The effects of Ca2+, Mg2+ and kynurenate on primary afferent synaptic potentials evoked in cat spinal cord neurones in vivo.

Walmsley, Bruce; Nicol, MJ

doi:10.1113/jphysiol.1991.sp018434

Cited by 18 publications

(7 citation statements)

References 25 publications

(32 reference statements)

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“…1979;Luscher, 1990), with some secondaries showing a near 70 % increase in connectivity (Luscher, 1990). It is becoming increasingly evident that, even at synapses where the incidence of failures is low enough to allow the connection to be revealed by averaging, transmission onto motoneurones can still be further augmented by procedures such as changing the firing frequency of the presynaptic neurone (Collins, Honig & Mendell, 1984;Koerber & Mendell, 1991), or in the case of dorsal-spinocerebellar tract neurones, perfusing the central canal with a calcium rich perfusate (Walmsley & Nicol, 1991). Thus, connectivity is perhaps best estimated from a knowledge of both the number of boutons given off by a presynaptic neurone onto individual target neurones, and the total number of boutons given off to the population of neurones of interest.…”

Section: Discussionmentioning

confidence: 99%

Monosynaptic EPSPs elicited by single interneurones and spindle afferents in trigeminal motoneurones of anaesthetized rats.

Grimwood

Appenteng

Curtis

1992

The Journal of Physiology

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Section: Discussionmentioning

confidence: 99%

Monosynaptic EPSPs elicited by single interneurones and spindle afferents in trigeminal motoneurones of anaesthetized rats.

Grimwood

Appenteng

Curtis

1992

The Journal of Physiology

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“…Spontaneous spike activity of DSCT neurons could arise from a number of sources, including primary afferent, intrasegmental, and supraspinal sources, and could be mediated by a variety of neurotransmitters (Myslinski and Randic, 1977;Pioro et al, 1984;Maxwell et al, 1990;McGonigle et al, 1996;Jankowska et al, 1997). Anatomical and electropharmacological evidence exists that the neurotransmitter released specifically from group I muscle afferents to Clarke's column DSCT neurons is an excitatory amino acid, such as GLU (Maxwell et al, 1990;Walmsley and Nicol, 1991).…”

Section: Excitatory Amino Acid-evoked Activitymentioning

confidence: 99%

State-Related Inhibition by GABA and Glycine of Transmission in Clarke's Column

2002

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During the state of active sleep (AS), Clarke's column dorsal spinocerebellar tract (DSCT) neurons undergo a marked reduction in their spontaneous and excitatory amino acid (EAA)-evoked responses. The present study was performed to examine the magnitude, consistency of AS-specific suppression, and potential role of classical inhibitory amino acids GABA and glycine (GLY) in mediating this phenomenon. AS-specific suppression of DSCT neurons, expressed as the reduction in mean spontaneous firing rate during AS versus the preceding episode of wakefulness, was compared across three consecutive sleep cycles (SC), each consisting of wakefulness (W), AS, and awakening from AS (RW). Spontaneous spike rate did not differ during W or RW between SC1, SC2, and SC3. AS-specific suppression of spontaneous firing rate was found to be consistent and measured 40.3, 31.5, and 41.6% in SC1, SC2, and SC3, respectively, indicating that such inhibition is marked and stable for pharmacological analyses. Microiontophoretic experiments were performed in which the magnitude of AS-specific suppression of spontaneous spike activity was measured over three consecutive SCs: SC1-control (no drug), SC2-test (drug), and SC3-recovery (no drug). The magnitude of AS-specific suppression during SC2-test measured only 11.7 or 14.6% in the presence of GABA(A) antagonist bicuculline (BIC) or GLY antagonist strychnine (STY), respectively. Coadministration of BIC and STY abolished AS-specific suppression. AS-specific suppression of EAA-evoked DSCT spike activity was also abolished in SC2-test after BIC or STY, respectively. We conclude that GABA and GLY mediate behavioral state-specific inhibition of ascending sensory transmission via Clarke's column DSCT neurons.

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“…Previous evidence suggests that also primary afferent fibres terminating in the spinal grey matter deep to the dorsal horn use glutamate as a neurotransmitter (Jahr and Yoshioka, 1986;Maxwell et a / . , 1990b;Walmsley and Nicol, 1991).…”

Section: Glutamate As a Putative Primary Afferent Neurotransmittermentioning

confidence: 99%

Enrichment of Glutamate‐like Immunoreactivity in Primary Afferent Terminals Throughout the Spinal Cord Dorsal Horn

Broman

Anderson

Ottersen

1993

Eur J of Neuroscience

106

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Although several lines of evidence indicate that glutamate is a neurotransmitter in primary afferent terminals, controversies exist on the proportion and types of such terminals that release glutamate. In the present study quantitative analysis of immunogold labelling was used to assess the presence of glutamate-like immunoreactivity in primary afferent terminals in laminae I-V of the rat spinal cord dorsal horn. Anterograde transport of choleragenoid-horseradish peroxidase from a spinal ganglion and tetramethyl benzidine histochemistry were used to identify primary afferent terminals in laminae I and III-V. Presumed C-fibre terminals in lamina II were identified on morphological criteria (dense sinusoid axon terminals). Primary afferent terminals in all dorsal horn laminae displayed significantly higher levels of glutamate-like immunoreactivity than pleomorphic vesicle-containing profiles in laminae III-IV and large neuronal cell bodies in laminae III-V. The density of gold particles over primary afferent terminals also significantly exceeded the average density of gold particles over laminae II and III-IV. The highest densities of gold particles were present over dense sinusoid axon terminals in lamina II. These findings suggest that glutamate, alone or in combination with other neuroactive compounds, is involved in the transfer of all sensory modalities from primary afferent fibres to dorsal horn neurons.

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The effects of Ca2+, Mg2+ and kynurenate on primary afferent synaptic potentials evoked in cat spinal cord neurones in vivo.

Cited by 18 publications

References 25 publications

Monosynaptic EPSPs elicited by single interneurones and spindle afferents in trigeminal motoneurones of anaesthetized rats.

Monosynaptic EPSPs elicited by single interneurones and spindle afferents in trigeminal motoneurones of anaesthetized rats.

State-Related Inhibition by GABA and Glycine of Transmission in Clarke's Column

Enrichment of Glutamate‐like Immunoreactivity in Primary Afferent Terminals Throughout the Spinal Cord Dorsal Horn

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