High- and low-threshold calcium currents in neurons acutely isolated from rat sensorimotor cortex

Sayer, Rod J.; Schwindt, P. C.; Crill, W. E.

doi:10.1016/0304-3940(90)90031-4

Cited by 93 publications

(52 citation statements)

References 18 publications

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“…For example, they are observed following presentation of visual stimuli (Hirsch et al 1995), whisker stimulation (Svoboda et al 1997), and during spontaneuous occurrence of hippocampal sharp wave (resulting from complex network-initiated spike bursts) in distal dendrites of pyramidal neurons in anesthetized animals in vivo (Komondi et al 1998). For a more detailed investigation of the electrophysiological characteristics of dendritic Ca 2ϩ potentials in pyramidal neurons, such potentials are often investigated in brain slices, following blockade of the Na ϩ and K ϩ channels (by external TTX ϩ TEA, or internal QX-314 ϩ Cs ϩ ) (Franz et al 1986;Sayer et al 1990Sayer et al , 1993Reuveni et Cd 2ϩ application to the proximal apical dendritic stem region (100-200 m from the soma) reduced the large subthreshold EPSP and abolished synaptically evoked action potentials, while having no effect on the EPSP evoked at Ϫ76mV. This suggests that the dendritic Ca 2ϩ "hump" potential mainly amplifies subthreshold EPSPs.…”

Section: Apical Dendritic Compartment Of Deep Layer Pyramidal Corticamentioning

confidence: 99%

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

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This review covers some recent findings of the electrophysiological mechanisms through which mesocortical dopamine modulates prefrontal cortical neurons. Dopamine has been shown to modulate several ionic conductances located along the soma-dendritic axis of prefrontal cortical pyramidal neurons. These ionic currents include high-voltage-activated calcium currents and slowly inactivating NaReceived May 12, 1998; revised May 27, 1998; accepted May 29, 1998. 162 C.R. Yang et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO Schizophrenia strikes one in one hundred people worldwide, regardless of cultural or racial origins. As the illness progresses and if it remains unattended, patients are frequently trapped in psychological, social, and economic devastation (Gottesman 1991;Jablensky 1995). Currently, our incomplete understanding of the neurobiological bases of schizophrenia suggests that defects in the genetic controls of brain development in such limbic regions (including temporal lobe structures such as hippocampus and the amygdala) as well as the prefrontal cortex (PFC) lead to cell loss or deformation, cytoarchitectural disorganization, and abnormal innervation in these brain regions (Roberts and Bruton 1990;Stevens 1992; Bogerts 1993;Shapiro 1993; Akbarian et al. 1993 Akbarian et al. , 1996Ross and Pearlson 1996;Weinberger 1996; Karayiorgou and Gogos 1997; Lewis 1997;Selemon et al. 1995Selemon et al. , 1998.Some results from recent imaging studies of brains from living schizophrenics have suggested that there are defective functional communications between the interconnected cortical (PFC and cingulate cortex) and limbic subcortical structures (thalamus, striatum, and temporal lobe limbic structures)(see reviews of Liddle 1996; Pfefferbaum and Marsh 1995; Andreasen 1997; Heckers et al. 1998). Findings from these studies suggest that in schizophrenics, abnormal recruitment of several interconnected cortical and subcortical structures may underlie such symptom clusters as psychomotor poverty, thought disorganization, and reality distortion (Liddle et al. 1992; Liddle 1996; Fletcher 1998; Heckers et al. 1998).As noted in Figure 1, the PFC receives converging limbic, association cortical, and mesocortical dopamine inputs. These inputs interact in the PFC and are involved functionally in high-level cognitive processes (Fuster 1995). Among the many brain regions that PFC output innervates, two important subcortical regions are emphasized in this review. These are the nucleus accumbens (where mesoaccumbens dopamine neurons terminate) and the ventral tegmental area (VTA, where the midbrain dopamine neurons reside) Groenewegen et al. 1990; Berendse et al. 1992a Berendse et al. , 1992bSesack and Pickel 1992;Gorelova and Yang 1997b). Several of the interconnected limbic, cortical, and subcortical structures known to be affected in schizophrenia are targets of the ascending midbrain dopamine systems that normally provide functional modulation of neurotransmission (Björklund and Lindvall 1984;Mogenson et ...

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Section: Apical Dendritic Compartment Of Deep Layer Pyramidal Corticamentioning

confidence: 99%

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

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“…In contrast, these behaviors are seen in immature, early postnatal neostriatal neurons (Trent et al, 1992) as predicted from our earlier work in immature cells (Bargas et al,199 1 b). This type of developmental elimination of LVA currents appears to be a characteristic of a great percentage of central neurons in descending motor pathways (i.e., pyramidal Betz neurons, spinal motoneurons; Llinas et al, 1988;Connors and Gutnick, 1990;Sayer et al, 1990;Mynlieff and Beam, 1992) whereas most ascending sensory neurons continue to manifest robust LVA currents (i.e., dorsal root ganglion neurons, dorsal horn spinal neurons, thalamic relay neurons, sensory cortex neurons, etc. ; Llinas et al, 1988;Tsien et al, 1988, Hemandez-Cruz and Pape, 1989Ryu and Randic, 1990;Sayer et al, 1990).…”

Section: Evidence For N-type Currentsmentioning

confidence: 99%

Cellular and molecular characterization of Ca2+ currents in acutely isolated, adult rat neostriatal neurons

et al. 1994

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Ca2+ currents in acutely isolated, adult rat neostriatal neurons were studied with whole-cell voltage-clamp techniques. In the vast majority of neurons (approximately 90%, n > 250), currents were exclusively of the high-voltage-activated (HVA) type. HVA currents activated near -40 mV and reached their maximum amplitude near 0 mV. Quasi-steady-state inactivation curves in many neurons were well fitted only with a sum of Boltzmann functions, suggesting that the HVA currents were heterogeneous. Although the block of whole-cell current by Cd2+ was well fitted with a single isotherm having an IC50 of near 1 microM, experiments with organic channel antagonists suggested that at least four types of HVA channels were expressed by most cells. On average, the L-channel antagonist nifedipine (5–10 microM) blocked 31 +/- 10% of the whole-cell current (n = 20), the N-channel antagonist omega- conotoxin GVIA (omega-CgTx) (2–5 microM) blocked 27 +/- 11% (n = 20), and the P-channel antagonist omega-agatoxin IVA (100–500 nM) blocked 21 +/- 10% (n = 18). In many neurons, the block by omega-CgTx was partially or completely reversible. In cells tested with a combination of these antagonists, 34 +/- 17% of the peak Ca2+ current remained unblocked (n = 13). Single-cell expression profiling of medium-sized neurons revealed the presence of rbA and rbB Ca2+ channel alpha 1 subunit mRNAs but low or undetectable levels of rbC mRNA (n = 12). These findings suggest that although adult neostriatal projection neurons do not express significant levels of LVA Ca2+ current, they do express a pharmacologically and structurally heterogeneous population of HVA currents.

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“…These models must take into account several types of voltage-gated conductances, some of them nonhomogeneously distributed on the neuronal membrane. For example, at least ten voltage-gated conductances were isolated from layer 5 (L5) pyramidal neurons (Bekkers 2000a;Berger et al 2001;Brown et al , 1994aColbert and Pan 2002;Foehring 1996;Foehring and Armstrong 1996;Foehring and Scroggs 1994;Foehring and Waters 1991;Foehring et al 2000;Korngreen and Sakmann 2000;Sayer et al 1990Sayer et al , 1993. Some of these conductances were observed to have nonhomogeneous density distributions along the apical dendrite of the neurons (Bekkers 2000b;Berger et al 2001;Korngreen and Sakmann 2000;Williams and Stuart 2000).…”

Section: Introductionmentioning

confidence: 99%

Constraining Compartmental Models Using Multiple Voltage Recordings and Genetic Algorithms

Keren

Peled²,

Korngreen³

2005

Journal of Neurophysiology

105

123

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Keren, Naomi, Noam Peled, and Alon Korngreen. Constraining compartmental models using multiple voltage recordings and genetic algorithms. J Neurophysiol 94: 3730 -3742, 2005. First published August 10, 2005; doi:10.1152/jn.00408.2005. Compartmental models with many nonlinearly and nonhomogeneous distributions of voltagegated conductances are routinely used to investigate the physiology of complex neurons. However, the number of loosely constrained parameters makes manually constructing the desired model a daunting if not impossible task. Recently, progress has been made using automated parameter search methods, such as genetic algorithms (GAs). However, these methods have been applied to somatically recorded action potentials using relatively simple target functions. Using a genetic minimization algorithm and a reduced compartmental model based on a previously published model of layer 5 neocortical pyramidal neurons we compared the efficacy of five cost functions (based on the waveform of the membrane potential, the interspike interval, trajectory density, and their combinations) to constrain the model. When the model was constrained using somatic recordings only, a combined cost function was found to be the most effective. This combined cost function was then applied to investigate the contribution of dendritic and axonal recordings to the ability of the GA to constrain the model. The more recording locations from the dendrite and the axon that were added to the data set the better was the genetic minimization algorithm able to constrain the compartmental model. Based on these simulations we propose an experimental scheme that, in combination with a genetic minimization algorithm, may be used to constrain compartmental models of neurons. I N T R O D U C T I O NThe majority of synapses in the CNS connect to dendrites. These dendrites transform information received from synapses into a code that is then translated by the axon to action potentials (APs) that are transmitted to other neurons. The properties and functions of dendrites in the CNS have been intensively studied especially over the past decade (for reviews see Johnston 1999;Johnston et al. 2003;Migliore and Shepherd 2002;Stuart et al. 1999), mainly as a result of patch-clamp recordings from visually identified dendrites in brain slices (Stuart et al. 1993) and novel imaging techniques (Antic 2003;Antic et al. 1999;Denk et al. 1994;Lasser-Ross et al. 1991; Tsien 1989). Action potentials initiated at or near the soma actively back-propagate into the dendritic tree (Bischofberger and Jonas 1997;Chen et al. 1997Chen et al. , 2002Häusser et al. 1995;Spruston et al. 1995;Stuart and Sakmann 1994). Furthermore, dendrites generate complex regenerative Ca 2ϩ and Na ϩ spikes (Amitai et al. 1993;Antic 2003;Ariav et al. 2003;Bischofberger and Jonas 1997;Johnston et al. 1996Johnston et al. , 2003Magee et al. 1996Magee et al. , 1998Martina et al. 2000;Migliore and Shepherd 2002;Schiller et al. 1997;Zhu 2000), modulate synaptic potentials (Magee 1999;Magee and Johnsto...

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High- and low-threshold calcium currents in neurons acutely isolated from rat sensorimotor cortex

Cited by 93 publications

References 18 publications

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Cellular and molecular characterization of Ca2+ currents in acutely isolated, adult rat neostriatal neurons

Constraining Compartmental Models Using Multiple Voltage Recordings and Genetic Algorithms

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