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13 Cards in this Set

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NTs discovered by Otto Loewi (1921) - looking at frog heart chambers. Saline solution appeared to transmit info between two chambers.

Criterion for NT: 1) produced within neuron 2) found within a neuron 3) when stimulated, neuron must release the NT, 4) when released it must act on post synaptic receptor and cause a biological effect 5) must be inactivated

Inactivation = reuptake mechanism or enzyme

Amino acids: glutamate and GABA
Biogenic Amines: acetylcholine, monoamines (serotonin and catcholamines - dopamine, noraderenaline, norepinephrine)

Peptides: Substance P
Others: ATP, Nitric Oxide

GLUTAMATE - excitatory NT - stimulate the neuron. Glu and GABA regulate whether a neuron is going to be stimulated or inhibited.

Used by multiple pathways - cortical association; coritco-thalamic; cortico-spinal; basal ganglia; hippocampal and cerebellar

PFC important for glutamate pathways - EF associated with PFC regions - abnormal NT pathways leading to these areas?

GLU binds to many different receptors - subtypes: NMDA, AMPA & Kainate, IONOTROPIC = control ion channels by receptors: regulate gate = VERY FAST

Metabotropic = Slower action: release of secondary messengers

Change neurotransmission - enhance synthesis, increase release, block reuptake, reduce metabolism (reduce enzymes which break them down) Drugs have many properties we can exploit to alter neurotransmission

S - over activity of Dopamine - pharmacologically reduce dopamine.

Drugs that block reupatke of Serotonin = anti-depressants (more release in synaptic cleft)

Amphetamine = blocks reuptake of dopamine (more in synaptic cleft)

Glutamate hypothesis - Kim (1980): reduced in cerebospinal fluid in S patients.

PCP and Ketamine (NMDA antagonists) produce both neg and pos symptoms of S

Genes can influence function of modulatory sites on the NMDA receptor or intra-cellular receptor interacting proteins which link glutamate receptors to signal transduction pathways (Harrison et al 2003; Moghaddam 2003)

Allelic variants of genes for Neuregeulin 1 (Stefansson et al 2002) influence the expression of NMDA receptors through activation of Erb4 receptors and GRM3 which encodes mGlu3 sybtype of metabotropic glutamate receptors (Egan et al 2004)

POST MORTEM - changes in glutamate receptor binding, transcription, subunit protein expression in PFC, thalamus and hippocampus of S patients (Clindon and Meador-Woodruff 2004)

Glutamate neurons regulate function of dopamine neurons - target of antipsychotic drugs - bursting of DA neurons (their response to environmental stimuli) is dependent on activation of NMDA receptors in these neurons

D2 receptors localised pre-synaptically on glutamate terminals and work to inhibit release of glutamate - reduced D2 receptor function produces increases in glutamate release

Regulation of DA dependent on glutamate function - reduce the function and there will be a misregulation of dopamine: potentially cause of psychoticism

Stahl (2007) - reduction in function of glutamate receptors linked to pos symptoms of S. Tonic inhibition: break on the DA pathway. Release the break and there is an overactivity of the system.

Dopamine Hypothesis - overactivity at dopaminergic synapses, likely in mesolimbic pathway coming from ventral tegmental area

SYNTHESIS = tyrosine + tyrosine hydrosylase = DOPA + DOPA decarboxylase = Dopamine + dopamine beta hydroxylase makes noradrenaline or monoamine oxidase to make DOPAC

Dorsal lateral PFC - working memory. Diff symptoms may be due to diff brain areas. Hypofunction in some tracts may lead to reduced activity.

Reduced NMDA receptor function - Neg and Cog affective symptoms

Redcued NMDA function in specific pathways - Pos symptoms - causing overactivity of dopamine

Overactivity at dopamine synapses and underactivity of NMDA important

Neg & Cog symptoms - pre frontal cortical regions (overactivity in the midbrain - original D2 hypothesis - may be due to underactivity in PFC.

Mesolimbic Dopamine Hypothesis - overactivity in midbrain regions is due to underactivity in PFC regions (due to glutamate reduction?)

Too little glutamate in mesolimbic region/too much in prefrontal region? D2 firing is observed in respective regions (rat studies)

Weinberger - extended dopamine hypothesis - pos symptoms caused by overactivity of dopaminergic synapses likely in mesolimbic pathway coming from VT area consequent to hypactivity at DA synapses in PFC regions

(neg & cog symptoms)

Loss of neurones in dorso-lateral PFC reduces its inhibitory effects on release of DA in NA - cause of neg symptoms?

DA Receptors
D1 = D1 and D5: activate neuron - activation of adenlyate cyclase

D2 = D2, D3 and D4: inhibition of adenlyate cyclase

Dependent on what it binds to - different effects

For S - D2 antagonists (block D2 receptors which are important for motor function)

D1 receptors most prevalent - in cerebal cortex and limbic system

D2 more selective - in hypothalamus