Electrophysiological Differences Between Neurogliaform Cells From Monkey and Rat Prefrontal Cortex

2007 ◽  
Vol 97 (2) ◽  
pp. 1030-1039 ◽  
Author(s):  
N. V. Povysheva ◽  
A. V. Zaitsev ◽  
S. Kröner ◽  
O. A. Krimer ◽  
D. C. Rotaru ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Input Resistance ◽  
Firing Frequency ◽  
Morphological Features ◽  
Inhibitory Neurons ◽  
Physiological Properties ◽  
Cortical Circuit ◽  
Current Steps ◽  
Constituent Elements ◽  
Whole Cell Recordings

Current dogma holds that a canonical cortical circuit is formed by cellular elements that are basically identical across species. However, detailed and direct comparisons between species of specific elements of this circuit are limited in number. In this study, we compared the morphological and physiological properties of neurogliaform (NGF) inhibitory neurons in the prefrontal cortex (PFC) of macaque monkeys and rats. In both species, NGF cells were readily identified based on their distinctive morphological features. Indeed, monkey NGF cells had only a few morphological features that differed from rat, including a larger soma, a greater number of dendrites, and a more compact axonal field. In contrast, whole cell recordings of the responses to injected current steps revealed important differences between monkey and rat NGF cells. Monkey NGF cells consistently generated a short-latency first spike riding on an initial depolarizing hump, whereas in rat NGF cells, the first spike appeared after a substantial delay riding on a depolarizing ramp not seen in monkey NGF cells. Thus although rat NGF cells are traditionally classified as late-spiking cells, monkey NGF cells did not meet this physiological criterion. In addition, NGF cells in monkey appeared to be more excitable than those in rat because they displayed a higher input resistance, a lower spike threshold, and a higher firing frequency. Finally, NGF cells in monkey showed a more prominent spike-frequency adaptation as compared with rat. Our findings indicate that the canonical cortical circuit differs in at least some aspects of its constituent elements across species.

scholarly journals Parvalbumin-Positive Basket Interneurons in Monkey and Rat Prefrontal Cortex

2008 ◽  
Vol 100 (4) ◽  
pp. 2348-2360 ◽  
Author(s):  
N. V. Povysheva ◽  
A. V. Zaitsev ◽  
D. C. Rotaru ◽  
G. Gonzalez-Burgos ◽  
D. A. Lewis ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Cortical Neurons ◽  
Input Resistance ◽  
Cell Types ◽  
Threshold Current ◽  
Electrophysiological Properties ◽  
Basket Cells ◽  
Physiological Properties ◽  
Axonal Arbor ◽  
Fast Spiking

Differences in the developmental origin and relative proportions of biochemically distinct classes of cortical neurons have been found between rodents and primates. In addition, species differences in the properties of certain cell types, such as neurogliaform cells, have also been reported. Consequently, in this study we compared the anatomical and physiological properties of parvalbumin (PV)-positive basket interneurons in the prefrontal cortex of macaque monkeys and rats. The somal size, total dendritic length, and horizontal and vertical spans of the axonal arbor were similar in monkeys and rats. Physiologically, PV basket cells could be identified as fast-spiking interneurons in both species, based on their short spike and high-frequency firing without adaptation. However, important interspecies differences in the intrinsic physiological properties were found. In monkeys, basket cells had a higher input resistance and a lower firing threshold, and they generated more spikes at near-threshold current intensities than those in rats. Thus monkey basket cells appeared to be more excitable. In addition, rat basket cells consistently fired the first spike with a substantial delay and generated spike trains interrupted by quiescent periods more often than monkey basket cells. The frequency of miniature excitatory postsynaptic potentials in basket cells was considerably higher in rats than that in monkeys. These differences between rats and monkeys in the electrophysiological properties of PV-positive basket cells may contribute to the differential patterns of neuronal activation observed in rats and monkeys performing working-memory tasks.

Firing Properties and Connectivity of Neurons in the Rat Lateral Central Nucleus of the Amygdala

2004 ◽  
Vol 92 (3) ◽  
pp. 1285-1294 ◽  
Author(s):  
Mikel Lopez De Armentia ◽  
Pankaj Sah
Keyword(s):  
Action Potentials ◽  
Slow Component ◽  
Cell Types ◽  
Firing Frequency ◽  
Central Nucleus ◽  
Sk Channels ◽  
Physiological Properties ◽  
Prolonged Delay ◽  
Firing Properties ◽  
Whole Cell Recordings

Using whole cell recordings from acute slices of the rat amygdala, we have examined the physiological properties of and synaptic connectivity to neurons in the lateral sector of the central amygdala (CeA). Based on their response to depolarizing current injections, CeA neurons could be divided into three types. Adapting neurons fired action potentials at the start of the current injections at high frequency and then showed complete spike-frequency adaptation with only six to seven action potentials evoked with suprathreshold current injections. Late-firing neurons fired action potentials with a prolonged delay at threshold but then discharged continuously with larger current injections. Repetitive firers discharged at the start of the current injection at threshold and then discharged continuously with larger current injections. All three cells showed prolonged afterhyperpolarizations (AHPs) that followed trains of action potentials. The AHP was longer lasting with a larger slow component in adapting neurons. The AHP in all cell types contained a fast component that was inhibited by the SK channel blocker UCL1848. The slow component, not blocked by UCL1848, was blocked by isoprenaline and was significantly larger in adapting neurons. Blockade of SK channels increased the discharge frequency in late firers and regular-spiking neurons but had no effect on adapting neurons. Blockade of the slow AHP with isoprenaline had no effect on any cell type. All cells received a mixed glutamatergic and GABAergic input from a medial pathway. Electrical stimulation of the lateral (LA) and basolateral (BLA) nuclei evoked a large monosynaptic glutamatergic response followed by a disynaptic inhibitory postsynaptic potential. Activation of neurons in the LA and BLA by puffer application of glutamate evoked a small monosynaptic response in 13 of 55 CeA neurons. Local application of glutamate to the CeL evoked a GABAergic response in all cells. These results show that at least three types of neurons are present in the CeA that can be distinguished on their firing properties. The firing frequency of two of these cell types is determined by activation of SK channels. Cells receive a small input from the LA and BLA but may receive inputs that course through these nuclei en route to the CeA.

scholarly journals GAD67-GFP+ Neurons in the Nucleus of Roller: A Possible Source of Inhibitory Input to Hypoglossal Motoneurons. I. Morphology and Firing Properties

2011 ◽  
Vol 105 (1) ◽  
pp. 235-248 ◽  
Author(s):  
J.F.M. van Brederode ◽  
Y. Yanagawa ◽  
A. J. Berger
Keyword(s):  
Time Course ◽  
Input Resistance ◽  
Threshold Current ◽  
Firing Frequency ◽  
Inhibitory Neurons ◽  
Morphological Properties ◽  
Inhibitory Input ◽  
Current Frequency ◽  
Oriented Parallel

In this study we examined the electrophysiological and morphological properties of inhibitory neurons located just ventrolateral to the hypoglossal motor (XII) nucleus in the Nucleus of Roller (NR). In vitro experiments were performed on medullary slices derived from postnatal day 5 (P5) to P15 GAD67-GFP knock-in mouse pups. on cell recordings from GFP+ cells in NR in rhythmic slices revealed that these neurons are spontaneously active, although their spiking activity does not exhibit inspiratory phase modulation. Morphologically, GFP+ cells were bi- or multipolar cells with small- to medium-sized cell bodies and small dendritic trees that were often oriented parallel to the border of the XII nucleus. GFP+ cells were classified as either tonic or phasic based on their firing responses to depolarizing step current stimulation in whole cell current clamp. Tonic GFP+ cells fired a regular train of action potentials (APs) throughout the duration of the pulse and often showed rebound spikes after a hyperpolarizing step. In contrast, phasic GFP+ neurons did not fire throughout the depolarizing current step but instead fired fewer than four APs at the onset of the pulse or fired multiple APs, but only after a marked delay. Phasic cells had a significantly smaller input resistance and shorter membrane time constant than tonic GFP+ cells. In addition, phasic GFP+ cells differed from tonic cells in the shape and time course of their spike afterpotentials, the minimum firing frequency at threshold current amplitude, and the slope of their current–frequency relationship. These results suggest that GABAergic neurons in the NR are morphologically and electrophysiologically heterogeneous cells that could provide tonic inhibitory synaptic input to HMs.

Physiological Properties of Late Inspiratory Neurons and Their Possible Involvement in Inspiratory Off-Switching in Cats

2002 ◽  
Vol 87 (2) ◽  
pp. 1057-1067 ◽  
Author(s):  
Akira Haji ◽  
Mari Okazaki ◽  
Hiromi Yamazaki ◽  
Ryuji Takeda
Keyword(s):  
Nmda Receptors ◽  
Gaba Release ◽  
Membrane Depolarization ◽  
Inhibitory Neurons ◽  
Acid Decarboxylase ◽  
Postsynaptic Potentials ◽  
Inspiratory Neurons ◽  
Small Constant ◽  
Physiological Properties ◽  
Decerebrate Cats

To assess the functional significance of late inspiratory (late-I) neurons in inspiratory off-switching (IOS), membrane potential and discharge properties were examined in vagotomized, decerebrate cats. During spontaneous IOS, late-I neurons displayed large membrane depolarization and associated discharge of action potentials that started in late inspiration, peaked at the end of inspiration, and ended during postinspiration. Depolarization was decreased by iontophoresis of dizocilpine and eliminated by tetrodotoxin. Stimulation of the vagus nerve or the nucleus parabrachialis medialis (NPBM) also evoked depolarization of late-I neurons and IOS. Waves of spontaneous chloride-dependent inhibitory postsynaptic potentials (IPSPs) preceded membrane depolarization during early inspiration and followed during postinspiration and stage 2 expiration of the respiratory cycle. Iontophoresed bicuculline depressed the IPSPs. Intravenous dizocilpine caused a greatly prolonged inspiratory discharge of the phrenic nerve (apneusis) and suppressed late-inspiratory depolarization as well as early-inspiratory IPSPs, resulting in a small constant depolarization throughout the apneusis. NPBM or vagal stimulation after dizocilpine produced small, stimulus-locked excitatory postsynaptic potentials (EPSPs) in late-I neurons. Neurobiotin-labeled late-I neurons revealed immunoreactivity for glutamic acid decarboxylase as well as N-methyl-d-aspartate (NMDA) receptors. These results suggest that late-I neurons are GABAergic inhibitory neurons, while the effects of bicuculline and dizocilpine indicate that they receive periodic waves of GABAergic IPSPs and glutamatergic EPSPs. The data lead to the conclusion that late-I neurons play an important inhibitory role in IOS. NMDA receptors are assumed to augment and/or synchronize late-inspiratory depolarization and discharge of late-I neurons, leading to GABA release and consequently off-switching of bulbar inspiratory neurons and phrenic motoneurons.

scholarly journals Muscarinic Acetylcholine Receptor Localization on Distinct Excitatory and Inhibitory Neurons Within the ACC and LPFC of the Rhesus Monkey

2022 ◽  
Vol 15 ◽  
Author(s):  
Alexandra Tsolias ◽  
Maria Medalla
Keyword(s):  
Prefrontal Cortex ◽  
Muscarinic Receptors ◽  
Calcium Binding ◽  
Pyramidal Neurons ◽  
Muscarinic Acetylcholine Receptor ◽  
Anterior Cingulate ◽  
Inhibitory Neurons ◽  
Receptor Localization ◽  
Cortical Inputs ◽  
Almost All

Acetylcholine (ACh) can act on pre- and post-synaptic muscarinic receptors (mAChR) in the cortex to influence a myriad of cognitive processes. Two functionally-distinct regions of the prefrontal cortex—the lateral prefrontal cortex (LPFC) and the anterior cingulate cortex (ACC)—are differentially innervated by ascending cholinergic pathways yet, the nature and organization of prefrontal-cholinergic circuitry in primates are not well understood. Using multi-channel immunohistochemical labeling and high-resolution microscopy, we found regional and laminar differences in the subcellular localization and the densities of excitatory and inhibitory subpopulations expressing m1 and m2 muscarinic receptors, the two predominant cortical mAChR subtypes, in the supragranular layers of LPFC and ACC in rhesus monkeys (Macaca mulatta). The subset of m1+/m2+ expressing SMI-32+ pyramidal neurons labeled in layer 3 (L3) was denser in LPFC than in ACC, while m1+/m2+ SMI-32+ neurons co-expressing the calcium-binding protein, calbindin (CB) was greater in ACC. Further, we found between-area differences in laminar m1+ dendritic expression, and m2+ presynaptic localization on cortico-cortical (VGLUT1+) and sub-cortical inputs (VGLUT2+), suggesting differential cholinergic modulation of top-down vs. bottom-up inputs in the two areas. While almost all inhibitory interneurons—identified by their expression of parvalbumin (PV+), CB+, and calretinin (CR+)—expressed m1+, the localization of m2+ differed by subtype and area. The ACC exhibited a greater proportion of m2+ inhibitory neurons compared to the LPFC and had a greater density of presynaptic m2+ localized on inhibitory (VGAT+) inputs targeting proximal somatodendritic compartments and axon initial segments of L3 pyramidal neurons. These data suggest a greater capacity for m2+-mediated cholinergic suppression of inhibition in the ACC compared to the LPFC. The anatomical localization of muscarinic receptors on ACC and LPFC micro-circuits shown here contributes to our understanding of diverse cholinergic neuromodulation of functionally-distinct prefrontal areas involved in goal-directed behavior, and how these interactions maybe disrupted in neuropsychiatric and neurological conditions.

scholarly journals Kynurenine pathway in post-mortem prefrontal cortex and cerebellum in schizophrenia: relationship with monoamines and symptomatology

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Amira Ben Afia ◽  
Èlia Vila ◽  
Karina S. MacDowell ◽  
Aida Ormazabal ◽  
Juan C. Leza ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
High Performance ◽  
Interaction Analysis ◽  
Kynurenine Pathway ◽  
Psychotic Symptoms ◽  
Post Mortem ◽  
Control Subjects ◽  
Network Interaction ◽  
Hydroxyindoleacetic Acid ◽  
Cortical Circuit

Abstract Background The cortico-cerebellar-thalamic-cortical circuit has been implicated in the emergence of psychotic symptoms in schizophrenia (SZ). The kynurenine pathway (KP) has been linked to alterations in glutamatergic and monoaminergic neurotransmission and to SZ symptomatology through the production of the metabolites quinolinic acid (QA) and kynurenic acid (KYNA). Methods This work describes alterations in KP in the post-mortem prefrontal cortex (PFC) and cerebellum (CB) of 15 chronic SZ patients and 14 control subjects in PFC and 13 control subjects in CB using immunoblot for protein levels and ELISA for interleukins and QA and KYNA determinations. Monoamine metabolites were analysed by high-performance liquid chromatography and SZ symptomatology was assessed by Positive and Negative Syndrome Scale (PANSS). The association of KP with inflammatory mediators, monoamine metabolism and SZ symptomatology was explored. Results In the PFC, the presence of the anti-inflammatory cytokine IL-10 together with IDO2 and KATII enzymes decreased in SZ, while TDO and KMO enzyme expression increased. A network interaction analysis showed that in the PFC IL-10 was coupled to the QA branch of the kynurenine pathway (TDO-KMO-QA), whereas IL-10 associated with KMO in CB. KYNA in the CB inversely correlated with negative and general PANSS psychopathology. Although there were no changes in monoamine metabolite content in the PFC in SZ, a network interaction analysis showed associations between dopamine and methoxyhydroxyphenylglycol degradation metabolite. Direct correlations were found between general PANSS psychopathology and the serotonin degradation metabolite, 5-hydroxyindoleacetic acid. Interestingly, KYNA in the CB inversely correlated with 5-hydroxyindoleacetic acid in the PFC. Conclusions Thus, this work found alterations in KP in two brain areas belonging to the cortico-cerebellar-thalamic-cortical circuit associated with SZ symptomatology, with a possible impact across areas in 5-HT degradation.

scholarly journals Functional properties of GABA synaptic inputs onto GABA neurons in monkey prefrontal cortex

2015 ◽  
Vol 113 (6) ◽  
pp. 1850-1861 ◽  
Author(s):  
Diana C. Rotaru ◽  
Cameron Olezene ◽  
Takeaki Miyamae ◽  
Nadezhda V. Povysheva ◽  
Aleksey V. Zaitsev ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Input Resistance ◽  
Synaptic Inputs ◽  
Gaba Neurons ◽  
Decay Times ◽  
Cortical Interneurons ◽  
Dorsolateral Prefrontal ◽  
Gaba Neuron ◽  
Fast Spiking ◽  
Monkey Prefrontal Cortex

In rodent cortex GABAA receptor (GABAAR)-mediated synapses are a significant source of input onto GABA neurons, and the properties of these inputs vary among GABA neuron subtypes that differ in molecular markers and firing patterns. Some features of cortical interneurons are different between rodents and primates, but it is not known whether inhibition of GABA neurons is prominent in the primate cortex and, if so, whether these inputs show heterogeneity across GABA neuron subtypes. We thus studied GABAAR-mediated miniature synaptic events in GABAergic interneurons in layer 3 of monkey dorsolateral prefrontal cortex (DLPFC). Interneurons were identified on the basis of their firing pattern as fast spiking (FS), regular spiking (RS), burst spiking (BS), or irregular spiking (IS). Miniature synaptic events were common in all of the recorded interneurons, and the frequency of these events was highest in FS neurons. The amplitude and kinetics of miniature inhibitory postsynaptic potentials (mIPSPs) also differed between DLPFC interneuron subtypes in a manner correlated with their input resistance and membrane time constant. FS neurons had the fastest mIPSP decay times and the strongest effects of the GABAAR modulator zolpidem, suggesting that the distinctive properties of inhibitory synaptic inputs onto FS cells are in part conferred by GABAARs containing α1 subunits. Moreover, mIPSCs differed between FS and RS interneurons in a manner consistent with the mIPSP findings. These results show that in the monkey DLPFC GABAAR-mediated synaptic inputs are prominent in layer 3 interneurons and may differentially regulate the activity of different interneuron subtypes.

Control of the Firing Patterns of Vibrissa Motoneurons by Modulatory and Phasic Synaptic Inputs: A Modeling Study

2010 ◽  
Vol 103 (5) ◽  
pp. 2684-2699 ◽  
Author(s):  
Omri Harish ◽  
David Golomb
Keyword(s):  
Firing Frequency ◽  
Low Frequencies ◽  
Firing Patterns ◽  
Firing Rates ◽  
Periodic Input ◽  
Potassium Conductances ◽  
Rhythmic Firing ◽  
Current Steps ◽  
Periodic Inputs ◽  
Serotonergic Modulation

Vibrissa motoneurons (vMNs) generate rhythmic firing that controls whisker movements, even without cortical, cerebellar, or sensory inputs. vMNs receive serotonergic modulation from brain stem areas, which mainly increases their persistent sodium conductance ( gNaP) and, possibly, phasic input from a putative central pattern generator (CPG). In response to serotonergic modulation or just-suprathreshold current steps, vMNs fire at low rates, below the firing frequency of exploratory whisking. In response to periodic inputs, vMNs exhibit nonlinear suprathreshold resonance in frequency ranges of exploratory whisking. To determine how firing patterns of vMNs are determined by their 1) intrinsic ionic conductances and 2) responses to periodic input from a putative CPG and to serotonergic modulation, we construct and analyze a single-compartment, conductance-based model of vMNs. Low firing rates are supported in extended regimes by adaptation currents and the minimal firing rate decreases with gNaP and increases with M-potassium and h-cation conductances. Suprathreshold resonance results from the locking properties of vMN firing to stimuli and from reduction of firing rates at low frequencies by slow M and afterhyperpolarization potassium conductances. h conductance only slightly affects the suprathreshold resonance. When a vMN is subjected to a small periodic CPG input, serotonergically induced gNaP elevation may transfer the system from quiescence to a firing state that is highly locked to the CPG input. Thus we conclude that for vMNs, the CPG controls firing frequency and phase and enables bursting, whereas serotonergic modulation controls transitions from quiescence to firing unless the CPG input is sufficiently strong.

Excitability Increase Induced by β-Adrenergic Receptor-Mediated Activation of Hyperpolarization-Activated Cation Channels in Rat Cerebellar Basket Cells

2000 ◽  
Vol 84 (4) ◽  
pp. 2026-2034 ◽  
Author(s):  
Fumihito Saitow ◽  
Shiro Konishi
Keyword(s):  
Preceding Paper ◽  
Input Resistance ◽  
Ionic Currents ◽  
Synaptic Activity ◽  
Basket Cells ◽  
Camp Analogue ◽  
Voltage Dependent ◽  
Current Clamp Mode ◽  
Old Rats ◽  
Whole Cell Recordings

In the preceding paper, we showed that norepinephrine (NE) enhances the spontaneous spike firings in cerebellar interneurons, basket cells (BCs), resulting in an increase in the frequency of BC-spike-triggered inhibitory postsynaptic currents (IPSCs) in Purkinje cells (PCs), and that the effects of NE on GABAergic BCs are mediated by β2-adrenergic receptors. This study aimed to further examine the ionic mechanism underlying the β-adrenoceptor-mediated facilitation of GABAergic transmission at the BC-PC synapses. Using cerebellar slices obtained from 15- to 21-day-old rats and whole cell recordings, we investigated ionic currents in the BCs and the effects of the β-agonist isoproterenol (ISP) as well as forskolin on the BC excitability. Hyperpolarizing voltage steps from a holding potential of −50 mV elicited a hyperpolarization-activated inward current, I h, in the BC. This current exhibited voltage-dependent activation that was accelerated by strong hyperpolarization, displaying two time constants, 84 ± 6 and 310 ± 40 ms, at −100 mV, and was inhibited by 20 μM ZD7288. ISP and forskolin, both at 20 μM, enhanced I h by shifting the activation curve by 5.9 and 9.3 mV toward positive voltages, respectively. Under the current-clamp mode, ISP produced a depolarization of 7 ± 3 mV in BCs and reduced their input resistance to 74 ± 6%. ISP and a cAMP analogue, Rp-cAMP-S, increased the frequency of spontaneous spikes recorded from BCs using the cell-attached mode. The I h inhibitor ZD7288 decreased the BC spike frequency and abolished the ISP-induced increase in spike discharges. The results suggest that NE depolarizes the BCs through β-adrenoceptor-mediated cAMP formation linking it to activation of I h, which is, at least in part, involved in noradrenergic afferent-mediated facilitation of GABAergic synaptic activity at BC-PC connections in the rat cerebellum.

Membrane Potential of CA3 Hippocampal Pyramidal Cells During Postnatal Development

2003 ◽  
Vol 90 (5) ◽  
pp. 2964-2972 ◽  
Author(s):  
Roman Tyzio ◽  
Anton Ivanov ◽  
Cristophe Bernard ◽  
Gregory L. Holmes ◽  
Yehezkiel Ben-Ari ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Postnatal Development ◽  
Developmental Change ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Whole Cell ◽  
Perforated Patch ◽  
Ca3 Pyramidal Cells ◽  
Whole Cell Recordings

A depolarized resting membrane potential has long been considered to be a universal feature of immature neurons. Despite the physiological importance, the underlying mechanisms of this developmental phenomenon are poorly understood. Using perforated-patch, whole cell, and cell-attached recordings, we measured the membrane potential in CA3 pyramidal cells in hippocampal slices from postnatal rats. With gramicidin perforated-patch recordings, membrane potential was –44 ± 4 (SE) mV at postnatal days P0–P2, and it progressively shifted to –67 ± 2 mV at P13–15. A similar developmental change of the membrane potential has been also observed with conventional whole cell recordings. However, the value of the membrane potential deduced from the reversal potential of N-methyl-d-aspartate channels in cell-attached recordings did not change with age and was –77 ± 2 mV at P2 and –77 ± 2 mV at P13–14. The membrane potential measured using whole cell recordings correlated with seal and input resistance, being most depolarized in neurons with high, several gigaohms, input resistance and low seal resistance. Simulations revealed that depolarized values of the membrane potential in whole cell and perforated-patch recordings could be explained by a shunt through the seal contact between the pipette and membrane. Thus the membrane potential of CA3 pyramidal cells appears to be strongly negative at birth and does not change during postnatal development.

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