No description available.

No description available.

Convergent lines of research suggest there exists an excitatory cholinergic input to the substantia nigra from the pedunculopontine tegmental nucleus and possibly the laterodorsal tegmental nucleus. Previous work has suggested that microinjection of cholinergic agonists into substantia nigra elicits behaviours performed with a high frequency but with a low current rate (Winn 1991). Experiments carried out during my PhD have demonstrated that: Microinjection of cholinergic agonists to anterior substantia nigra (SN) elicited increased consumption of palatable food such as spaghetti but not rat maintenance diet in pre-satiated rats. Stimulation of behaviour was achieved using direct agonists for either muscarinic or nicotinic cholinergic receptors (carbachol and nicotine respectively). Stimulation of behaviour was also achieved using the indirect cholinergic agonist neostigmine which blocks the de-activation of endogenous acetylcholine by AChE. Increased feeding elicited by cholinergic stimulation of the anterior SN was abolished by a selective lesion of ascending dopamine (DA) neurones which significantly depleted caudate DA levels but left accumbens DA levels unaltered. A behaviourally potent dose of carbachol caused a significant increase in the response to different doses of nicotine suggesting an additive effect of muscarinic and nicotinic stimulation at the doses used. Administration of cholinergic agonists to the VTA or SN caused indistinguishable effects on responding for conditioned reinforcement. Cholinergic stimulation caused increased responding for a conditioned reinforcer and also reinstated responding at the primary reward source. The functional significance of the cholinergic innervation of the DA- containing neurones of the substantia nigra is discussed with reference to its relationship to the neighbouring ventral tegmental area, and their innervation of the caudate-putamen and the nucleus accumbens. Cholinergic neurones in the PPTg and LDTN appear to exert a tonic control over the activity of midbrain DA-containing neurones. It is suggested that cholinergic control of midbrain DA-containing neurones facilitates the processing of information in the striatum and hence influence the selection of an appropriate behavioural response to a given situation.

The role of the pedunculopontine tegmental nucleus (PPTg) in the control of behavioural processes was investigated in this thesis. This was achieved through examination of: (1) Conditioned place preference formation: PPTg lesioned rats were not impaired in forming an appropriate place preference, regardless of their deprivation state. (2) Reward-related responding: both food deprived and non-deprived lesioned rats displayed disinhibited intake across a gradient of sucrose rewards, the degree of disinhibition increasing as the reward became stronger. This disinhibited responding was disassociated from simple approach behaviour as shown by similar runway completion times across control and lesioned rats. (3) Radial arm maze performance: PPTg lesioned rats were impaired in their ability to retrospectively plan and forage in a random foraging task. This impairment was seen in both acquisition and retention tasks. PPTg lesioned rats were also impaired in the acquisition of a spatial working memory task in which they had to prospectively plan and execute responses. (4) These behavioural tasks are related to striatal output. To complement them anatomical experiments examining altered striatal outflow on neurotransmitter expression in the PPTg were conducted. Neither dopamine receptor blockade nor 6- hydroxydopamine (6-OHDA) lesions of striatal dopamine produced changes in nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase expression in the PPTg. This work did, however, lay the foundation for future experimentation to address this question. The combination of these findings extends current literature to outline a role for the PPTg in the control of complex behaviours that have been previously associated with sites higher up the neuraxis. This thesis demonstrates that removal of the PPTg results in behaviours that are inappropriate and disinhibited. In conclusion the PPTg is important for both accurate response selection and execution of goal directed behaviours, elements crucial for effective behavioural responding.

No description available.

No description available.

Abstract Recent studies demonstrated that LPS treated Sprague-Dawley rats induced a reduction (Phase I), followed by an augmentation (Phase II) and a secondary decrease (Phase III) in the power density of vasomotor components (0-0.8 Hz) in systemic arterial pressure signals. The molecular mechanisms underlie the progression toward death in the brain stem is unclear. In order to find out the differentially expressed genes between LPS-treated RVLM and saline-treated RVLM, we used suppression subtractive hybridization,a method commonly used to search differentially expressed genes, and subtractive cDNA library construction. At present, we have found some differentially expressed genes and these genes are up-regulation expression. These genes may be involved in the progression toward death in the rat brain stem.

Thesis (Ph. D.)--Biomedical Engineering, Georgia Institute of Technology, 2008. / LaPlaca, Michelle, Committee Chair ; McDevitt, Todd, Committee Member ; Lee, Robert, Committee Member ; Archer, David, Committee Member ; Lambert, Nevin, Committee Member.

Repeated, intense, cutaneous stimulation results in the gradual development of inhibition of spinal interneurones. This change in neuronal activity could not be demonstrated in rats whose spinal cords had been transected, and was considered to be the consequence of supraspinal mechanisms. . Experiments sere carried out to determine which areas of the brain were involved. Unitary recordings from neurones situated in nucleus reticularis pontis-caudalis, nucleus reticularis giganto-cellularis, nucleus reticularis parvocellularis and nucleus medulla oblongata pars ventralis demonstrated a progressively increasing excitatory response to repeated intense cutaneous stimulation. These areas were shown to have direct projections to the spinal cord, by retrograde transport of horseradish peroxidase. Cells in nucleus reticularis gigantocellularis, which demonstrated a progressively increasing excitatory response, could also be antidromically activated from the spinal cord. Repeated stimulation of some of these areas produced a progressive inhibition of spinal interneurones which was similar to that resulting from cutaneous stimulation. It would appear that nucleus reticularis gigantocellularis and nucleus reticularis pontis-caudalis are involved in the development of a progressive inhibition of spinal interneurones. A similar role for other reticular and raphe nuclei can not be excluded on the basis of evidence presently available. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

Signals for each of the five tastes have previously been shown to be processed by distinct labeled lines from taste receptor cells (TRCs) on the tongue to the ganglion neurons that innervate them. Furthermore, different tastes have been shown to be represented by distinct neurons in the taste cortex. We recorded calcium activity using fiber photometry from genetically defined populations in the mouse rostral nucleus of the solitary tract (rNST), the first brain station receiving taste signals from the tongue. We found that Somatostatin- (Sst) expressing cells respond exclusively to bitter chemicals while Calretinin- (Calb2) expressing cells respond exclusively to sweet chemicals. Immunostaining and viral strategies demonstrated that Sst and Calb2 mark distinct neuronal populations in the rNST. We then showed that optogenetic activation of Sst and Calb2 cells elicits prototypical bitter and sweet behaviors, respectively and demonstrate that ablation of these cells strongly impairs aversion to bitter tastants and attraction to sweet tastants, respectively. These findings reveal how taste information is propagated into the brain.