuccessful. In addition, highly purified non-neuronal cultures (greater than or equal to 99.5%) were prepared from the dorsal root ganglia of 12-day chick embryos, but cultures enriched with dorsal root neurons could only be partially purified (82%). Specific activity of butyrylcholinesterase in cerebral non-neuronal cells was found to vary inversely with the density of non-neuronal cells.

Animals↗
PubMed1982

Neuronal stimulation of non-neuronal (glial) cell proliferation: lack of specificity between different regions of the nervous system.

Purified and recombined primary cultures of neurons and non-neuronal (glial) cells were prepared from the cerebral hemispheres of 10-day chick embryos. Addition of cerebral neurons to homologous non-neuronal cultures stimulated incorporation of [3H]thymidine by 2.8-fold and increased the frequency of labelling of the non-neuronal cells by 3.5-fold as visualized by autoradiography. In contrast, cerebral neurons did not stimulate the proliferation of either embryonic chick fibroblasts or leptomeningeal cells. Furthermore, addition of either fibroblasts or extra non-neuronal cells did not stimulate non-neuronal cel proliferation. These data demonstrate for the first time that neurons isolated from the central nervous system can selectively stimulate the proliferation of homologous non-neuronal cells. Cell proliferation was also studied in cultures containing both homologous and heterologous combinations of neuronal and non-neuronal cells prepared from several different portions of the nervous system (cerebral hemispheres, optic lobes, sympathetic ganglia, and sensory ganglia). Addition of embryonic neurons stimulated non-neuronal cell proliferation in all cell combinations. Thus, neurons isolated from one region of the nervous system can stimulate the proliferation of non-neuronal cells isolated from other neural regions.

Animals↗
PubMedDate not supplied

Increased neurons containing neuronal nitric oxide synthase in the brain of a hypoxic-ischemic neonatal rat model.

We evaluated the temporal profile of the number of neurons containing neuronal nitric oxide synthase (nNOS neurons) in the brain of a neonatal hypoxic-ischemic rat model. Hypoxic-ischemic insults were produced in the brains of 7-day-old rat pups using a combination of unilateral carotid artery ligation and hypoxic (8% oxygen) exposure. Sections of brain from rats killed at 0-24 h after the onset of hypoxia were stained immunohistochemically using a polyclonal anti-nNOS antibody. Histological changes of neuronal injury were evaluated in the adjacent Nissl stained sections. The number of nNOS neurons in the hemisphere ipsilateral to the carotid ligation was significantly increased (P < 0.05) at 3 h, when the neuronal injury consisted of clusters of degenerating hyperchromic neurons. Neuronal degeneration and an increased number of nNOS neurons were seen only in the ipsilateral hemisphere and the increase was most prominent in the dorsolateral area of the striatum. The increase in the number of nNOS neurons continued at 6 h, when the area of neuronal injury continued to expand. At 24 h, the neuronal injury was diffuse, and the number of nNOS neurons on the ipsilateral side significantly decreased. The increase of the number of nNOS neurons in the early phase of neonatal neuronal injury suggests its possible involvement in the hypoxic-ischemic injury. The delineation of its role in neuronal injury may lead to an improvement in managing neonatal hypoxic-ischemic brain injury.

Animals↗
PubMed1999

Preferential loss of large neocortical neurons during HIV infection: a study of the size distribution of neocortical neurons in the human brain.

The infection with human immunodeficiency virus (HIV) is associated with a global and severe loss of neocortical neurons. However, there is limited knowledge concerning whether all neurons are equally susceptible to damage during HIV infection. Other studies have reported low vulnerability of small interneurons and high vulnerability of large motor neurons. Thus, it is natural to suggest that HIV infection, which causes damage to neurons in several ways, may predominantly affect large neurons in the neocortex. In this study we have used three unbiased stereological probes: Cavalieri's principle, the optical dissector and the rotator method, to obtain both total neocortical neuron number and their size distribution in formalin-fixed brains from six male acquired immunodeficiency syndrome (AIDS) patients and six male controls. The material is a selection of a large material choosing the youngest. The number of neurons in neocortex was reduced by 25% from 24.4 x 10(9) in controls to 18.3 x 10(9) in the AIDS patients; the reduction is similar to that of 27% found in the large material. In the normal size distribution of the neocortical neurons most neurons were smaller than 5000 micron3 and no sampled neurons were larger than 28,000 micron3. In addition, the absolute size distribution of neocortical neurons showed a significant decrease of the largest group of neurons by 50% (2p = 0.01) in the AIDS group, while there was no significant difference between controls and AIDS patients in the number of small neurons. The pattern of reduction in the number of large neocortical neurons was found in frontal, temporal, parietal as well as in occipital regions. This suggests that large neurons are more sensitive than small neurons to the destruction caused by the HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Mechanosensory S-neurons rather than AH-neurons appear to generate a rhythmic motor pattern in guinea-pig distal colon.

Simultaneous intracellular recordings were made from myenteric neurons and circular muscle (CM) cells in isolated, stretched segments of guinea-pig distal colon. We have shown previously that maintained stretch generates a repetitive and coordinated discharge of ascending excitatory and descending inhibitory neuronal reflex pathways in the distal colon. In the presence of nifedipine (1-2 microm) to paralyse the muscle, simultaneous recordings were made from 25 pairs of AH (after-hyperpolarization)-neurons and CM cells separated by 100-500 microm. In all 25 AH-neurons, proximal process potentials (PPPs) were never recorded, even though at the same time, all recordings from neighbouring CM cells showed an ongoing discharge of inhibitory junction potentials (IJPs) anally, or excitatory junction potentials (EJPs) orally. In fact, 24 of 25 AH-neurons were totally silent, while in one AH-cell, some spontaneous fast excitatory postsynaptic potentials (FEPSPs) were recorded. All 10 electrically silent AH-cells that were injected with neurobiotin were found to be multipolar Dogiel type II neurons. In contrast, when recordings were made from myenteric S-neurons, two distinct electrical patterns of electrical activity were recorded. Recordings from 25 of 48 S-neurons showed spontaneous FEPSPs, the majority of which (22 of 25) showed periods when discrete clusters of FEPSPs (mean duration 88 ms) could be temporally correlated with the onset of EJPs or anal IJPs in the CM. Nine S-neurons were electrically quiescent. The second distinct electrical pattern in 14 S-neurons consisted of bursts, or prolonged trains of action potentials, which could be reduced to proximal process potentials (PPPs) in six of these 14 neurons during membrane hyperpolarization. Unlike FEPSPs, PPPs were resistant to a low Ca(2+)-high Mg(2+) solution and did not change in amplitude during hyperpolarizing pulses. Mechanosensory S-neurons were found to be uniaxonal or pseudounipolar filamentous neurons, with morphologies consistent with interneurons. No slow EPSPs were ever recorded from AH- or S-type neurons when IJPs or EJPs occurred in the CM. In summary, we have identified a population of mechanosensory S-neurons in the myenteric plexus of the distal colon which appear to be largely stretch sensitive, rather than muscle-tension sensitive, since they generate ongoing trains of action potentials in the presence of nifedipine. No evidence was found to suggest that in paralysed preparations, the repetitive firing in ascending excitatory or descending inhibitory nerve pathways was initiated by myenteric AH-neurons, or slow synaptic transmission.

Action Potentials↗
PubMed1993

Neuronal activity changes of ventromedial hypothalamic neurons and associated temperature responses in rats following scrotal thermal stimulation.

Experiments were conducted to determine whether ventromedial hypothalamic (VMH) neurons were responsive to thermal warming or cooling of the scrotum. Extracellular neuronal activity of VMH neurons was monitored in anesthetized groups of normothermic (core temperature maintained at 37 degrees C) or hypothermic (core temperatures allowed to decrease, 33.3 +/- 1.1 degrees C) male, Sprague-Dawley rats along with colonic (Tc), interscapular brown adipose tissue (TIBAT), tail (Tt), and scrotal (Tsc) temperatures during 30-min periods of scrotal cooling (small ice peak) or scrotal warming (small sealed pack containing 40 degrees C tap water). In the normothermic group (65 VMH neurons recorded in total), 20 VMH neurons (31%) were classified as warm-responsive neurons (WRNs) (i.e., increased firing rate with scrotal warming and (or) decreased firing rates with scrotal cooling); 7 VMH neurons (11%) were classified as cold-responsive neurons (CRNs) (i.e., increased firing rate with scrotal cooling and (or) decreased firing rate with scrotal warming); and 38 VMH neurons (58%) were thermal nonresponsive neurons (TNRNs). In the hypothermic group (total of 85 VMH neurons recorded), 14 neurons (16%) were WRNs, 15 neurons (18%) were CRNs, and 56 neurons (66%) were TNRNs. Results indicated that VMH neurons can respond selectively to changes in scrotal temperature, as previously shown for preoptic-anterior hypothalamic neurons. Scrotal cooling and warming caused marked changes in T(sc) values in both the hypothermic and normothermic rats, but significant increases in TIBAT values indicative of brown adipose tissue thermogenesis did not occur.

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