Effect of tetanus toxin on the excitatory and the inhibitory post‐synaptic potentials in the cat motoneurone.

Kanda, Kenro; Takano, K.

doi:10.1113/jphysiol.1983.sp014536

Cited by 37 publications

(15 citation statements)

References 36 publications

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“…Release of GABA recovered with seizure remission. Tetanus toxin may affect other transmitter systems, however, at least at the higher doses used in acute studies (Duchen and Tonge, 1973;Albus and Habermann, 1983;Kanda and Takano, 1983;Bevan and Wendon, 1984;Penner et al, 1986). The specificity of the low dose of toxin used in the chronic model remains to be tested, but electro-physiologic recordings clearly show that excitatory synaptic transmission remains effective in vitro in hippocampal slices from such animals (Jefferys, 1989).…”

Section: Discussionmentioning

confidence: 99%

Lack of Change in Neurochemical Markers During the Postepileptic Phase of Intrahippocampal Tetanus Toxin Syndrome in Rats

et al. 1990

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The chronic epileptic syndrome induced by injecting tetanus toxin into rat hippocampus causes functional changes that essentially are permanent, outlasting the period of active seizures by at least 1 year. These long-term changes have been characterized by an impaired performance on a range of behavioral tasks, which in turn have been associated with a physiologic depression of hippocampal evoked responses but not with any discernible histopathology. In the present study, we examined the hippocampi of rats in the postseizure phase of the tetanus toxin model and observed no significant changes in the concentration of neurochemical markers for six neurotransmitters. Therefore, the long-term reduction in hippocampal excitability cannot be attributed to any major loss of afferents or hippocampal neurons using aspartate, acetylcholine, gamma-aminobutyric acid (GABA), glutamate, norepinephrine (NE), or serotonin as their transmitters.

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Section: Discussionmentioning

confidence: 99%

Lack of Change in Neurochemical Markers During the Postepileptic Phase of Intrahippocampal Tetanus Toxin Syndrome in Rats

et al. 1990

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“…Certainly the toxin can block synaptic transmission peripherally for several weeks and it has been shown at the skeletal neuromuscular junction that recovery of synaptic function depends on the growth of new terminals rather than the repair of old ones (Duchen, 1973;Duchen & Tonge, 1973). In the central nervous system, the direct effect of the toxin appears to be generally excitatory, through a presynaptic block ofinhibitory transmission (see Mellanby & Green, 1980 Collingridge, Thompson, Davies & Mellanby, 1981;Wellhoner, 1982), although it can also block synaptic excitation (Kanda & Takano, 1983). Even if the block of inhibition were sufficiently long-lasting it would be in the wrong sense to account directly for the depression of CA3 excitability reported here.…”

Section: Discussionmentioning

confidence: 99%

Long‐term changes in hippocampal physiology and learning ability of rats after intrahippocampal tetanus toxin.

Brace¹,

Jefferys²,

Mellanby³

1985

The Journal of Physiology

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SUMMARY1. A chronic epileptic syndrome can be induced by injecting minute doses of tetanus toxin into rat hippocampi. This causes intermittent epileptic fits over a period of 2-4 weeks, after which the fits cease, and the electroencephalogram (e.e.g.) appears to return to normal over the following 2-3 weeks. However, once they have recovered from the seizures, the rats exhibit a remarkably persistent impairment of learning and memory, which is the subject of the present study.2. Learning ability was assessed using a radial arm maze task, in which the rats had to visit each of eight arms for a food reward. The toxin-injected rats learnt this task more slowly than control-injected.3. Evoked potentials from the CA3 pyramidal cells were recorded in terminal experiments under halothane anaesthesia. Long term potentiation ofthe post-synaptic response to the commissural pathway from the contralateral hippocampus appeared to be unaffected by the previous toxin treatment, at least over periods of up to 5 h.4. The toxin-injected group differed from the control in having consistently smaller post-synaptic population spikes in their evoked responses, so that stimuli were less effective in exciting the post-synaptic neurones. This applied both to the contralateral commissural input, and to the ipsilateral mossy fibre input.5. No differences were found between the toxin and control groups in the size of the antidromic population spike in the commissural response, or in the population excitatory post-synaptic potential (e.p.s.p.) for either input. Thus the depressed output from CA3 pyramidal cells cannot be explained either by a loss of these neurones (confirming earlier neuropathological observations), or by a loss ofexcitatory afferents.6. While its precise cause remains unknown, the depressed output from the CA3 region was statistically correlated with the learning impairment, and we believe provides a reasonable explanation of this behavioural deficit.

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“…Our results indicate that synaptic input plays a key role in determining a pattern of recruitment since the high dose led to a recruitment pattern that shifts and expands in range with respect to control. TeNT not only blocks synaptic inhibition, but also excitation, as shown both in vivo (Curtis et al 1976;Kanda and Takano 1983) and in vitro (Gobbi et al 1993). …”

Section: Synaptic Organization As Factor That Influences Recruitmentmentioning

confidence: 94%

“…In summary, we conclude that a recruitment order based solely in size-related factors does not produce a rule to rank motoneurons as a function of neuronal sensitivity. The use of TeNT does not modify this view since it has been shown that TeNT does not alter the excitability of either spinal (Kanda and Takano 1983;Wiegand and Wellhöner 1979), cranial motoneurons in vivo (González-Forero et al 2002a), or cultured neurons (Dimpfel 1979).…”

Section: Intrinsic Correlates To Recruitment Ordermentioning

confidence: 99%

Recruitment Order of Cat Abducens Motoneurons and Internuclear Neurons

Pastor

González-Forero

2003

Journal of Neurophysiology

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Abducens neurons undergo a dose-dependent synaptic blockade (either disinhibition or complete blockade) when tetanus neurotoxin (TeNT) is injected into the lateral rectus muscle at either a low (0.5) or a high dose (5 ng/kg). We studied the firing pattern and recruitment order in abducens neurons both in control and after TeNT injection. The eye position threshold for recruitment of control abducens neurons was exponentially related to the eye position and velocity sensitivities. We also found a constancy of recruitment threshold for different eye movement modalities (spontaneous, optokinetic, and vestibular). Exponential relationships were found, as well, for eye velocity sensitivity during saccades and for position and velocity sensitivities during the vestibulo-ocular reflex. Likewise, inverse relationships were found between recruitment threshold or position sensitivity with the antidromic latency in control abducens neurons. These relationships, however, did not apply following TeNT treatment. Neuronal firing after TeNT appeared either disinhibited (low dose) or depressed (high dose), but the relationships between neuronal sensitivities and recruitment still applied. However, the pattern of recruitment shifted toward the treated side as more inputs were blocked by the low-and high-dose treatments, respectively. Nonetheless, although the recruitment-to-sensitivity relationships persisted under the TeNT synaptic blockade, we conclude that synaptic inputs are determinant for establishing the recruitment threshold and recruitment spacing of abducens motoneurons and internuclear neurons.

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Effect of tetanus toxin on the excitatory and the inhibitory post‐synaptic potentials in the cat motoneurone.

Cited by 37 publications

References 36 publications

Lack of Change in Neurochemical Markers During the Postepileptic Phase of Intrahippocampal Tetanus Toxin Syndrome in Rats

Lack of Change in Neurochemical Markers During the Postepileptic Phase of Intrahippocampal Tetanus Toxin Syndrome in Rats

Long‐term changes in hippocampal physiology and learning ability of rats after intrahippocampal tetanus toxin.

Recruitment Order of Cat Abducens Motoneurons and Internuclear Neurons

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