Changes in membrane currents during Pavlovian conditioning of single cortical neurons

Woody, Charles D.; Gruen, Ehud; Birt, Dorwin

doi:10.1016/0006-8993(91)90688-r

Cited by 66 publications

(31 citation statements)

References 43 publications

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“…An increase in postsynaptic neuronal excitability has been advocated as a possible mechanism of plasticity, for instance in some forms of motor learning (Woody et al, 1991). In the present study, MT of the target biceps muscle was not significantly altered by any of the interventions.…”

Section: Mechanisms and Modulation Of Deafferentation-induced Plasticitysupporting

confidence: 51%

Modulation of Plasticity in Human Motor Cortex after Forearm Ischemic Nerve Block

1998

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Deafferentation leads to cortical reorganization that may be functionally beneficial or maladaptive. Therefore, we were interested in learning whether it is possible to purposely modulate deafferentation-induced reorganization. Transient forearm deafferentation was induced by ischemic nerve block (INB) in healthy volunteers. The following five interventions were tested: INB alone; INB plus low-frequency (0.1 Hz) repetitive transcranial magnetic stimulation of the motor cortex ipsilateral to INB (INBϩrTMS i ); rTMS i alone; INB plus rTMS of the motor cortex contralateral to INB (INBϩrTMS c ); and rTMS c alone. Plastic changes in the motor cortex contralateral to deafferentation were probed with TMS, measuring motor threshold (MT), motor evoked-potential (MEP) size, and intracortical inhibition (ICI) and facilitation (ICF) to the biceps brachii muscle proximal to the level of deafferentation. INB alone induced a moderate increase in MEP size, which was significantly enhanced by INBϩrTMS c but blocked by INBϩrTMS i . INB alone had no effect on ICI or ICF, whereas INBϩrTMS c reduced ICI and increased ICF, and conversely, INBϩrTMS i deepened ICI and suppressed ICF. rTMS i and rTMS c alone were ineffective in changing any of these parameters. These findings indicate that the deafferented motor cortex becomes modifiable by inputs that are normally subthreshold for inducing changes in excitability. The deafferentation-induced plastic changes can be up-regulated by direct stimulation of the "plastic" cortex and likely via inhibitory projections down-regulated by stimulation of the opposite cortex. This modulation of cortical plasticity by noninvasive means might be used to facilitate plasticity when it is primarily beneficial or to suppress it when it is predominately maladaptive.

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Section: Mechanisms and Modulation Of Deafferentation-induced Plasticitysupporting

confidence: 51%

Modulation of Plasticity in Human Motor Cortex after Forearm Ischemic Nerve Block

1998

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“…Such changes have been observed in both vertebrate (Disterhoft et al, 1986(Disterhoft et al, , 1988aLoTurco et al, 1988;Coulter et al, 1989;deJonge et al, 1990;Woody et al, 1991;Moyer et al, 1993Moyer et al, , 1994bPower et al, 1995;Thompson et al, 1996b) and invertebrate Kandel, 1978, 1980;Hawkins et al, 1983;Alkon, 1984;Crow, 1985a,b;Carew and Sahley, 1986;Scholz and Byrne, 1987;Hawkins et al, 1993) preparations. The convergence between observed reductions in calcium-activated potassium conductances across such diverse organisms as Hermissenda (Alkon, 1984) and rabbits (Disterhoft et al, 1986) illustrates the significance of these changes as conserved mechanisms of learning-related plasticity at the cellular level across phylogeny.…”

Section: Discussionmentioning

confidence: 91%

“…We deemed this to be a scientifically acceptable procedure for several reasons. First, previous blind studies conducted in our laboratory (Disterhoft et al, 1986(Disterhoft et al, , 1988bdeJonge et al, 1990) and other laboratories (LoTurco et al, 1988;Coulter et al, 1989;Sanchez-Andres and Alkon, 1991;Woody et al, 1991) have observed conditioning-specific changes in postsynaptic properties of hippocampal or cortical neurons. That is, a substantial amount of data exists supporting the basic phenomenon of postsynaptic excitability changes in cortical neurons after eyeblink conditioning.…”

Section: Methodsmentioning

confidence: 94%

Trace Eyeblink Conditioning Increases CA1 Excitability in a Transient and Learning-Specific Manner

Thompson²,

1996

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Time-dependent, learning-related changes in hippocampal excitability were evaluated by recording from rabbit CA1 pyramidal neurons in slices prepared at various times after acquisition of trace eyeblink conditioning. Increased excitability (reduced postburst afterhyperpolarizations and reduced spike-frequency adaptation) was seen as early as 1 hr after acquisition to behavioral criterion, was maximal in neurons studied 24 hr later, and returned to baseline within 7 d, whereas behavioral performance remained asymptotic for months. Neurons were held at Ϫ67 mV to equate voltage-dependent effects. No learningrelated effects were observed on input resistance, actionpotential amplitude or duration, or resting membrane potential. The excitability changes were learning-specific, because they were not seen in neurons from very slow learning (exhibited Ͻ30% conditioned responses after 15 training sessions) or from pseudoconditioned control rabbits. Neurons from rabbits that displayed asymptotic behavioral performance after longterm retention testing (an additional training session 14 d after learning) were also indistinguishable from control neurons. Thus, the increased excitability of CA1 neurons was not performance-or memory-dependent. Rather, the time course of increased excitability may represent a critical window during which learning-specific alterations in postsynaptic excitability of hippocampal neurons are important for consolidation of the learned association elsewhere in the brain.

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“…97 The mechanisms underlying these effects are incompletely understood, but they could include modulation of LTP-or LTD-like processes, 98 as well as nonspecific changes such as generalized postsynaptic excitability enhancements. 99 These well documented effects of noninvasive brain stimulation in healthy subjects support possible application in stroke patients.…”

Section: Noninvasive Brain Stimulationmentioning

confidence: 88%

Noninvasive brain stimulation in stroke rehabilitation

Webster

Celnik

Cohen

2006

NeuroRX

145

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Summary:Stroke is a common disorder that produces a major burden to society, largely through long-lasting motor disability in survivors. Recent studies have broadened our understanding of the processes underlying recovery of motor function after stroke. Bilateral motor regions of the brain experience substantial reorganization after stroke, including changes in the strength of interhemispheric inhibitory interactions. Our understanding of the extent to which different forms of reorganization contribute to behavioral gains in the rehabilitative process, although still limited, has led to the formulation of novel interventional strategies to regain motor function. Transcranial magnetic (TMS) and DC (tDCS) electrical stimulation are noninvasive brain stimulation techniques that modulate cortical excitability in both healthy individuals and stroke patients. These techniques can enhance the effect of training on performance of various motor tasks, including those that mimic activities of daily living. This review looks at the effects of TMS and tDCS on motor cortical function and motor performance in healthy volunteers and in patients with stroke. Both techniques can either enhance or suppress cortical excitability, and may move to the clinical arena as strategies to enhance the beneficial effects of customarily used neurorehabilitative treatments after stroke.

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Changes in membrane currents during Pavlovian conditioning of single cortical neurons

Cited by 66 publications

References 43 publications

Modulation of Plasticity in Human Motor Cortex after Forearm Ischemic Nerve Block

Modulation of Plasticity in Human Motor Cortex after Forearm Ischemic Nerve Block

Trace Eyeblink Conditioning Increases CA1 Excitability in a Transient and Learning-Specific Manner

Noninvasive brain stimulation in stroke rehabilitation

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