Biomedical subjects

Andrew Talk

Publications and source records attributed to Andrew Talk.

3 recordsLinked to original sources

PubMed2005

Cingulate cortical coding of context-dependent latent inhibition.

Neuronal activity of the auditory thalamus, amygdala, cingulate cortex, and substantia nigra was recorded during the administration of a behavioral test for latent inhibition (LI) or the retardation of behavioral conditioning because of preexposure of the conditional stimulus (CS). Following CS preexposure, both the preexposed CS and a control CS predicted avoidable footshock. LI occurred as significantly fewer avoidance conditioned avoidance responses after the preexposed CS than after the control CS. Attenuation of neuronal responses to the preexposed CS, or neural LI, occurred in all monitored areas. One group of subjects (Oryctolagus cuniculus) then received context extinction, and additional groups experienced novel context exposure or handling. Context extinction enhanced behavioral responding to the preexposed CS, eliminating LI. Context extinction also eliminated cingulate cortical neural LI by enhancing posterior cingulate cortical responses to the preexposed CS and attenuating anterior cingulate cortical responses to the control CS. Present and past results are interpreted to indicate that LI is (a) a failure of response retrieval and/or expression mediated by interfering CS-context associations and (b) a product of interactions of the posterior cingulate cortex and the hippocampus.

Acoustic Stimulation↗

PubMed2004

Independent generation of theta rhythm in the hippocampus and posterior cingulate cortex.

Theta rhythmicity of field potentials recorded in the posterior cingulate cortex is thought to have a septo-hippocampal origin, principally because phase reversal of this theta occurs in the dorsal hippocampus, but not in the posterior cingulate cortex. In the current study, theta activity of cue-elicited field potentials and multiple unit activity in posterior cingulate cortical areas 29b and 29c/d, and in the associated anterior ventral (AV) thalamic nucleus, was monitored while rabbits underwent discriminative avoidance conditioning. Theta activity in the field potentials occurred during training in areas 29b and 29c/d, and was severely attenuated by electrolytic lesions in the dorsal hippocampus. Significant theta rhythmicity was not evident in multiple unit activity recorded from area 29c/d, either in lesioned or sham-operated subjects. However, theta-like modulation was evident in the multiple unit activity of area 29b, and in the AV thalamic nucleus, occurring in synchrony with the field potential oscillations. Theta rhythmicity of unit activity in these areas was unaffected by dorsal hippocampal lesions. These results suggest that theta-frequency oscillations apparent in posterior cingulate cortical field potentials are volume-conducted from the dorsal hippocampus, but that theta-like unit activity in posterior cingulate cortical area 29b and in the AV thalamic nucleus occurs independently of hippocampal theta.

Analysis of Variance↗

PubMed2004

Effects of conditioning during amygdalar inactivation on training-induced neuronal plasticity in the medial geniculate nucleus and cingulate cortex in rabbits (Oryctolagus cuniculus).

This study addressed the amygdala's role in avoidance conditioning in rabbits (Oryctolagus cuniculus). Intra-amygdalar muscimol infusion before 60 or 120 conditioning trials blocked training-induced neuronal activity (TIA) in the medial geniculate (MG) nucleus. One hundred twenty trials with muscimol blocked TIA permanently, during conditioning with muscimol and then later without muscimol; 60 trials with muscimol blocked TIA only when muscimol was present. Cingulate cortical TIA was blocked only when muscimol was present. Behavioral learning did not occur with muscimol, but later learning was facilitated (i.e., savings occurred) in rabbits initially given muscimol plus training. These results define the time period wherein amygdalar processes initiate TIA in the MG nucleus and suggest that distinct forms of amygdalar processes induce TIA in the MG nucleus and cingulate cortex.

Action Potentials↗