Brain research
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To determine if classical conditioning produces general or specific modification of responses to acoustic conditioned stimuli (CS), frequency receptive fields (RF) of neurons in guinea pig auditory cortex were determined before and up to 24 h after fear conditioning. Highly specific RF plasticity characterized by maximal increased responses to the CS frequency and decreased responses to the pretraining best frequency (BF) and other frequencies was observed in 70% of conditioning cases. ⋯ Sensitization training produced general increased responses across the RF without CS specificity. The findings indicate that associative processes produce systematic modification of the auditory system's processing of frequency information and exemplify the advantages of combining receptive field analysis with behavioral training in the study of the neural bases of learning and memory.
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Retrograde tracing and immunocytochemistry were used to examine the axon collateralization of brainstem serotonin (5-HT) and norepinephrine (NE) cells to the periaqueductal gray (PAG) and spinal cord. Tyrosine hydroxylase (TH)-immunofluorescent neurons which collateralize to the PAG and the cervical spinal cord were found in all brainstem catecholamine cell groups previously shown to contain neurons which project to the spinal cord, including the A5 and A7 cell groups, locus coeruleus, subcoeruleus and the C1 cell group. Many TH-immunofluorescent cells which project to the PAG but not to the spinal cord were also found. ⋯ Finally, a population of neurons in the NRM and adjacent reticular formation and in the region of several pontomedullary catecholamine cell groups collateralized to the PAG and spinal cord, but were neither 5-HT nor TH-immunofluorescent. Taken together, these findings raise the possibility that the noradrenergic contribution to the spinal antinociceptive effects produced by PAG electrical stimulation results, in part, from antidromic activation of brainstem noradrenergic neurons that have axon collaterals projecting to the PAG and spinal cord. In contrast, the 5-HT contribution to the spinal antinociceptive effects produced by PAG electrical stimulation is more likely to derive, as previously proposed, from orthodromic activation of raphe-spinal serotonergic axons.
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Prolonged neurological dysfunction that results from an insult to the brain is often attributed to irreversible structural damage such as loss of neurons or axonal degeneration. For example, following cerebral ischemia even partial hippocampal CA1 neuronal loss has been proposed to be sufficient to result in deficits in hippocampal dependent spatial memory. This study examined if hippocampal CA1 neuronal loss and/or axonal injury was necessary to produce prolonged spatial memory deficits resulting from traumatic brain injury (TBI). ⋯ M. = +/- 69) per 10(6) micron2, respectively. Additionally, no overt evidence of axonal injury was observed in any forebrain structure including major intrinsic or extrinsic connecting hippocampal pathways. These data strongly suggest that mild to moderate TBI is capable of producing prolonged spatial memory deficits in the rat without evidence of either neuronal cell death in the intrinsic hippocampus or overt axonal injury in hippocampal pathways.
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As well as substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) have recently been found in the superficial dorsal horn of the spinal cord; NKA originating mainly in fine primary afferents. We have investigated the effects of these tachykinins and a range of analogues on somatosensory responses of single identified dorsal horn neurons, when applied ionophoretically to the region of the substantia gelatinosa. Behavioural reflex tests of thermal nociception were carried out in parallel. ⋯ Evidence from receptor-selective antagonists supports that obtained with agonists for the roles of particular NK receptors in somatosensory processing. NK-2, but not NK-1 or NK-3 antagonists attenuated endogenous thermal nociceptive responses, supporting the hypothesis that an NK-2 agonist (such as NKA) may normally participate in expression of thermal nociception in the superficial dorsal horn. Behavioural experiments showing increased response latencies with a putative NK-2 selective antagonist further supported the involvement of NK-2 receptors in thermal nociception.
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The effects of hyper- and hypocapnia on oxidative metabolism were evaluated by near-infrared (NIR) multiwavelength spectroscopy in intact brain and skeletal muscle tissues of the anesthetized cat. A 3-wavelength NIR algorithm was used to monitor cytochrome a,a3 oxidation state, regional blood volume, and tissue oxyhemoglobin and O2 stores simultaneously in brain and muscle in ventilated animals. Incremental hypercapnia was produced in 10 cats by raising arterial pCO2 from 27.0 +/- 1.3 to 95.1 +/- 1.9 mmHg with inspired CO2. ⋯ Hypocapnia produced by hyperventilation in 8 cats lowered paCO2 from 28.5 +/- 0.4 to 13.5 +/- 0.5 mmHg. Hypocapnia decreased cerebral HbO2, blood volume, and cytochrome a,a3 redox level (P less than 0.05), but NIR changes were not seen in skeletal muscle. These experiments demonstrate preferential distribution of oxygen to brain during hypercapnia and the ability of NIR spectroscopy to assess regional oxygenation in multiple tissues non-invasively.