Medial geniculate lesions block amygdalar and cingulothalamic learning-related neuronal activity.

This study assessed the role of the thalamic medial geniculate (MG) nucleus in discriminative avoidance learning, wherein rabbits acquire a locomotory response to a tone [conditioned stimulus (CS)+] to avoid a foot shock, and they learn to ignore a different tone (CS-) not predictive of foot shock. Limbic (anterior and medial dorsal) thalamic, cingulate cortical, or amygdalar lesions severely impair acquisition, and neurons in these areas develop training-induced activity (TIA): more firing to the CS+ than to the CS-. MG neurons exhibit TIA during learning and project to the amygdala. The MG neurons may supply afferents essential for amygdalar and cingulothalamic TIA and for avoidance learning. To test this hypothesis, bilateral electrolytic or excitotoxic ibotenic acid MG nuclear lesions were induced, and multiunit recording electrodes were chronically implanted into the anterior and posterior cingulate cortex, the anterior-ventral and medial-dorsal thalamic nuclei, and the basolateral nucleus of the amygdala before training. Learning was severely impaired and TIA was abolished in all areas in rabbits with lesions. Thus learning and TIA require the integrity of the MG nucleus. Only damage in the medial MG division was significantly correlated with the learning deficit. The lesions abolished the sensory response of amygdalar neurons, and they attenuated (but did not eliminate) the sensory response of cingulothalamic neurons, suggesting the existence of extra geniculate sources of auditory transmission to the cingulothalamic areas.

Visual system degeneration induced by blast overpressure.

The effect of blast overpressure on visual system pathology was studied in 14 male Sprague-Dawley rats weighing 360-432 g. Blast overpressure was simulated using a compressed-air driven shock tube, with the aim of studying a range of overpressures causing sublethal injury. Neither control (unexposed) rats nor rats exposed to 83 kiloPascals (kPa) overpressure showed evidence of visual system pathology. Neurological injury to brain visual pathways was observed in male rats surviving blast overpressure exposures of 104-110 kPa and 129-173 kPa. Optic nerve fiber degeneration was ipsilateral to the blast pressure wave. The optic chiasm contained small numbers of degenerated fibers. Optic tract fiber degeneration was present bilaterally, but was predominantly ipsilateral. Optic tract fiber degeneration was followed to nuclear groups at the level of the midbrain, midbrain-diencephalic junction, and the thalamus where degenerated fibers arborized among the neurons of: (i) the superior colliculus, (ii) pretectal region, and (iii) the lateral geniculate body. The superior colliculus contained fiber degeneration localized principally to two superficial layers (i) the stratum opticum (layer III) and (ii) stratum cinereum (layer II). The pretectal area contained degenerated fibers which were widespread in (i) the nucleus of the optic tract, (ii) olivary pretectal nucleus, (iii) anterior pretectal nucleus, and (iv) the posterior pretectal nucleus. Degenerated fibers in the lateral geniculate body were not universally distributed. They appeared to arborize among neurons of the dorsal and ventral nuclei: the ventral lateral geniculate nucleus (parvocellular and magnocellular parts); and the dorsal lateral geniculate nucleus. The axonopathy observed in the central visual pathways and nuclei of the rat brain are consistent with the presence of blast overpressure induced injury to the retina. The orbital cavities of the human skull contain frontally-directed eyeballs for binocular vision. Humans looking directly into an oncoming blast wave place both eyes at risk. With bilateral visual system injury, neurological deficits may include loss or impairments of ocular movements, and of the pupillary and accommodation reflexes, retinal hemorrhages, scotomas, and general blindness. These findings suggest that the retina should be investigated for the presence of traumatic or ischemic cellular injury, hemorrhages, scotomas, and retinal detachment.

The effects of subcortical lesions on evoked potentials and spontaneous high frequency (gamma-band) oscillating potentials in rat auditory cortex.

Functional subdivisions of auditory cortex in the rat were identified based on the distribution of temporal components of the mid-latency auditory evoked potential (MAEP) recorded with a multichannel epipial electrode array. Spontaneous data collected from the same location exhibited spindle-shaped bursts of oscillations in the gamma-band (20-40 Hz) whose location and spatial distribution were similar to that of the MAEP complex in that the bursts were localized to primary and secondary auditory cortex, the principle targets of thalamocortical projections. This suggested that the neural generators of these electrophysiological events may be similar. However, ablation of the medial geniculate nucleus (MG) of the thalamus revealed that while this nucleus is required for the generation of MAEPs, it is not required for the generation of spontaneous gamma-band oscillations. Ablation of subcortical cholinergic nuclei revealed that cholinergic input via the thalamus or the basal forebrain is not necessary for the generation of either MAEPs or spontaneous gamma-band oscillations recorded in this study. These results indicated that there may be networks of cells in sensory cortical areas endowed with an intrinsic capacity to oscillate independently of sensory or cholinergic input, but that may be modulated by this input.

Involvement of subcortical and cortical afferents to the lateral nucleus of the amygdala in fear conditioning measured with fear-potentiated startle in rats trained concurrently with auditory and visual conditioned stimuli.

The goal of this work was to test the involvement, in fear conditioning, of afferents to the lateral nucleus of the amygdala originating from the auditory thalamus, auditory cortex, and perirhinal area. The acoustic startle reflex was used as the behavioral index of conditioning because it is reliably enhanced in the presence of a conditioned stimulus (CS) previously paired with a footshock. Auditory and visual CSs were used to assess the modality specificity of lesions to the above brain areas. Pre- or posttraining lesions of the entire auditory thalamus including the ventral, dorsal, and medial divisions of the medial geniculate body, the posterior intralaminar nucleus, and the suprageniculate nucleus, completely blocked fear-potentiated startle to the auditory CS, but had no effect on fear-potentiated startle to the visual CS. Posttraining lesions mostly restricted to the ventral and dorsal divisions of the medial geniculate body specifically disrupted fear-potentiated startle to the auditory CS. However, retraining in rats sustaining ventral and dorsal medial geniculate body lesions led to reliable fear-potentiated startle to the auditory CS. Posttraining lesions mostly restricted to the medial division of the medial geniculate body, posterior intralaminar, and suprageniculate nuclei did not disrupt fear-potentiated startle. These results indicate that the auditory thalamus is specifically involved, through either its direct or indirect amygdaloid afferents, in fear conditioning to auditory CSs. Pre- or posttraining lesions mostly restricted to the primary auditory cortex did not reliably attenuate fear-potentiated startle to the auditory or visual CSs. Extensive posttraining lesions of the perirhinal area (including secondary auditory cortices), but not its rostral aspect alone, blocked fear-potentiated startle to both CSs. However, reliable potentiated startle was observed to both CSs following similarly extensive pretraining lesions of the perirhinal area. Because post- but not pretraining lesions of the perirhinal area blocked fear-potentiated startle nonspecifically, at least with regard to auditory and visual CSs, the results are consistent with the involvement of the perirhinal area in general memory functions such as information storage or retrieval. Alternatively, the secondary auditory and/or perirhinal cortices might function as multimodal sensory relays to the amygdala.