Intertrial unconditioned stimuli preferentially interfere with delay conditioning.

2010 ◽  
Vol 36 (2) ◽  
pp. 232-242 ◽  
Author(s):  
Douglas A. Williams ◽  
Heather K. MacKenzie ◽  
Kenneth W. Johns
Keyword(s):  
Delay Conditioning

UCR diminution in trace and delay conditioning.

1969 ◽  
Vol 79 (2, Pt.1) ◽  
pp. 246-248 ◽  
Author(s):  
William W. Grings ◽  
Anne M. Schell
Keyword(s):  
Delay Conditioning

scholarly journals The effects of stimulus distribution form during trace conditioning

2018 ◽  
Vol 72 (2) ◽  
pp. 285-297 ◽  
Author(s):  
Charlotte Bonardi ◽  
Dómhnall J Jennings
Keyword(s):  
Associative Strength ◽  
Auditory Stimulus ◽  
Trace Conditioning ◽  
Response Rates ◽  
Second Phase ◽  
Fixed Duration ◽  
Trace Interval ◽  
Delay Conditioning ◽  
Performance Effect ◽  
Distribution Form

Three experiments examined the effect of distribution form of the trace interval on trace conditioning. In Experiments 1 and 2, two groups of rats were conditioned to a fixed-duration conditioned stimulus (CS) in a trace interval procedure; rats in Group Fix received a fixed-duration trace interval, whereas for rats in Group Var the trace interval was of variable duration. Responding during the CS was higher in Group Var than in Group Fix, whereas during the trace interval this difference in responding reversed—Group Fix showed higher response rates than Group Var. Experiment 3 examined whether the greater response rate observed during the CS in Group Var was due to a performance effect or the acquisition of greater associative strength by the CS. Following trace conditioning, the rats from Experiment 1 underwent a second phase of delay conditioning with the same CS; a 5-s auditory stimulus was presented in compound with the last 5 s of the 15-s CS, and the unconditioned stimulus (US) was delivered at the offset of the CSs. On test with the auditory stimulus alone, subjects in Group Var showed lower response rates during the auditory stimulus than subjects in Group Fix. We interpreted these findings as evidence that the superior responding in Group Var during the CS was a result of it acquiring greater associative strength than in Group Fix.

scholarly journals Effects of US intensity on heart rate in delay conditioning and pseudoconditioning

1970 ◽  
Vol 19 (1) ◽  
pp. 15-17
Author(s):  
William F. Caul ◽  
Robert E. Miller ◽  
James H. Banks
Keyword(s):  
Heart Rate ◽  
Delay Conditioning

Properties of Conditioned Abducens Nerve Responses in a Highly Reduced In Vitro Brain Stem Preparation From the Turtle

1999 ◽  
Vol 81 (3) ◽  
pp. 1242-1250 ◽  
Author(s):  
Curtis W. Anderson ◽  
Joyce Keifer
Keyword(s):  
Brain Stem ◽  
Red Nucleus ◽  
Abducens Nerve ◽  
Unconditioned Response ◽  
Stem Tissue ◽  
Delay Conditioning ◽  
Conditioned Responses ◽  
A Site ◽  
Classically Conditioned

Properties of conditioned abducens nerve responses in a highly reduced in vitro brain stem preparation from the turtle. Previous work suggested that the cerebellum and red nucleus are not necessary for the acquisition, extinction, and reacquistion of the in vitro classically conditioned abducens nerve response in the turtle. These findings are extended in the present study by obtaining conditioned responses (CRs) in preparations that received a partial ablation of the brain stem circuitry. In addition to removing all tissue rostral to and including the midbrain and cerebellum, a transection was made just caudal to the emergence of the IXth nerve. Such ablations result in a 4-mm-thick section of brain stem tissue that functionally eliminates the sustained component of the unconditioned response (UR) while leaving only a phasic component. We refer to this region of brain stem tissue caudal to the IXth nerve as the “caudal premotor blink region.” Neural discharge was recorded from the abducens nerve following a single shock unconditioned stimulus (US) applied to the ipsilateral trigeminal nerve. When the US was paired with a conditioned stimulus (CS) applied to the posterior eighth, or auditory, nerve using a delay conditioning paradigm, a positive slope of CR acquisition was recorded in the abducens nerve, and CR extinction was recorded when the stimuli were alternated. Resumption of paired stimuli resulted in reacquisition. Quantitative analysis of the CRs in preparations in which the caudal premotor blink region had been removed and those with cerebellar/red nucleus lesions showed that both types of preparations had abnormally short latency CR onsets compared with preparations in which these regions were intact. Preparations with brain stem transections had significantly earlier CR offsets as more CRs terminated as short bursts when compared with intact or cerebellar lesioned preparations. These data suggest that a highly reduced in vitro brain stem preparation from the turtle can be classically conditioned. Furthermore, the caudal brain stem is not a site of acquisition in this reduced preparation, but it contributes to the sustained activity of both the UR and CR. Finally, the unusually short CR onset latencies following lesions to the cerebellum are not further exacerbated by removal of the caudal brain stem. These studies suggest that convergence of CS and US synaptic inputs onto the abducens nerve reflex circuitry may underlie acquisition in this reduced preparation, but that mechanisms that control learned CR timing arise from the cerebellorubral system.

scholarly journals Active Inference and Learning in the Cerebellum

2016 ◽  
Vol 28 (9) ◽  
pp. 1812-1839 ◽  
Author(s):  
Karl Friston ◽  
Ivan Herreros
Keyword(s):  
Eyeblink Conditioning ◽  
Predictive Coding ◽  
Trace Conditioning ◽  
Face Validity ◽  
Active Inference ◽  
Focal Lesions ◽  
Delay Conditioning ◽  
Neuronal Populations ◽  
Intrinsic Connectivity ◽  
The Face

This letter offers a computational account of Pavlovian conditioning in the cerebellum based on active inference and predictive coding. Using eyeblink conditioning as a canonical paradigm, we formulate a minimal generative model that can account for spontaneous blinking, startle responses, and (delay or trace) conditioning. We then establish the face validity of the model using simulated responses to unconditioned and conditioned stimuli to reproduce the sorts of behavior that are observed empirically. The scheme’s anatomical validity is then addressed by associating variables in the predictive coding scheme with nuclei and neuronal populations to match the (extrinsic and intrinsic) connectivity of the cerebellar (eyeblink conditioning) system. Finally, we try to establish predictive validity by reproducing selective failures of delay conditioning, trace conditioning, and extinction using (simulated and reversible) focal lesions. Although rather metaphorical, the ensuing scheme can account for a remarkable range of anatomical and neurophysiological aspects of cerebellar circuitry—and the specificity of lesion-deficit mappings that have been established experimentally. From a computational perspective, this work shows how conditioning or learning can be formulated in terms of minimizing variational free energy (or maximizing Bayesian model evidence) using exactly the same principles that underlie predictive coding in perception.

A Stress-Induced Shift From Trace to Delay Conditioning Depends on the Mineralocorticoid Receptor

2015 ◽  
Vol 78 (12) ◽  
pp. 830-839 ◽  
Author(s):  
Susanne Vogel ◽  
Floris Klumpers ◽  
Marijn C.W. Kroes ◽  
Krista T. Oplaat ◽  
Harm J. Krugers ◽  
...  
Keyword(s):  
Mineralocorticoid Receptor ◽  
Delay Conditioning

scholarly journals Cerebellar Cortex Contributions to the Expression and Timing of Conditioned Eyelid Responses

2010 ◽  
Vol 103 (4) ◽  
pp. 2039-2049 ◽  
Author(s):  
Brian E. Kalmbach ◽  
Tobin Davis ◽  
Tatsuya Ohyama ◽  
Frank Riusech ◽  
William L. Nores ◽  
...  
Keyword(s):  
Purkinje Cells ◽  
Cerebellar Cortex ◽  
Local Anesthetic ◽  
Eyelid Conditioning ◽  
Trace Conditioning ◽  
Anterior Lobe ◽  
Short Latency ◽  
Delay Conditioning ◽  
Conditioned Responses ◽  
Primary Fissure

We used micro-infusions during eyelid conditioning in rabbits to investigate the relative contributions of cerebellar cortex and the underlying deep nuclei (DCN) to the expression of cerebellar learning. These tests were conducted using two forms of cerebellum-dependent eyelid conditioning for which the relative roles of cerebellar cortex and DCN are controversial: delay conditioning, which is largely unaffected by forebrain lesions, and trace conditioning, which involves interactions between forebrain and cerebellum. For rabbits trained with delay conditioning, silencing cerebellar cortex by micro-infusions of the local anesthetic lidocaine unmasked stereotyped short-latency responses. This was also the case after extinction as observed previously with reversible blockade of cerebellar cortex output. Conversely, increasing cerebellar cortex activity by micro-infusions of the GABAA antagonist picrotoxin reversibly abolished conditioned responses. Effective cannula placements were clustered around the primary fissure and deeper in lobules hemispheric lobule IV (HIV) and hemispheric lobule V (HV) of anterior lobe. In well-trained trace conditioned rabbits, silencing this same area of cerebellar cortex or reversibly blocking cerebellar cortex output also unmasked short-latency responses. Because Purkinje cells are the sole output of cerebellar cortex, these results provide evidence that the expression of well-timed conditioned responses requires a well-timed decrease in the activity of Purkinje cells in anterior lobe. The parallels between results from delay and trace conditioning suggest similar contributions of plasticity in cerebellar cortex and DCN in both instances.

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