Character of evoked responses of the dorsomedial thalamic nucleus to stimulation of the periamygdalar cortex and area amygdaloidea anterior in rats

Sidorov, B. M.; Podachin, V. P.

doi:10.1007/bf01060193

Cited by 1 publication

(3 citation statements)

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“…Due to the absence of interneurones in the rodent MD ( Kuroda et al., 1998 ) and VB ( Ralston, 1983; Barbaresi et al., 1986; Harris and Hendrickson, 1987; Ohara and Lieberman, 1993 ), all recordings can be presumed to be from thalamocortical neurones. Both quiescent (68%) and spontaneously active (32%) MD neurones were recorded from, which is consistent with MD neurone population activity previously reported ( Fernandez de Molina and Ispizua, 1972; Sidorov and Podachin, 1982 ). The magnitude of evoked responses (in terms of evoked action potentials) in the MD upon stimulation of the PFC was, on average, much greater than that evoked upon stimulation of the amygdala.…”

Section: Resultssupporting

confidence: 89%

“…Single short-latency (6–50 ms) spikes were evoked in the MD upon stimulation of both the PFC and amygdala, with long latency (300–200 ms) bursts also evoked in the MD upon stimulation of the PFC only: response parameters consistent with those previously observed. The distribution of the evoked response latencies into these two broad ranges is similar to the previously reported MD population activity ( Fernandez de Molina and Ispizua, 1972; Sidorov and Podachin, 1982 ). In the VB, recordings were made from quiescent neurones in which long-latency (300–400 ms) bursts comprising 2–6 spikes were evoked upon vibrissal deflection.…”

Section: Resultssupporting

confidence: 86%

“…Both types of electrode were advanced into their appropriate stereotaxic location using micromanipulators (PFC: AP +9.5 mm from lambda; ML 0.8 mm; amygdala AP +1.7 mm from lambda; ML 3.7 mm at a 21° angle) ( Paxinos and Watson, 1998 ). Using such an approach it is possible to use electrical stimulation of the PFC and amygdala to evoke either excitatory or inhibitory responses, as described previously ( Fernandez de Molina and Ispizua, 1972; Sidorov and Podachin, 1982 ). Recordings were made from both quiescent and spontaneously firing neurones, with the experimental protocol performed adjusted accordingly.…”

Section: Methodsmentioning

confidence: 99%

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Neuronal activity patterns in the mediodorsal thalamus and related cognitive circuits are modulated by metabotropic glutamate receptors

Copeland

Neale²,

Salt

2015

Neuropharmacology

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The mediodorsal thalamus (MD) likely plays an important role in cognition as it receives abundant afferent connections from the amygdala and prefrontal cortex (PFC). Indeed, disturbed activity within the MD is thought to precipitate cognitive deficits associated with schizophrenia. As compounds acting at the Group II metabotropic glutamate (mGlu) receptors (subtypes mGlu2/mGlu3) have efficacy in animal models of schizophrenia, we investigated whether a Group II agonist and an mGlu2 positive allosteric modulator (PAM) could modulate MD activity. Extracellular single-unit recordings were made in vivo from MD neurones in anaesthetised rats. Responses were elicited by electrical stimulation of the PFC and/or amygdala, with Group II compounds locally applied as required. The Group II agonist reduced inhibition evoked in the MD: an effect manifested as an increase in short-latency responses, and a decrease in long-latency burst-firing. This disinhibitory action of the Group II receptors in the MD represents a mechanism of potential therapeutic importance as increased inhibition in the MD has been associated with cognitive deficit-onset. Furthermore, as co-application of the mGlu2 PAM did not potentiate the Group II agonist effects in the MD, we suggest that the Group II disinhibitory effect is majority-mediated via mGlu3. This heterogeneity in Group II receptor thalamic physiology bears consequence, as compounds active exclusively at the mGlu2 subtype are unlikely to perturb maladapted MD firing patterns associated with cognitive deficits, with activity at mGlu3 receptors possibly more appropriate. Indeed, polymorphisms in the mGlu3, but not the mGlu2, gene have been detected in patients with schizophrenia.

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Section: Resultssupporting

confidence: 89%

Section: Resultssupporting

confidence: 86%

Section: Methodsmentioning

confidence: 99%

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