Involvement of cortical and thalamic auditory regions in retention of differential bradycardiac conditioning to acoustic conditioned stimuli in rabbits

Theodore W. Jarrell, Christopher G. Gentile, Lizabeth M. Romanski, Philip McCabe, Neil Schneiderman

Research output: Contribution to journalArticle

96 Citations (Scopus)

Abstract

Our previous findings indicate that lesions in the medial division of the medial geniculate nucleus (mMGN) prevent the acquisition of differential conditioning of bradycardia to acoustic stimuli in rabbits. In the present experiment, the effect of lesions in mMGN on retention of differential bradycardiac conditioning was examined. In addition, the possible involvement of auditory cortex in differential conditioning was investigated. Electrodes were chronically implanted in mMGN, the ventral division of the medial geniculate nucleus (vMGN), or auditory cortex. After 7 days of recovery, animals received one differential Pavlovian conditioning session. At the end of the session, lesions were produced through the implanted electrodes. All animals demonstrated differential bradycardiac conditioning during the prelesion session. Animals with vMGN lesions also demonstrated differential conditioning during the postlesion session. However, mMGN and auditory cortex lesion animals failed to demonstrate differential conditioning during the postlesion session due to an increased response magnitude to the unpaired tone (CS-). These data support the hypothesis that mMGN plays a role in differential conditioning of bradycardia to tonal stimuli. In addition, these findings suggest that a possible corticothalamic pathway may be involved in the inhibition of the response to the CS-.

Original languageEnglish
Pages (from-to)285-294
Number of pages10
JournalBrain Research
Volume412
Issue number2
DOIs
StatePublished - Jun 2 1987

Fingerprint

Geniculate Bodies
Acoustics
Rabbits
Auditory Cortex
Bradycardia
Implanted Electrodes
Electrodes

Keywords

  • Auditory cortex
  • Bradycardia
  • Corticothalamic pathway
  • Differential Pavlovian conditioning
  • Medial geniculate
  • Rabbit
  • Response inhibition

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Involvement of cortical and thalamic auditory regions in retention of differential bradycardiac conditioning to acoustic conditioned stimuli in rabbits. / Jarrell, Theodore W.; Gentile, Christopher G.; Romanski, Lizabeth M.; McCabe, Philip; Schneiderman, Neil.

In: Brain Research, Vol. 412, No. 2, 02.06.1987, p. 285-294.

Research output: Contribution to journalArticle

@article{306be09b3efd4394b963a7872ab99c70,
title = "Involvement of cortical and thalamic auditory regions in retention of differential bradycardiac conditioning to acoustic conditioned stimuli in rabbits",
abstract = "Our previous findings indicate that lesions in the medial division of the medial geniculate nucleus (mMGN) prevent the acquisition of differential conditioning of bradycardia to acoustic stimuli in rabbits. In the present experiment, the effect of lesions in mMGN on retention of differential bradycardiac conditioning was examined. In addition, the possible involvement of auditory cortex in differential conditioning was investigated. Electrodes were chronically implanted in mMGN, the ventral division of the medial geniculate nucleus (vMGN), or auditory cortex. After 7 days of recovery, animals received one differential Pavlovian conditioning session. At the end of the session, lesions were produced through the implanted electrodes. All animals demonstrated differential bradycardiac conditioning during the prelesion session. Animals with vMGN lesions also demonstrated differential conditioning during the postlesion session. However, mMGN and auditory cortex lesion animals failed to demonstrate differential conditioning during the postlesion session due to an increased response magnitude to the unpaired tone (CS-). These data support the hypothesis that mMGN plays a role in differential conditioning of bradycardia to tonal stimuli. In addition, these findings suggest that a possible corticothalamic pathway may be involved in the inhibition of the response to the CS-.",
keywords = "Auditory cortex, Bradycardia, Corticothalamic pathway, Differential Pavlovian conditioning, Medial geniculate, Rabbit, Response inhibition",
author = "Jarrell, {Theodore W.} and Gentile, {Christopher G.} and Romanski, {Lizabeth M.} and Philip McCabe and Neil Schneiderman",
year = "1987",
month = "6",
day = "2",
doi = "10.1016/0006-8993(87)91135-8",
language = "English",
volume = "412",
pages = "285--294",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Involvement of cortical and thalamic auditory regions in retention of differential bradycardiac conditioning to acoustic conditioned stimuli in rabbits

AU - Jarrell, Theodore W.

AU - Gentile, Christopher G.

AU - Romanski, Lizabeth M.

AU - McCabe, Philip

AU - Schneiderman, Neil

PY - 1987/6/2

Y1 - 1987/6/2

N2 - Our previous findings indicate that lesions in the medial division of the medial geniculate nucleus (mMGN) prevent the acquisition of differential conditioning of bradycardia to acoustic stimuli in rabbits. In the present experiment, the effect of lesions in mMGN on retention of differential bradycardiac conditioning was examined. In addition, the possible involvement of auditory cortex in differential conditioning was investigated. Electrodes were chronically implanted in mMGN, the ventral division of the medial geniculate nucleus (vMGN), or auditory cortex. After 7 days of recovery, animals received one differential Pavlovian conditioning session. At the end of the session, lesions were produced through the implanted electrodes. All animals demonstrated differential bradycardiac conditioning during the prelesion session. Animals with vMGN lesions also demonstrated differential conditioning during the postlesion session. However, mMGN and auditory cortex lesion animals failed to demonstrate differential conditioning during the postlesion session due to an increased response magnitude to the unpaired tone (CS-). These data support the hypothesis that mMGN plays a role in differential conditioning of bradycardia to tonal stimuli. In addition, these findings suggest that a possible corticothalamic pathway may be involved in the inhibition of the response to the CS-.

AB - Our previous findings indicate that lesions in the medial division of the medial geniculate nucleus (mMGN) prevent the acquisition of differential conditioning of bradycardia to acoustic stimuli in rabbits. In the present experiment, the effect of lesions in mMGN on retention of differential bradycardiac conditioning was examined. In addition, the possible involvement of auditory cortex in differential conditioning was investigated. Electrodes were chronically implanted in mMGN, the ventral division of the medial geniculate nucleus (vMGN), or auditory cortex. After 7 days of recovery, animals received one differential Pavlovian conditioning session. At the end of the session, lesions were produced through the implanted electrodes. All animals demonstrated differential bradycardiac conditioning during the prelesion session. Animals with vMGN lesions also demonstrated differential conditioning during the postlesion session. However, mMGN and auditory cortex lesion animals failed to demonstrate differential conditioning during the postlesion session due to an increased response magnitude to the unpaired tone (CS-). These data support the hypothesis that mMGN plays a role in differential conditioning of bradycardia to tonal stimuli. In addition, these findings suggest that a possible corticothalamic pathway may be involved in the inhibition of the response to the CS-.

KW - Auditory cortex

KW - Bradycardia

KW - Corticothalamic pathway

KW - Differential Pavlovian conditioning

KW - Medial geniculate

KW - Rabbit

KW - Response inhibition

UR - http://www.scopus.com/inward/record.url?scp=0023187502&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023187502&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(87)91135-8

DO - 10.1016/0006-8993(87)91135-8

M3 - Article

C2 - 3607469

AN - SCOPUS:0023187502

VL - 412

SP - 285

EP - 294

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 2

ER -