Neural encoding in orbitofrontal cortex and basolateral amygdala during olfactory discrimination learning. (1/3478)

Orbitofrontal cortex (OFC) is part of a network of structures involved in adaptive behavior and decision making. Interconnections between OFC and basolateral amygdala (ABL) may be critical for encoding the motivational significance of stimuli used to guide behavior. Indeed, much research indicates that neurons in OFC and ABL fire selectively to cues based on their associative significance. In the current study recordings were made in each region within a behavioral paradigm that allowed comparison of the development of associative encoding over the course of learning. In each recording session, rats were presented with novel odors that were informative about the outcome of making a response and had to learn to withhold a response after sampling an odor that signaled a negative outcome. In some cases, reversal training was performed in the same session as the initial learning. Ninety-six of the 328 neurons recorded in OFC and 60 of the 229 neurons recorded in ABL exhibited selective activity during evaluation of the odor cues after learning had occurred. A substantial proportion of those neurons in ABL developed selective activity very early in training, and many reversed selectivity rapidly after reversal. In contrast, those neurons in OFC rarely exhibited selective activity during odor evaluation before the rats reached the criterion for learning, and far fewer reversed selectivity after reversal. The findings support a model in which ABL encodes the motivational significance of cues and OFC uses this information in the selection and execution of an appropriate behavioral strategy.  (+info)

Distinct populations of NMDA receptors at subcortical and cortical inputs to principal cells of the lateral amygdala. (2/3478)

Fear conditioning involves the transmission of sensory stimuli to the amygdala from the thalamus and cortex. These input synapses are prime candidates for sites of plasticity critical to the learning in fear conditioning. Because N-methyl-D-aspartate (NMDA)-dependent mechanisms have been implicated in fear learning, we investigated the contribution of NMDA receptors to synaptic transmission at putative cortical and thalamic inputs using visualized whole cell recording in amygdala brain slices. Whereas NMDA receptors are present at both of these pathways, differences were observed. First, the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-receptor-mediated component of the synaptic response, relative to the NMDA component, is smaller at thalamic than cortical input synapses. Second, thalamic NMDA responses are more sensitive to Mg2+. These findings suggest that there are distinct populations of NMDA receptors at cortical and thalamic inputs to the lateral amygdala. Differences such as these might underlie unique contributions of the two pathways to fear conditioning.  (+info)

Dose-related effects of single focal irradiation in the medial temporal lobe structures in rats--magnetic resonance imaging and histological study. (3/3478)

The dose-related effects of single focal irradiation on the medial temporal lobe in rats were investigated by sequential magnetic resonance imaging and histological examination. Irradiation of 200 Gy as a maximum dose using 4 mm collimators with a gamma unit created an area of necrosis consistently at the target site within 2 weeks after irradiation. Irradiation of 100 Gy caused necrosis within 10 weeks, and 75 Gy caused necrosis within one year. Irradiation of less than 50 Gy did not induce necrosis consistently, although a restricted area of necrosis was created in the medial temporal structures including the intraparenchymal portion of the optic tract. 75 Gy may be the optimum dose for creating necrosis consistently in the medial temporal lobe structures. However, careful dose planning considering both dose-time and dose-volume relationships in necrosis development is necessary to avoid injury to vulnerable neural structures such as the optic tract when applying radiosurgical techniques to treat functional brain disorders in medial temporal lobe structures such as temporal lobe epilepsy.  (+info)

A quantitative MR study of the hippocampal formation, the amygdala, and the temporal horn of the lateral ventricle in healthy subjects 40 to 90 years of age. (4/3478)

BACKGROUND AND PURPOSE: Several investigators have defined normal age-specific values for the medial temporal lobe structures in neurologically normal elderly subjects, but, to our knowledge, no one has reported those values for a large sample of healthy volunteers. The purpose of our study was to define normal age-specific values for the hippocampal formation, the amygdala, and the temporal horn of the lateral ventricle by age group, ranging from 40 to 90 years, in order to generate a guideline for the quantitative MR diagnosis and differential diagnosis for early Alzheimer disease. METHODS: MR-based volumetric measurements of the hippocampal formation, the amygdala, and the temporal horn, standardized by total intracranial volume, were obtained from oblique coronal and sagittal T1-weighted MR images in 619 healthy volunteers and two cadaveric specimens. RESULTS: Differences in standardized volumes of the hippocampal formation, the amygdala, and the temporal horn were significant among the 61- to 70-year-old, 71- to 80-year-old, and 81- to 90-year-old groups, and were not significant between the 40- to 50-year-old and 51- to 60-year-old groups. We found no significant differences in side or sex among the age groups for any of the structures. CONCLUSION: Differences in the mean value and in the 95% normal range of standardized volumes of the hippocampal formation, the amygdala, and the temporal horn correspond to differences in age among healthy subjects; therefore, age should be considered a factor in correlative research, especially in that involving patients in the early stages of Alzheimer disease.  (+info)

The human amygdala plays an important role in gaze monitoring. A PET study. (5/3478)

Social contact often initially depends on ascertaining the direction of the other person's gaze. We determined the brain areas involved in gaze monitoring by a functional neuroimaging study. Discrimination between the direction of gaze significantly activated a region in the left amygdala during eye-contact and no eye-contact tasks to the same extent. However, a region in the right amygdala was specifically activated only during the eye-contact task. Results confirm that the left amygdala plays a general role in the interpretation of eye gaze direction, and that the activity of the right amygdala of the subject increases when another individual's gaze is directed towards him. This suggests that the human amygdala plays a role in reading social signals from the face.  (+info)

Differential regulation of the expression of corticotropin-releasing factor receptor type 2 (CRF2) in hypothalamus and amygdala of the immature rat by sensory input and food intake. (6/3478)

The physiological consequences of activating corticotropin-releasing factor receptor type 2 (CRF2) are not fully understood. The neuroanatomic distribution of this CRF receptor family member is consistent with roles in mediating the actions of CRF and similar ligands on food intake control and integrative aspects of stress-related behaviors. However, CRF2 expression in the adult rat is not influenced by stress, corticosterone (CORT), or food intake. In immature rat we have demonstrated striking downregulation of CRF2mRNA in hypothalamic ventromedial nucleus (VMH) after 24 hr of maternal deprivation, a paradigm consisting of both physiological/psychological stress and food deprivation. The current study aimed to distinguish which element or elements of maternal deprivation govern CRF2mRNA expression by isolating the effects of food intake and discrete maternal sensory cues on CRF2mRNA levels in VMH and in reciprocally communicating amygdala nuclei. In maternally deprived pups, CRF2mRNA levels in VMH and basomedial (BMA) and medial (MEA) amygdala nuclei were 62, 72, and 102% of control levels, respectively. Sensory inputs of grooming and handling as well as of the pups' own suckling activity-but not food intake-fully restored CRF2mRNA expression in VMH. In contrast, all manipulations tended to increase CRF2mRNA levels in BMA of maternally deprived rats, and surrogate grooming increased CRF2mRNA expression significantly above that of nondeprived controls. CRF2mRNA expression was not influenced significantly by plasma adrenocorticotropic hormone (ACTH) and CORT levels. Thus, in the immature rat, (1) CRF2 expression is regulated differentially in hypothalamic and amygdala regions, and (2) CRF2mRNA levels in VMH are governed primarily by maternal or suckling-derived sensory input rather than food intake or peripheral stress hormones. These findings indicate a region-specific regulation of CRF2mRNA, supporting the participation of the receptor in neurochemically defined circuits integrating sensory cues to influence specific behavioral and visceral functions.  (+info)

Differential regulation of glucocorticoid receptor messenger RNA (GR-mRNA) by maternal deprivation in immature rat hypothalamus and limbic regions. (7/3478)

Maternal deprivation (MDep) of neonatal rats significantly influences the hypothalamic-pituitary-adrenal (HPA) axis. This study hypothesized that GR-mRNA modulation constituted an early, critical mechanism for the acute effects of MDep on neuroendocrine stress-responses. GR-mRNA hybridization signal in hippocampal CA1, hypothalamic paraventricular nucleus (PVN) and frontal cortex was significantly reduced immediately following 24 h MDep. In amygdala, cingulate cortex, PVN and CA1, apparent gender-dependent MDep effects on GR-mRNA expression were observed, without significant differences in absolute levels. Thus, rapid, region-specific MDep effects on GR-mRNA expression in HPA-regulating areas are shown, consistent with involvement of GR-expression in mechanisms of MDep influence on HPA tone.  (+info)

Differential effects of metabotropic glutamate receptor antagonists on bursting activity in the amygdala. (8/3478)

Differential effects of metabotropic glutamate receptor antagonists on bursting activity in the amygdala. Metabotropic glutamate receptors (mGluRs) are implicated in both the activation and inhibition of epileptiform bursting activity in seizure models. We examined the role of mGluR agonists and antagonists on bursting in vitro with whole cell recordings from neurons in the basolateral amygdala (BLA) of amygdala-kindled rats. The broad-spectrum mGluR agonist 1S,3R-1-aminocyclopentane dicarboxylate (1S,3R-ACPD, 100 microM) and the group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG, 20 microM) evoked bursting in BLA neurons from amygdala-kindled rats but not in control neurons. Neither the group II agonist (2S,3S,4S)-alpha-(carboxycyclopropyl)-glycine (L-CCG-I, 10 microM) nor the group III agonist L-2-amino-4-phosphonobutyrate (L-AP4, 100 microM) evoked bursting. The agonist-induced bursting was inhibited by the mGluR1 antagonists (+)-alpha-methyl-4-carboxyphenylglycine [(+)-MCPG, 500 microM] and (S)-4-carboxy-3-hydroxyphenylglycine [(S)-4C3HPG, 300 microM]. Kindling enhanced synaptic strength from the lateral amygdala (LA) to the BLA, resulting in synaptically driven bursts at low stimulus intensity. Bursting was abolished by (S)-4C3HPG. Further increasing stimulus intensity in the presence of (S)-4C3HPG (300 microM) evoked action potential firing similar to control neurons but did not induce epileptiform bursting. In kindled rats, the same threshold stimulation that evoked epileptiform bursting in the absence of drugs elicited excitatory postsynaptic potentials in (S)-4C3HPG. In contrast (+)-MCPG had no effect on afferent-evoked bursting in kindled neurons. Because (+)-MCPG is a mGluR2 antagonist, whereas (S)-4C3HPG is a mGluR2 agonist, the different effects of these compounds suggest that mGluR2 activation decreases excitability. Together these data suggest that group I mGluRs may facilitate and group II mGluRs may attenuate epileptiform bursting observed in kindled rats. The mixed agonist-antagonist (S)-4C3HPG restored synaptic transmission to control levels at the LA-BLA synapse in kindled animals. The different actions of (S)-4C3HPG and (+)-MCPG on LA-evoked bursting suggests that the mGluR1 antagonist-mGluR2 agonist properties may be the distinctive pharmacology necessary for future anticonvulsant compounds.  (+info)

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